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pathway</title> <meta name="description" content="Search results for: signaling pathway"> <meta name="keywords" content="signaling pathway"> <meta name="viewport" content="width=device-width, initial-scale=1, minimum-scale=1, maximum-scale=1, user-scalable=no"> <meta charset="utf-8"> <link href="https://cdn.waset.org/favicon.ico" type="image/x-icon" rel="shortcut icon"> <link href="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/css/bootstrap.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/plugins/fontawesome/css/all.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/css/site.css?v=150220211555" rel="stylesheet"> </head> <body> <header> <div class="container"> <nav class="navbar navbar-expand-lg navbar-light"> <a class="navbar-brand" href="https://waset.org"> <img src="https://cdn.waset.org/static/images/wasetc.png" alt="Open Science Research Excellence" title="Open Science Research Excellence" /> </a> <button class="d-block d-lg-none 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action="https://publications.waset.org/abstracts/search"> <div id="custom-search-input"> <div class="input-group"> <i class="fas fa-search"></i> <input type="text" class="search-query" name="q" placeholder="Author, Title, Abstract, Keywords" value="signaling pathway"> <input type="submit" class="btn_search" value="Search"> </div> </div> </form> </div> </div> <div class="row mt-3"> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Commenced</strong> in January 2007</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Frequency:</strong> Monthly</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Edition:</strong> International</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Paper Count:</strong> 973</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: signaling pathway</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">973</span> Metabolomics Profile Recognition for Cancer Diagnostics</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Valentina%20L.%20Kouznetsova">Valentina L. Kouznetsova</a>, <a href="https://publications.waset.org/abstracts/search?q=Jonathan%20W.%20Wang"> Jonathan W. Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Igor%20F.%20Tsigelny"> Igor F. Tsigelny</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Metabolomics has become a rising field of research for various diseases, particularly cancer. Increases or decreases in metabolite concentrations in the human body are indicative of various cancers. Further elucidation of metabolic pathways and their significance in cancer research may greatly spur medicinal discovery. We analyzed the metabolomics profiles of lung cancer. Thirty-three metabolites were selected as significant. These metabolites are involved in 37 metabolic pathways delivered by MetaboAnalyst software. The top pathways are glyoxylate and dicarboxylate pathway (its hubs are formic acid and glyoxylic acid) along with Citrate cycle pathway followed by Taurine and hypotaurine pathway (the hubs in the latter are taurine and sulfoacetaldehyde) and Glycine, serine, and threonine pathway (the hubs are glycine and L-serine). We studied interactions of the metabolites with the proteins involved in cancer-related signaling networks, and developed an approach to metabolomics biomarker use in cancer diagnostics. Our analysis showed that a significant part of lung-cancer-related metabolites interacts with main cancer-related signaling pathways present in this network: PI3K–mTOR–AKT pathway, RAS–RAF–ERK1/2 pathway, and NFKB pathway. These results can be employed for use of metabolomics profiles in elucidation of the related cancer proteins signaling networks. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cancer" title="cancer">cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=metabolites" title=" metabolites"> metabolites</a>, <a href="https://publications.waset.org/abstracts/search?q=metabolic%20pathway" title=" metabolic pathway"> metabolic pathway</a>, <a href="https://publications.waset.org/abstracts/search?q=signaling%20pathway" title=" signaling pathway"> signaling pathway</a> </p> <a href="https://publications.waset.org/abstracts/54096/metabolomics-profile-recognition-for-cancer-diagnostics" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/54096.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">401</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">972</span> Network Based Molecular Profiling of Intracranial Ependymoma over Spinal Ependymoma</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hyeon%20Su%20Kim">Hyeon Su Kim</a>, <a href="https://publications.waset.org/abstracts/search?q=Sungjin%20Park"> Sungjin Park</a>, <a href="https://publications.waset.org/abstracts/search?q=Hae%20Ryung%20Chang"> Hae Ryung Chang</a>, <a href="https://publications.waset.org/abstracts/search?q=Hae%20Rim%20Jung"> Hae Rim Jung</a>, <a href="https://publications.waset.org/abstracts/search?q=Young%20Zoo%20Ahn"> Young Zoo Ahn</a>, <a href="https://publications.waset.org/abstracts/search?q=Yon%20Hui%20Kim"> Yon Hui Kim</a>, <a href="https://publications.waset.org/abstracts/search?q=Seungyoon%20Nam"> Seungyoon Nam</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Ependymoma, one of the most common parenchymal spinal cord tumor, represents 3-6% of all CNS tumor. Especially intracranial ependymomas, which are more frequent in childhood, have a more poor prognosis and more malignant than spinal ependymomas. Although there are growing needs to understand pathogenesis, detailed molecular understanding of pathogenesis remains to be explored. A cancer cell is composed of complex signaling pathway networks, and identifying interaction between genes and/or proteins are crucial for understanding these pathways. Therefore, we explored each ependymoma in terms of differential expressed genes and signaling networks. We used Microsoft Excel™ to manipulate microarray data gathered from NCBI’s GEO Database. To analyze and visualize signaling network, we used web-based PATHOME algorithm and Cytoscape. We show HOX family and NEFL are down-regulated but SCL family is up-regulated in cerebrum and posterior fossa cancers over a spinal cancer, and JAK/STAT signaling pathway and Chemokine signaling pathway are significantly different in the both intracranial ependymoma comparing to spinal ependymoma. We are considering there may be an age-dependent mechanism under different histological pathogenesis. We annotated mutation data of each gene subsequently in order to find potential target genes. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=systems%20biology" title="systems biology">systems biology</a>, <a href="https://publications.waset.org/abstracts/search?q=ependymoma" title=" ependymoma"> ependymoma</a>, <a href="https://publications.waset.org/abstracts/search?q=deg" title=" deg"> deg</a>, <a href="https://publications.waset.org/abstracts/search?q=network%20analysis" title=" network analysis"> network analysis</a> </p> <a href="https://publications.waset.org/abstracts/50168/network-based-molecular-profiling-of-intracranial-ependymoma-over-spinal-ependymoma" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/50168.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">298</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">971</span> Intensive Crosstalk between Autophagy and Intracellular Signaling Regulates Osteosarcoma Cell Survival Response under Cisplatin Stress</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Jyothi%20Nagraj">Jyothi Nagraj</a>, <a href="https://publications.waset.org/abstracts/search?q=Sudeshna%20Mukherjee"> Sudeshna Mukherjee</a>, <a href="https://publications.waset.org/abstracts/search?q=Rajdeep%20Chowdhury"> Rajdeep Chowdhury</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Autophagy has recently been linked with cancer cell survival post drug insult contributing to acquisition of resistance. However, the molecular signaling governing autophagic survival response is poorly explored. In our study, in osteosarcoma (OS) cells cisplatin shock was found to activate both MAPK and autophagy signaling. An activation of JNK and autophagy acted as pro-survival strategy, while ERK1/2 triggered apoptotic signals upon cisplatin stress. An increased sensitivity of the cells to cisplatin was obtained with simultaneous inhibition of both autophagy and JNK pathway. Furthermore, we observed that the autophagic stimulation upon drug stress regulates other developmentally active signaling pathways like the Hippo pathway in OS cells. Cisplatin resistant cells were thereafter developed by repetitive drug exposure followed by clonal selection. Basal levels of autophagy were found to be high in resistant cells to. However, the signaling mechanism leading to autophagic up-regulation and its regulatory effect differed in OS cells upon attaining drug resistance. Our results provide valuable clues to regulatory dynamics of autophagy that can be considered for development of improved therapeutic strategy against resistant type cancers. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=JNK" title="JNK">JNK</a>, <a href="https://publications.waset.org/abstracts/search?q=autophagy" title=" autophagy"> autophagy</a>, <a href="https://publications.waset.org/abstracts/search?q=drug%20resistance" title=" drug resistance"> drug resistance</a>, <a href="https://publications.waset.org/abstracts/search?q=cancer" title=" cancer"> cancer</a> </p> <a href="https://publications.waset.org/abstracts/63712/intensive-crosstalk-between-autophagy-and-intracellular-signaling-regulates-osteosarcoma-cell-survival-response-under-cisplatin-stress" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/63712.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">290</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">970</span> Photobiomodulation Activates WNT/β-catenin Signaling for Wound Healing in an in Vitro Diabetic Wound Model</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Dimakatso%20B.%20Gumede">Dimakatso B. Gumede</a>, <a href="https://publications.waset.org/abstracts/search?q=Nicolette%20N.%20Houreld"> Nicolette N. Houreld</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Diabetic foot ulcers (DFUs) are a complication of diabetes mellitus (DM), a metabolic disease caused by insulin resistance or insufficiency, resulting in hyperglycaemia and low-grade chronic inflammation. Current therapies for treating DFUs include wound debridement, glycaemic control, and wound dressing. However, these therapies are moderately effective as there is a recurrence of these ulcers and an increased risk of lower limb amputations. Photobiomodulation (PBM), which is the application of non-invasive low-level light for wound healing at the spectrum of 660-1000 nm, has shown great promise in accelerating the healing of chronic wounds. However, its underlying mechanisms are not clearly defined. Studies have indicated that PBM induces wound healing via the activation of signaling pathways that are involved in tissue repair, such as the transforming growth factor-β (TGF-β). However, other signaling pathways, such as the WNT/β-catenin pathway, which is also critical for wound repair, have not been investigated. This study aimed to elucidate if PBM at 660 nm and a fluence of 5 J/cm² activates the WNT/β-catenin signaling pathway for wound healing in a diabetic cellular model. Human dermal fibroblasts (WS1) were continuously cultured high-glucose (26.5 mM D-glucose) environment to create a diabetic cellular model. A central scratch was created in the diabetic model to ‘wound’ the cells. The diabetic wounded (DW) cells were thereafter irradiated at 660 nm and a fluence of 5 J/cm². Cell migration, gene expression and protein assays were conducted at 24- and 48-h post-PBM. The results showed that PBM at 660 nm and a fluence of 5 J/cm² significantly increased cell migration in diabetic wounded cells at 24-h post-PBM. The expression of CTNNB1, ACTA2, COL1A1 and COL3A1 genes was also increased in DW cells post-PBM. Furthermore, there was increased cytoplasmic accumulation and nuclear localization of β-catenin at 24 h post-PBM. The findings in this study demonstrate that PBM activates the WNT/β-catenin signaling pathway by inducing the accumulation of β-catenin in diabetic wounded cells, leading to increased cell migration and expression of wound repair markers. These results thus indicate that PBM has the potential to improve wound healing in diabetic ulcers via activation of the WNT/β-catenin signaling pathway. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=wound%20healing" title="wound healing">wound healing</a>, <a href="https://publications.waset.org/abstracts/search?q=diabetic%20ulcers" title=" diabetic ulcers"> diabetic ulcers</a>, <a href="https://publications.waset.org/abstracts/search?q=photobiomodulation" title=" photobiomodulation"> photobiomodulation</a>, <a href="https://publications.waset.org/abstracts/search?q=WNT%2F%CE%B2-catenin" title=" WNT/β-catenin"> WNT/β-catenin</a>, <a href="https://publications.waset.org/abstracts/search?q=signalling%20pathway" title=" signalling pathway"> signalling pathway</a> </p> <a href="https://publications.waset.org/abstracts/188444/photobiomodulation-activates-wntv-catenin-signaling-for-wound-healing-in-an-in-vitro-diabetic-wound-model" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/188444.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">40</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">969</span> TNF Receptor-Associated Factor 6 (TRAF6) Mediating the Angiotensin-Induced Non-Canonical TGFβ Pathway Activation and Differentiation of c-kit+ Cardiac Stem Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Qing%20Cao">Qing Cao</a>, <a href="https://publications.waset.org/abstracts/search?q=Fei%20Wang"> Fei Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yu-Qiang%20Wang"> Yu-Qiang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Li-Ya%20Huang"> Li-Ya Huang</a>, <a href="https://publications.waset.org/abstracts/search?q=Tian-Tian%20Sang"> Tian-Tian Sang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shu-Yan%20Chen"> Shu-Yan Chen</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Aims: TNF Receptor-Associated Factor 6 (TRAF6) acts as a multifunctional regulator of the Transforming Growth Factor (TGF)-β signaling pathway, and mediates Smad-independent JNK and p38 activation via TGF-β. This study was performed to test the hypothesis that TGF-β/TRAF6 is essential for angiotensin-II (Ang II)-induced differentiation of rat c-kit+ Cardiac Stem Cells (CSCs). Methods and Results: c-kit+ CSCs were isolated from neonatal Sprague Dawley (SD) rats, and their c-kit status was confirmed with immunofluorescence staining. A TGF-β type I receptor inhibitor (SB431542) or the small interfering RNA (siRNA)-mediated knockdown of TRAF6 were used to investigate the role of TRAF6 in TGF-β signaling. Rescue of TRAF6 siRNA transfected cells with a 3'UTR deleted siRNA insensitive construct was conducted to rule out the off target effects of the siRNA. TRAF6 dominant negative (TRAF6DN) vector was constructed and used to infect c-kit+ CSCs, and western blotting was used to assess the expression of TRAF6, JNK, p38, cardiac-specific proteins, and Wnt signaling proteins. Physical interactions between TRAF6 and TGFβ receptors were studied by coimmunoprecipitation. Cardiac differentiation was suppressed in the absence of TRAF6. Forced expression of TRAF6 enhanced the expression of TGF-β-activated kinase1 (TAK1), and inhibited Wnt signaling. Furthermore, TRAF6 increased the expression of cardiac-specific proteins (cTnT and Cx-43) but inhibited the expression of Wnt3a. Conclusions: Our data suggest that TRAF6 plays an important role in Ang II induced differentiation of c-kit+ CSCs via the non-canonical signaling pathway. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cardiac%20stem%20cells" title="cardiac stem cells">cardiac stem cells</a>, <a href="https://publications.waset.org/abstracts/search?q=differentiation" title=" differentiation"> differentiation</a>, <a href="https://publications.waset.org/abstracts/search?q=TGF-%CE%B2" title=" TGF-β"> TGF-β</a>, <a href="https://publications.waset.org/abstracts/search?q=TRAF6" title=" TRAF6"> TRAF6</a>, <a href="https://publications.waset.org/abstracts/search?q=ubiquitination" title=" ubiquitination"> ubiquitination</a>, <a href="https://publications.waset.org/abstracts/search?q=Wnt" title=" Wnt"> Wnt</a> </p> <a href="https://publications.waset.org/abstracts/10048/tnf-receptor-associated-factor-6-traf6-mediating-the-angiotensin-induced-non-canonical-tgfv-pathway-activation-and-differentiation-of-c-kit-cardiac-stem-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/10048.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">401</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">968</span> Competition Between the Effects of Pesticides and Immune-activation on the Expression of Toll Pathway Genes</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Dani%20Sukkar">Dani Sukkar</a>, <a href="https://publications.waset.org/abstracts/search?q=Ali%20Kanso"> Ali Kanso</a>, <a href="https://publications.waset.org/abstracts/search?q=Philippe%20Laval-Gilly"> Philippe Laval-Gilly</a>, <a href="https://publications.waset.org/abstracts/search?q=Jairo%20Falla-Angel"> Jairo Falla-Angel</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The honeybees' immune system is challenged by different risk factors that induce various responses. However, complex scenarios where bees are exposed to different pesticides simultaneously with immune activation are not well evaluated. The Toll pathway is one of the main signaling pathways studied in invertebrate immune responses, and it is a good indicator of the effect of such complex interactions in addition to key signaling elements of other pathways like Relish of the immune deficiency (IMD) pathway or Eater, the phagocytosis receptor or vitellogenin levels. Honeybee hemocytes extracted from 5th instar larvae were exposed to imidacloprid and/or amitraz with or without the presence of the zymosan a as an immune activator. The gene expression of multiple immune related genes were studied, including spaetzle, Toll, myD88, relish, eater and vitellogenin, by real-time polymerase chain reaction after RNA extraction. The results demonstrated that the Toll pathway is mainly affected by the pesticides; imidacloprid and amitraz, especially by their different combinations. Furthermore, immune activation by zymosan A, a fungal cell-wall component, acts to mitigate to some extent the effect of pesticides on the different levels of the Toll pathway. In addition, imidacloprid, amitraz, and zymosan A have complex and context-specific interactions depending on the levels of immune activation and the pathway evaluated affecting immune-gene expression differently. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=toll%20pathway" title="toll pathway">toll pathway</a>, <a href="https://publications.waset.org/abstracts/search?q=immune%20modulation" title=" immune modulation"> immune modulation</a>, <a href="https://publications.waset.org/abstracts/search?q=%CE%B2-glucan" title=" β-glucan"> β-glucan</a>, <a href="https://publications.waset.org/abstracts/search?q=imidacloprid" title=" imidacloprid"> imidacloprid</a>, <a href="https://publications.waset.org/abstracts/search?q=amitraz" title=" amitraz"> amitraz</a>, <a href="https://publications.waset.org/abstracts/search?q=honeybees" title=" honeybees"> honeybees</a>, <a href="https://publications.waset.org/abstracts/search?q=immune%20genes" title=" immune genes"> immune genes</a> </p> <a href="https://publications.waset.org/abstracts/172811/competition-between-the-effects-of-pesticides-and-immune-activation-on-the-expression-of-toll-pathway-genes" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/172811.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">87</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">967</span> Computational Identification of Signalling Pathways in Protein Interaction Networks</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Angela%20U.%20Makolo">Angela U. Makolo</a>, <a href="https://publications.waset.org/abstracts/search?q=Temitayo%20A.%20Olagunju"> Temitayo A. Olagunju</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The knowledge of signaling pathways is central to understanding the biological mechanisms of organisms since it has been identified that in eukaryotic organisms, the number of signaling pathways determines the number of ways the organism will react to external stimuli. Signaling pathways are studied using protein interaction networks constructed from protein-protein interaction data obtained using high throughput experimental procedures. However, these high throughput methods are known to produce very high rates of false positive and negative interactions. In order to construct a useful protein interaction network from this noisy data, computational methods are applied to validate the protein-protein interactions. In this study, a computational technique to identify signaling pathways from a protein interaction network constructed using validated protein-protein interaction data was designed. A weighted interaction graph of the Saccharomyces cerevisiae (Baker’s Yeast) organism using the proteins as the nodes and interactions between them as edges was constructed. The weights were obtained using Bayesian probabilistic network to estimate the posterior probability of interaction between two proteins given the gene expression measurement as biological evidence. Only interactions above a threshold were accepted for the network model. A pathway was formalized as a simple path in the interaction network from a starting protein and an ending protein of interest. We were able to identify some pathway segments, one of which is a segment of the pathway that signals the start of the process of meiosis in S. cerevisiae. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Bayesian%20networks" title="Bayesian networks">Bayesian networks</a>, <a href="https://publications.waset.org/abstracts/search?q=protein%20interaction%20networks" title=" protein interaction networks"> protein interaction networks</a>, <a href="https://publications.waset.org/abstracts/search?q=Saccharomyces%20cerevisiae" title=" Saccharomyces cerevisiae"> Saccharomyces cerevisiae</a>, <a href="https://publications.waset.org/abstracts/search?q=signalling%20pathways" title=" signalling pathways"> signalling pathways</a> </p> <a href="https://publications.waset.org/abstracts/22095/computational-identification-of-signalling-pathways-in-protein-interaction-networks" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/22095.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">543</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">966</span> Genome-Wide Functional Analysis of Phosphatase in Cryptococcus neoformans</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Jae-Hyung%20Jin">Jae-Hyung Jin</a>, <a href="https://publications.waset.org/abstracts/search?q=Kyung-Tae%20Lee"> Kyung-Tae Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=Yee-Seul%20So"> Yee-Seul So</a>, <a href="https://publications.waset.org/abstracts/search?q=Eunji%20Jeong"> Eunji Jeong</a>, <a href="https://publications.waset.org/abstracts/search?q=Yeonseon%20Lee"> Yeonseon Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=Dongpil%20Lee"> Dongpil Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=Dong-Gi%20Lee"> Dong-Gi Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=Yong-Sun%20Bahn"> Yong-Sun Bahn</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Cryptococcus neoformans causes cryptococcal meningoencephalitis mainly in immunocompromised patients as well as immunocompetent people. But therapeutic options are limited to treat cryptococcosis. Some signaling pathways including cyclic AMP pathway, MAPK pathway, and calcineurin pathway play a central role in the regulation of the growth, differentiation, and virulence of C. neoformans. To understand signaling networks regulating the virulence of C. neoformans, we selected the 114 putative phosphatase genes, one of the major components of signaling networks, in the genome of C. neoformans. We identified putative phosphatases based on annotation in C. neoformans var. grubii genome database provided by the Broad Institute and National Center for Biotechnology Information (NCBI) and performed a BLAST search of phosphatases of Saccharomyces cerevisiae, Aspergillus nidulans, Candida albicans and Fusarium graminearum to Cryptococcus neoformans. We classified putative phosphatases into 14 groups based on InterPro phosphatase domain annotation. Here, we constructed 170 signature-tagged gene-deletion strains through homologous recombination methods for 91 putative phosphatases. We examined their phenotypic traits under 30 different in vitro conditions, including growth, differentiation, stress response, antifungal resistance and virulence-factor production. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=human%20fungal%20pathogen" title="human fungal pathogen">human fungal pathogen</a>, <a href="https://publications.waset.org/abstracts/search?q=phosphatase" title=" phosphatase"> phosphatase</a>, <a href="https://publications.waset.org/abstracts/search?q=deletion%20library" title=" deletion library"> deletion library</a>, <a href="https://publications.waset.org/abstracts/search?q=functional%20genomics" title=" functional genomics"> functional genomics</a> </p> <a href="https://publications.waset.org/abstracts/63313/genome-wide-functional-analysis-of-phosphatase-in-cryptococcus-neoformans" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/63313.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">364</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">965</span> Sirt1 Promotes C2C12 Myoblast Cell Proliferation by Myostatin Signaling Pathway</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang">Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun"> Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Ruilin%20Xue"> Ruilin Xue</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Backgrounds: Previous studies showed that Sirt1 plays an important role in C2C12 myoblast cell proliferation, but the mechanism(s) involved in this process remains unclear. This work was undertaken to determine if Myostatin participates in the regulation of C2C12 proliferation by Sirt1. Methods: We administrated the Sirt1 activator resveratrol, inhibitor Nicotinamide (NAM) and Myostatin inhibitor SB431542 on C2C12 myoblast cells. Cell viability was evaluated by CCK8 assay. The expression of Sirt1 and MyoD were detected by qRT-PCR. Utilizing western blot to determinate the expression of myostatin, P107 and p-P107. Results: Our results showed that resveratrol promoted the proliferation of C2C12 myoblast cells, while NAM suppressed the proliferation of C2C12 myoblast cells; SB431542 promoted the proliferation of C2C12 myoblast cells and attenuated the inhibition effect of NAM on C2C12 myoblast cells proliferation; Resveratrol can significantly increase the expression of Sirt1 and MyoD, decrease the expression of Myostatin, while NAM can significantly down-regulate the expression of Sirt1, MyoD and the phosphorylation of P107(p-P107), but up-regulate the expression of Myostatin and the protein P107; SB431542 can significantly mitigate the effect of NAM on the expression of MyoD, P107, and p-P107. Conclusions: Taken together, these results indicate that Sirt1 promotes the proliferation of C2C12 myoblast cells via Myostatin signaling pathway. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sirt1" title="Sirt1">Sirt1</a>, <a href="https://publications.waset.org/abstracts/search?q=C2C12%20cells" title=" C2C12 cells"> C2C12 cells</a>, <a href="https://publications.waset.org/abstracts/search?q=proliferation" title=" proliferation"> proliferation</a>, <a href="https://publications.waset.org/abstracts/search?q=myostatin%20signaling%20pathway" title=" myostatin signaling pathway "> myostatin signaling pathway </a> </p> <a href="https://publications.waset.org/abstracts/21780/sirt1-promotes-c2c12-myoblast-cell-proliferation-by-myostatin-signaling-pathway" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/21780.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">450</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">964</span> Neuroprotective Effect of Tangeretin against Potassium Dichromate-Induced Acute Brain Injury via Modulating AKT/Nrf2 Signaling Pathway in Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ahmed%20A.%20Sedik">Ahmed A. Sedik</a>, <a href="https://publications.waset.org/abstracts/search?q=Doaa%20Mahmoud%20Shuaib"> Doaa Mahmoud Shuaib</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Brain injury is a cause of disability and death worldwide. Potassium dichromate (PD) is an environmental contaminant widely recognized as teratogenic, carcinogenic, and mutagenic towards animals and humans. The aim of the present study was to investigate the possible neuroprotective effects of tangeretin (TNG) on PD-induced brain injury in rats. Forty male adult Wistar rats were randomly and blindly allocated into four groups (8 rats /group). The first group received saline intranasally (i.n.). The second group received a single dose of PD (2 mg/kg, i.n.). The third group received TNG (50 mg/kg; orally) for 14 days, followed by i.n. of PD on the last day of the experiment. Four groups received TNG (100 mg/kg; orally) for 14 days, followed by i.n. of PD on the last day of the experiment. 18- hours after the final treatment, behavioral parameters, neuro-biochemical indices, FTIR analysis, and histopathological studies were evaluated. Results of the present study revealed that rats intoxicated with PD promoted oxidative stress and inflammation via an increase in MDA and a decrease in Nrf2 signaling pathway and GSH levels with an increase in brain contents of TNF-α, IL-10, and NF-kβ and reduced AKT levels in brain homogenates. Treatment with TNG (100 mg/kg; orally) ameliorated behavioral, cholinergic activities and oxidative stress, decreased the elevated levels of pro-inflammatory mediators; TNF-α, IL-10, and NF-κβ elevated AKT pathway with corrected FTIR spectra with a decrease in brain content of chromium residues detected by atomic absorption spectrometry. Also, TNG administration restored the morphological changes as degenerated neurons and necrosis associated with PD intoxication. Additionally, TNG decreased Caspase-3 expression in the brain of PD rats. TNG plays a crucial role in AKT/Nrf2 pathway that is responsible for their antioxidant, anti-inflammatory effects, and apoptotic pathway against PD-induced brain injury in rats. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=tangeretin" title="tangeretin">tangeretin</a>, <a href="https://publications.waset.org/abstracts/search?q=potassium%20dichromate" title=" potassium dichromate"> potassium dichromate</a>, <a href="https://publications.waset.org/abstracts/search?q=brain%20injury" title=" brain injury"> brain injury</a>, <a href="https://publications.waset.org/abstracts/search?q=AKT%2FNrf2%20signaling%20pathway" title=" AKT/Nrf2 signaling pathway"> AKT/Nrf2 signaling pathway</a>, <a href="https://publications.waset.org/abstracts/search?q=FTIR" title=" FTIR"> FTIR</a>, <a href="https://publications.waset.org/abstracts/search?q=atomic%20absorption%20spectrometry" title=" atomic absorption spectrometry"> atomic absorption spectrometry</a> </p> <a href="https://publications.waset.org/abstracts/155926/neuroprotective-effect-of-tangeretin-against-potassium-dichromate-induced-acute-brain-injury-via-modulating-aktnrf2-signaling-pathway-in-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/155926.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">103</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">963</span> Sulforaphane Attenuates Fibrosis of Dystrophic Muscle in Mdx Mice via Nrf2-Mediated Inhibition of TGF-β/Smad Signaling</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Ruilin%20Xue"> Ruilin Xue</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Backgrounds: A few lines of evidence show that Sulforaphane (SFN) has anti-fibrosis effect in liver tissue via Nrf2-mediated inhibition of TGF-β/Smad signaling. However, its effects on muscular dystrophic fibrosis remain unknown. This work was undertaken to evaluate the effects of SFN on fibrosis in dystrophic muscle. Methods: 3-month-old male mdx mice were treated with SFN by gavage (2 mg/kg body weight per day) for 3 months. Gastrocnemius, tibial anterior and triceps brachii muscles were collected for related analysis. Fibrosis in skeletal muscles was analyzed by Sirius red staining. Histology and morphology of skeletal muscles were investigated by H&E staining. Moreover, the expressions of Nrf2, NQO1, HO-1, and TGF-β/Smad signaling pathway were detected by western blot, qRT-PCR, immunohistochemistry and immunofluorescence assays. Results: Our results demonstrated that SFN treatment significantly decreased and improved morphological features in mdx muscles. Moreover, SFN increased the expression of muscle phase II enzymes NQO1 and HO-1 and significantly decreased the expression of TGF-β1，p-smad2, p-smad3, α-SMA, fibronectin, collagen I, PAI-1, and TIMP-1 in Nrf2 dependent manner. Additionally, SFN significantly decreased the expression of CD45 and TNF-α. Conclusions: Collectively, these results show that SFN can ameliorate muscle fibrosis in mdx mice by Nrf2-induced inhibition of TGF-β/Smad signaling pathway, which indicate Nrf2 may be useful for the treatment of muscular dystrophy. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sulforaphane" title="sulforaphane">sulforaphane</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=TGF-%CE%B2%2Fsmad%20signaling" title=" TGF-β/smad signaling"> TGF-β/smad signaling</a>, <a href="https://publications.waset.org/abstracts/search?q=duchenne%20muscular%20dystrophy" title=" duchenne muscular dystrophy"> duchenne muscular dystrophy</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title=" fibrosis"> fibrosis</a> </p> <a href="https://publications.waset.org/abstracts/19674/sulforaphane-attenuates-fibrosis-of-dystrophic-muscle-in-mdx-mice-via-nrf2-mediated-inhibition-of-tgf-vsmad-signaling" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/19674.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">441</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">962</span> Evaluation of Important Transcription Factors and Kinases in Regulating the Signaling Pathways of Cancer Stem Cells With Low and High Proliferation Rate Derived From Colorectal Cancer</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mohammad%20Hossein%20Habibi">Mohammad Hossein Habibi</a>, <a href="https://publications.waset.org/abstracts/search?q=Atena%20Sadat%20Hosseini"> Atena Sadat Hosseini</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Colorectal cancer is the third leading cause of cancer-related death in the world. Colorectal cancer screening, early detection, and treatment programs could benefit from the most up-to-date information on the disease's burden, given the present worldwide trend of increasing colorectal cancer incidence. Tumor recurrence and resistance are exacerbated by the presence of chemotherapy-resistant cancer stem cells that can generate rapidly proliferating tumor cells. In addition, tumor cells can evolve chemoresistance through adaptation mechanisms. In this work, we used in silico analysis to select suitable GEO datasets. In this study, we compared slow-growing cancer stem cells with high-growth colorectal cancer-derived cancer stem cells. We then evaluated the signal pathways, transcription factors, and kinases associated with these two types of cancer stem cells. A total of 980 upregulated genes and 870 downregulated genes were clustered. MAPK signaling pathway, AGE-RAGE signaling pathway in diabetic complications, Fc gamma R-mediated phagocytosis, and Steroid biosynthesis signaling pathways were observed in upregulated genes. Also, caffeine metabolism, amino sugar and nucleotide sugar metabolism, TNF signaling pathway, and cytosolic DNA-sensing pathway were involved in downregulated genes. In the next step, we evaluated the best transcription factors and kinases in two types of cancer stem cells. In this regard, NR2F2, ZEB2, HEY1, and HDGF as transcription factors and PRDM5, SMAD, CBP, and KDM2B as critical kinases in upregulated genes. On the other hand, IRF1, SPDEF, NCOA1, and STAT1 transcription factors and CTNNB1 and CDH7 kinases were regulated low expression genes. Using bioinformatics analysis in the present study, we conducted an in-depth study of colorectal cancer stem cells at low and high growth rates so that we could take further steps to detect and even target these cells. Naturally, more additional tests are needed in this direction. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=colorectal%20cancer" title="colorectal cancer">colorectal cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=bioinformatics%20analysis" title=" bioinformatics analysis"> bioinformatics analysis</a>, <a href="https://publications.waset.org/abstracts/search?q=transcription%20factor" title=" transcription factor"> transcription factor</a>, <a href="https://publications.waset.org/abstracts/search?q=kinases" title=" kinases"> kinases</a>, <a href="https://publications.waset.org/abstracts/search?q=cancer%20stem%20cells" title=" cancer stem cells"> cancer stem cells</a> </p> <a href="https://publications.waset.org/abstracts/149949/evaluation-of-important-transcription-factors-and-kinases-in-regulating-the-signaling-pathways-of-cancer-stem-cells-with-low-and-high-proliferation-rate-derived-from-colorectal-cancer" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/149949.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">126</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">961</span> Stem Cell Differentiation Toward Secretory Progenitors after Intestinal Ischemia-Reperfusion in a Rat is Accompanied by Inhibited Notch Signaling Cascade</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Igor%20Sukhotnik">Igor Sukhotnik</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Objectives: Notch signaling is thought to act to drive cell versification in the lining of the small intestine. When Notch signaling is blocked, proliferation ceases, and epithelial cells become secretory. The purpose of the present study was to evaluate the role of Notch signaling pathway in stem cell differentiation in a rat model of intestinal ischemia-reperfusion (IR). Methods: Male Sprague-Dawley rats were randomly divided into four experimental groups: Sham-24 and Sham-48 rats underwent laparotomy and were killed 24 or 48 h later, respectively; IR-24 and IR-48 rats underwent occlusion of SMA and portal vein for 30 min followed by 24 or 48 h of reperfusion, respectively. Notch-related gene and protein expression were determined using Real Time PCR, Western blotting and immunohistochemistry. Wax histology and immunohistochemistry was used to determine cell differentiation toward absorptive (enterocytes) or secretory progenitors (goblet cells, enteroendocrine cells or Paneth cells). Results: IR-48 rats exhibited a significant decrease in Notch-1 protein expression (Western blot) that was coincided with a significant decrease in the number of Notch-1 positive cells (immunohistochemistry) in jejunum and ileum as well as Hes-1 positive cells in jejunum and ileum compared to Sham-48 rats. A significant down-regulation of Notch signaling related genes and proteins in IR animals was accompanied by a significant increase in the number of goblet and Paneth cells and decreased number of absorptive cells compared to control rats. Conclusions: Forty-eight hours following intestinal IR in rats, inhibited Notch signaling pathway was accompanied by intestinal stem cells differentiation toward secretory progenitors. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Intestine" title="Intestine">Intestine</a>, <a href="https://publications.waset.org/abstracts/search?q=notch" title=" notch"> notch</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemia-reperfusion" title=" ischemia-reperfusion"> ischemia-reperfusion</a>, <a href="https://publications.waset.org/abstracts/search?q=cell%20differentiation" title=" cell differentiation"> cell differentiation</a>, <a href="https://publications.waset.org/abstracts/search?q=secretory" title=" secretory"> secretory</a> </p> <a href="https://publications.waset.org/abstracts/170973/stem-cell-differentiation-toward-secretory-progenitors-after-intestinal-ischemia-reperfusion-in-a-rat-is-accompanied-by-inhibited-notch-signaling-cascade" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/170973.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">58</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">960</span> A Novel Application of CORDYCEPIN (Cordycepssinensis Extract): Maintaining Stem Cell Pluripotency and Improving iPS Generation Efficiency</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Shih-Ping%20Liu">Shih-Ping Liu</a>, <a href="https://publications.waset.org/abstracts/search?q=Cheng-Hsuan%20Chang"> Cheng-Hsuan Chang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yu-Chuen%20Huang"> Yu-Chuen Huang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shih-Yin%20Chen"> Shih-Yin Chen</a>, <a href="https://publications.waset.org/abstracts/search?q=Woei-Cherng%20Shyu"> Woei-Cherng Shyu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Embryonic stem cells (ES) and induced pluripotnet stem cells (iPS) are both pluripotent stem cells. For mouse stem cells culture technology, leukemia inhibitory factor (LIF) was used to maintain the pluripotency of stem cells in vitro. However, LIF is an expensive reagent. The goal of this study was to find out a pure compound extracted from Chinese herbal medicine that could maintain stem cells pluripotency to replace LIF and improve the iPS generation efficiency. From 20 candidates traditional Chinese medicine we found that Cordycepsmilitaris triggered the up-regulation of stem cells activating genes (Oct4 and Sox2) expression levels in MEF cells. Cordycepin, a major active component of Cordycepsmilitaris, also could up-regulate Oct4 and Sox2 gene expression. Furthermore, we used ES and iPS cells and treated them with different concentrations of Cordycepin (replaced LIF in the culture medium) to test whether it was useful to maintain the pluripotency. The results showed higher expression levels of several stem cells markers in 10 μM Cordycepin-treated ES and iPS cells compared to controls that did not contain LIF, including alkaline phosphatase, SSEA1, and Nanog. Embryonic body formation and differentiation confirmed that 10 μM Cordycepin-containing medium was capable to maintain stem cells pluripotency after four times passages. For mechanism analysis, microarray analysis indicated extracellular matrix and Jak/Stat signaling pathway as the top two deregulated pathways. In ECM pathway, we determined that the integrin αVβ5 expression levels and phosphorylated Src levels increased after Cordycepin treatment. In addition, the phosphorylated Jak2 and phosphorylated Sat3 protein levels were increased after Cordycepin treatment and suppressed with the Jak2 inhibitor, AG490. The expression of cytokines associated with Jak2/Stat3 signaling pathway were also up-regulated by Q-PCR and ELISA assay. Lastly, we used Oct4-GFP MEF cells to test iPS generation efficiency following Cordycepin treatment. We observed that 10 Μm Cordycepin significantly increased the iPS generation efficiency in day 21. In conclusion, we demonstrated Cordycepin could maintain the pluripotency of stem cells through both of ECM and Jak2/Stat3 signaling pathway and improved iPS generation efficiency. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cordycepin" title="cordycepin">cordycepin</a>, <a href="https://publications.waset.org/abstracts/search?q=iPS%20cells" title=" iPS cells"> iPS cells</a>, <a href="https://publications.waset.org/abstracts/search?q=Jak2%2FStat3%20signaling%20pathway" title=" Jak2/Stat3 signaling pathway"> Jak2/Stat3 signaling pathway</a>, <a href="https://publications.waset.org/abstracts/search?q=molecular%20biology" title=" molecular biology"> molecular biology</a> </p> <a href="https://publications.waset.org/abstracts/6862/a-novel-application-of-cordycepin-cordycepssinensis-extract-maintaining-stem-cell-pluripotency-and-improving-ips-generation-efficiency" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/6862.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">438</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">959</span> Therapeutic Effects of Toll Like Receptor 9 Ligand CpG-ODN on Radiation Injury</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Jianming%20Cai">Jianming Cai</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Exposure to ionizing radiation causes severe damage to human body and an safe and effective radioprotector is urgently required for alleviating radiation damage. In 2008, flagellin, an agonist of TLR5, was found to exert radioprotective effects on radiation injury through activating NF-kB signaling pathway. From then, the radioprotective effects of TLR ligands has shed new lights on radiation protection. CpG-ODN is an unmethylated oligonucleotide which activates TLR9 signaling pathway. In this study, we demonstrated that CpG-ODN has therapeutic effects on radiation injuries induced by γ ray and 12C6+ heavy ion particles. Our data showed that CpG-ODN increased the survival rate of mice after whole body irradiation and increased the number of leukocytes as well as the bone marrow cells. CpG-ODN also alleviated radiation damage on intestinal crypt through regulating apoptosis signaling pathway including bcl2, bax, and caspase 3 etc. By using a radiation-induced pulmonary fibrosis model, we found that CpG-ODN could alleviate structural damage, within 20 week after whole–thorax 15Gy irradiation. In this model, Th1/Th2 imbalance induced by irradiation was also reversed by CpG-ODN. We also found that TGFβ-Smad signaling pathway was regulated by CpG-ODN, which accounts for the therapeutic effects of CpG-ODN in radiation-induced pulmonary injury. On another hand, for high LET radiation protection, we investigated protective effects of CpG-ODN against 12C6+ heavy ion irradiation and found that after CpG-ODN treatment, the apoptosis and cell cycle arrest induced by 12C6+ irradiation was reduced. CpG-ODN also reduced the expression of Bax and caspase 3, while increased the level of bcl2. Then we detected the effect of CpG-ODN on heavy ion induced immune dysfunction. Our data showed that CpG-ODN increased the survival rate of mice and also the leukocytes after 12C6+ irradiation. Besides, the structural damage of immune organ such as thymus and spleen was also alleviated by CpG-ODN treatment. In conclusion, we found that TLR9 ligand, CpG-ODN reduced radiation injuries in response to γ ray and 12C6+ heavy ion irradiation. On one hand, CpG-ODN inhibited the activation of apoptosis induced by radiation through regulating bcl2, bax and caspase 3. On another hand, through activating TLR9, CpG-ODN recruit MyD88-IRAK-TRAF6 complex, activating TAK1, IRF5 and NF-kB pathway, and thus alleviates radiation damage. This study provides novel insights into protection and therapy of radiation damages. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=TLR9" title="TLR9">TLR9</a>, <a href="https://publications.waset.org/abstracts/search?q=CpG-ODN" title=" CpG-ODN"> CpG-ODN</a>, <a href="https://publications.waset.org/abstracts/search?q=radiation%20injury" title=" radiation injury"> radiation injury</a>, <a href="https://publications.waset.org/abstracts/search?q=high%20LET%20radiation" title=" high LET radiation"> high LET radiation</a> </p> <a href="https://publications.waset.org/abstracts/35124/therapeutic-effects-of-toll-like-receptor-9-ligand-cpg-odn-on-radiation-injury" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/35124.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">480</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">958</span> Unravelling of the TOR Signaling Pathway in Human Fungal Pathogen Cryptococcus neoformans </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Yee-Seul%20So">Yee-Seul So</a>, <a href="https://publications.waset.org/abstracts/search?q=Guiseppe%20Ianiri"> Guiseppe Ianiri</a>, <a href="https://publications.waset.org/abstracts/search?q=Alex%20Idnurm"> Alex Idnurm</a>, <a href="https://publications.waset.org/abstracts/search?q=Yong-Sun%20Bahn"> Yong-Sun Bahn</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Tor1 is a serine/threonine protein kinase that is widely conserved across eukaryotic species. Tor1 was first identified in Saccharomyces cerevisiae as a target of rapamycin (TOR). The TOR pathway has been implicated in regulating cellular responses to nutrients, proliferation, translation, transcription, autophagy, and ribosome biogenesis. Here we identified two homologues of S. cerevisiae Tor proteins, CNAG_06642 (Tor1) and CNAG_05220 (Tlk1, TOR-like kinase 1), in Cryptococcus neoformans causing a life-threatening fungal meningoencephalitis. Both Tor1 and Tlk1 have rapamycin-binding (RB) domains but Tlk1 has truncated RB form. To study the TOR-signaling pathway in the fungal pathogen, we attempt to construct the tor1Δ and tlk1Δ mutants and phenotypically analyze them. Although we failed to construct the tor1Δ mutant, we successfully construct the tlk1Δ mutant. The tlk1Δ mutant does not exhibit any discernable phenotypes, suggesting that Tlk1 is dispensable in C. neoformans. The essentiality of TOR1 is independently confirmed by constructing the TOR1 promoter replacement strain by using a copper transporter 4 (CTR4) promoter and the TOR1/tor1 heterozygous mutant in diploid C. neoformans strain background followed by sporulation analysis. To further analyze the function of Tor1, we construct TOR1 overexpression mutant using a constitutively active histone H3 in C. neoformans. We find that the Tor1 overexpression mutant is resistant to rapamycin but the tlk1Δ mutant does not exhibit any altered resistance to rapamycin, further confirming that Tor1, but not Tlk1, is critical for TOR signaling. Furthermore, we found that Tor1 is involved in response to diverse stresses, including genotoxic stress, oxidative stress, thermo-stress, antifungal drug treatment, and production of melanin. To identify any TOR-related transcription factors, we screened C. neoformans transcription factor library that we constructed in our previous study and identified several potential downstream factors of Tor1, including Atf1, Crg1 and Bzp3. In conclusion, the current study provides insight into the role of the TOR signaling pathway in human fungal pathogens as well as C. neoformans. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=fungal%20pathogen" title="fungal pathogen">fungal pathogen</a>, <a href="https://publications.waset.org/abstracts/search?q=serine%2Fthreonine%20kinase" title=" serine/threonine kinase"> serine/threonine kinase</a>, <a href="https://publications.waset.org/abstracts/search?q=target%20of%20rapamycin" title=" target of rapamycin"> target of rapamycin</a>, <a href="https://publications.waset.org/abstracts/search?q=transcription%20factor" title=" transcription factor"> transcription factor</a> </p> <a href="https://publications.waset.org/abstracts/69093/unravelling-of-the-tor-signaling-pathway-in-human-fungal-pathogen-cryptococcus-neoformans" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/69093.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">221</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">957</span> STAT6 Mediates Local and Systemic Fibrosis and Type Ii Immune Response via Macrophage Polarization during Acute and Chronic Pancreatitis in Murine Model</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hager%20Elsheikh">Hager Elsheikh</a>, <a href="https://publications.waset.org/abstracts/search?q=Matthias%20Sendler"> Matthias Sendler</a>, <a href="https://publications.waset.org/abstracts/search?q=Juliana%20Glaubnitz"> Juliana Glaubnitz</a> </p> <p class="card-text"><strong>Abstract:</strong></p> In pancreatitis, an inflammatory reaction occurs in the pancreatic secretory cells due to premature activation of proteases, leading to pancreatic self-digestion and necrotic cell death of acinar cells. Acute pancreatitis in patients is characterized by a severe immune reaction that could lead to serious complications, such as organ failure or septic shock, if left untreated. Chronic pancreatitis is a recurrence of episodes of acute pancreatitis resulting in a fibro-inflammatory immune response, in which the type 2 immune response is primarily driven by AAMs in the pancreas. One of the most important signaling pathways for M2 macrophage activation is the IL-4/STAT6 pathway. Pancreatic fibrosis is induced by the hyperactivation of pancreatic stellate cells by dysregulation in the inflammatory response, leading to further damage, autodigestion and possibly necrosis of pancreatic acinar cells. The aim of this research is to investigate the effect of STAT6 knockout in disease severity and development of fibrosis wound healing in the presence of different macrophage populations, regulated by the type 2 immune response, after inducing chronic and/or acute pancreatitis in mice models via cerulean injection. We further investigate the influence of the JAK/STAT6 signaling pathway on the balance of fibrosis and regeneration in STAT6 deficient and wild-type mice. The characterization of resident and recruited macrophages will provide insight into the influence of the JAK/STAT6 signaling pathway on infiltrating cells and, ultimately, tissue fibrosis and disease severity. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=acute%20and%20chronic%20pancreatitis" title="acute and chronic pancreatitis">acute and chronic pancreatitis</a>, <a href="https://publications.waset.org/abstracts/search?q=tissue%20regeneration" title=" tissue regeneration"> tissue regeneration</a>, <a href="https://publications.waset.org/abstracts/search?q=macrophage%20polarization" title=" macrophage polarization"> macrophage polarization</a>, <a href="https://publications.waset.org/abstracts/search?q=Gastroenterology" title=" Gastroenterology"> Gastroenterology</a> </p> <a href="https://publications.waset.org/abstracts/173320/stat6-mediates-local-and-systemic-fibrosis-and-type-ii-immune-response-via-macrophage-polarization-during-acute-and-chronic-pancreatitis-in-murine-model" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/173320.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">68</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">956</span> IPO Price Performance and Signaling</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chih-Hsiang%20Chang">Chih-Hsiang Chang</a>, <a href="https://publications.waset.org/abstracts/search?q=I-Fan%20Ho"> I-Fan Ho</a> </p> <p class="card-text"><strong>Abstract:</strong></p> This study examines the credibility of the signaling as explanation for IPO initial underpricing. Findings reveal the initial underpricing and the long-term underperformance of IPOs in Taiwan. However, we only find weak support for signaling as explanation of IPO underpricing. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=signaling" title="signaling">signaling</a>, <a href="https://publications.waset.org/abstracts/search?q=IPO%20initial%20underpricing" title=" IPO initial underpricing"> IPO initial underpricing</a>, <a href="https://publications.waset.org/abstracts/search?q=IPO%20long-term%20underperformance" title=" IPO long-term underperformance"> IPO long-term underperformance</a>, <a href="https://publications.waset.org/abstracts/search?q=Taiwan%E2%80%99s%20stock%20market" title=" Taiwan’s stock market"> Taiwan’s stock market</a> </p> <a href="https://publications.waset.org/abstracts/22348/ipo-price-performance-and-signaling" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/22348.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">461</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">955</span> Effect of Serine/Threonine Kinases on Autophagy Mechanism</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ozlem%20Oral">Ozlem Oral</a>, <a href="https://publications.waset.org/abstracts/search?q=Seval%20Kilic"> Seval Kilic</a>, <a href="https://publications.waset.org/abstracts/search?q=Ozlem%20Yedier"> Ozlem Yedier</a>, <a href="https://publications.waset.org/abstracts/search?q=Serap%20Dokmeci"> Serap Dokmeci</a>, <a href="https://publications.waset.org/abstracts/search?q=Devrim%20Gozuacik"> Devrim Gozuacik</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Autophagy is a degradation pathway, activating under stress conditions. It digests macromolecules, such as abnormal proteins and long-lived organelles by engulfing them and by subsequent delivery of the cargo to lysosomes. The members of the phospholipid-dependent serine/threonine kinases, involved in many signaling pathways, which are necessary for the regulation of cellular metabolic activation. Previous studies implicate that, serine/threonine kinases have crucial roles in the mechanism of many diseases depend on the activated and/or inactivated signaling pathway. Data indicates, the signaling pathways activated by serine/threonine kinases are also involved in activation of autophagy mechanism. However, the information about the effect of serine/threonine kinases on autophagy mechanism and the roles of these effects in disease formation is limited. In this study, we investigated the effect of activated serine/threonine kinases on autophagic pathway. We performed a commonly used autophagy technique, GFP-LC3 dot formation and by using microscopy analyses, we evaluated promotion and/or inhibition of autophagy in serine/threonine kinase-overexpressed fibroblasts as well as cancer cells. In addition, we carried out confocal microscopy analyses and examined autophagic flux by utilizing the differential pH sensitivities of RFP and GFP in mRFP-GFP-LC3 probe. Based on the shRNA-library based screening, we identified autophagy-related proteins affected by serine/threonine kinases. We further studied the involvement of serine/threonine kinases on the molecular mechanism of newly identified autophagy proteins and found that, autophagic pathway is indirectly controlled by serine/threonine kinases via specific autophagic proteins. Our data indicate the molecular connection between two critical cellular mechanisms, which have important roles in the formation of many disease pathologies, particularly cancer. This project is supported by TUBITAK-1001-Scientific and Technological Research Projects Funding Program, Project No: 114Z836. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=autophagy" title="autophagy">autophagy</a>, <a href="https://publications.waset.org/abstracts/search?q=GFP-LC3%20dot%20formation%20assay" title=" GFP-LC3 dot formation assay"> GFP-LC3 dot formation assay</a>, <a href="https://publications.waset.org/abstracts/search?q=serine%2Fthreonine%20kinases" title=" serine/threonine kinases"> serine/threonine kinases</a>, <a href="https://publications.waset.org/abstracts/search?q=shRNA-library%20screening" title=" shRNA-library screening"> shRNA-library screening</a> </p> <a href="https://publications.waset.org/abstracts/50879/effect-of-serinethreonine-kinases-on-autophagy-mechanism" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/50879.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">292</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">954</span> Comparison of Serum Levels of Secreted Frizzler Protein 5 in Patients with Type 2 Diabetes Mellitus Treated and Not Treated with Metformin</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Irma%20Gabriela%20Lopez-Moreno">Irma Gabriela Lopez-Moreno</a>, <a href="https://publications.waset.org/abstracts/search?q=Elva%20Perez-Luque"> Elva Perez-Luque</a>, <a href="https://publications.waset.org/abstracts/search?q=Herlinda%20Aguilar-Zavala"> Herlinda Aguilar-Zavala</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: Type 2 Diabetes Mellitus (T2DM) is characterized by combination of insulin resistance and deterioration of insulin secretion. Sfrp5 is a protein that antagonizes Wnt5a proteins by preventing it from reaching its receptor and activating the Wnt/β-catenin signaling pathway, this pathway is one of the most important regulators of adipogenesis. Although metformin decreases glucose levels its mechanisms of action are not fully known but it has been implicated in the inhibition of the Wnt/β-catenin signaling pathway. Objective: The objective was evaluating the effects of metformin on serum levels of Sfrp5 in patients with T2DM treated and not treated with metformin. Methods: Two groups of patients were selected: one group of T2DM patients treated with metformin (n = 35) and another group of subjects with recent diagnosis of T2DM untreated (n = 35) with a mean age of 48 ± 9 years. In these subjects anthropometric measures were taken as weight, height, waist and hip circumference, were calculated the percentage of body fat, visceral fat and muscle mass. In addition, were measured glucose levels, lipid profile, adiponectin and Sfrp5. Results: Sfrp5 were higher in metformin-treated patients compared to the untreated group (19.9 vs 13.6 ng/mL p < 0.001), a negative correlation was found between Sfrp5 levels and total cholesterol levels (r= -0.25, p = 0.03) and percentage of visceral fat (r = -0.26, p = 0.03) and a positive correlation with HDL cholesterol levels (r = 0.31, p = 0.01) and adiponectin (r=0.65, p = < 0.001). Conclusions: The findings show that metformin consumption increased levels of Sfrp5, which may lead to a decrease in the activation of the WNT/β-catenin pathway impacting on adipogenesis. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=adiponectin" title="adiponectin">adiponectin</a>, <a href="https://publications.waset.org/abstracts/search?q=diabetes" title=" diabetes"> diabetes</a>, <a href="https://publications.waset.org/abstracts/search?q=metformin" title=" metformin"> metformin</a>, <a href="https://publications.waset.org/abstracts/search?q=Sfrp5" title=" Sfrp5"> Sfrp5</a> </p> <a href="https://publications.waset.org/abstracts/86854/comparison-of-serum-levels-of-secreted-frizzler-protein-5-in-patients-with-type-2-diabetes-mellitus-treated-and-not-treated-with-metformin" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/86854.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">177</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">953</span> Therapeutic Application of Light and Electromagnetic Fields to Reduce Hyper-Inflammation Triggered by COVID-19 </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Blanche%20Aguida">Blanche Aguida</a>, <a href="https://publications.waset.org/abstracts/search?q=Marootpong%20Pooam"> Marootpong Pooam</a>, <a href="https://publications.waset.org/abstracts/search?q=Nathalie%20Jourdan"> Nathalie Jourdan</a>, <a href="https://publications.waset.org/abstracts/search?q=Margaret%20Ahmad"> Margaret Ahmad</a> </p> <p class="card-text"><strong>Abstract:</strong></p> COVID-19-related morbidity is associated with exaggerated inflammation and cytokine production in the lungs, leading to acute respiratory failure. The cellular mechanisms underlying these so-called ‘cytokine storms’ are regulated through the Toll-like receptor 4 (TLR4) signaling pathway and by reactive oxygen species (ROS). Both light (photobiomodulation) and magnetic fields (e.g., pulsed electromagnetic field) stimulation are non-invasive therapies known to confer anti-inflammatory effects and regulate ROS signaling pathways. Here we show that daily exposure to two 10-minute intervals of moderate-intensity infra-red light significantly lowered the inflammatory response induced via the TLR4 receptor signaling pathway in human cell cultures. Anti-inflammatory effects were likewise achieved by electromagnetic field exposure of cells to daily 10-minute intervals of either pulsed electromagnetic fields (PEMF) or to low-level static magnetic fields. Because current illumination and electromagnetic field therapies have no known side effects and are already approved for some medical uses, we have here developed protocols for verification in clinical trials of COVID 19 infection. These treatments are affordable, simple to implement, and may help to resolve the acute respiratory distress of COVID 19 patients both in the home and in the hospital. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=COVID%2019" title="COVID 19">COVID 19</a>, <a href="https://publications.waset.org/abstracts/search?q=electromagnetic%20fields%20therapy" title=" electromagnetic fields therapy"> electromagnetic fields therapy</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=photobiomodulation%20therapy" title=" photobiomodulation therapy"> photobiomodulation therapy</a> </p> <a href="https://publications.waset.org/abstracts/135632/therapeutic-application-of-light-and-electromagnetic-fields-to-reduce-hyper-inflammation-triggered-by-covid-19" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/135632.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">144</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">952</span> Auricular Electroacupuncture Rescued Epilepsy Seizure by Attenuating TLR-2 Inflammatory Pathway in the Kainic Acid-Induced Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=I-Han%20Hsiao">I-Han Hsiao</a>, <a href="https://publications.waset.org/abstracts/search?q=Chun-Ping%20Huang"> Chun-Ping Huang</a>, <a href="https://publications.waset.org/abstracts/search?q=Ching-Liang%20Hsieh"> Ching-Liang Hsieh</a>, <a href="https://publications.waset.org/abstracts/search?q=Yi-Wen%20Lin"> Yi-Wen Lin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Epilepsy is chronic brain disorder that results in the sporadic occurrence of spontaneous seizures in the temporal lobe, cerebral cortex, and hippocampus. Clinical antiepileptic medicines are often ineffective or little benefits in the small amount of patients and usually initiate severe side effects. This inflammation contributes to enhanced neuronal excitability and the onset of epilepsy. Auricular electric-stimulation (AES) can increase parasympathetic activity and stimulate the solitary tract nucleus to induce the cholinergic anti-inflammatory pathway. Furthermore, it may be a therapeutic strategy for the treatment of epilepsy. In the present study, we want to investigate the effects of AES on inflammatory mediators in kainic acid (KA)-induced epileptic seizure rats. Experimental KA injection increased expression of TLR-2 pathway associated inflammatory mediators, were further reduced by either 2Hz or 15 Hz AES in the prefrontal cortex, hippocampus, and somatosensory cortex. We suggest that AES can successfully control the epileptic seizure by down-regulation of inflammation signaling pathway. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=auricular%20electric-stimulation" title="auricular electric-stimulation">auricular electric-stimulation</a>, <a href="https://publications.waset.org/abstracts/search?q=epileptic%20seizures" title=" epileptic seizures"> epileptic seizures</a>, <a href="https://publications.waset.org/abstracts/search?q=anti-inflammation" title=" anti-inflammation"> anti-inflammation</a> </p> <a href="https://publications.waset.org/abstracts/84898/auricular-electroacupuncture-rescued-epilepsy-seizure-by-attenuating-tlr-2-inflammatory-pathway-in-the-kainic-acid-induced-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/84898.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">185</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">951</span> The Role of Cholesterol Oxidase of Mycobacterium tuberculosis in the Down-Regulation of TLR2-Signaling Pathway in Human Macrophages during Infection Process</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Michal%20Kielbik">Michal Kielbik</a>, <a href="https://publications.waset.org/abstracts/search?q=Izabela%20Szulc-Kielbik"> Izabela Szulc-Kielbik</a>, <a href="https://publications.waset.org/abstracts/search?q=Anna%20Brzostek"> Anna Brzostek</a>, <a href="https://publications.waset.org/abstracts/search?q=Jaroslaw%20Dziadek"> Jaroslaw Dziadek</a>, <a href="https://publications.waset.org/abstracts/search?q=Magdalena%20Klink"> Magdalena Klink</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The goal of many research groups in the world is to find new components that are important for survival of mycobacteria in the host cells. Mycobacterium tuberculosis (Mtb) possesses a number of enzymes degrading cholesterol that are considered to be an important factor for its survival and persistence in host macrophages. One of them - cholesterol oxidase (ChoD), although not being essential for cholesterol degradation, is discussed as a virulence compound, however its involvement in macrophages’ response to Mtb is still not sufficiently determined. The recognition of tubercle bacilli antigens by pathogen recognition receptors is crucial for the initiation of the host innate immune response. An important receptor that has been implicated in the recognition and/or uptake of Mtb is Toll-like receptor type 2 (TLR2). Engagement of TLR2 results in the activation and phosphorylation of intracellular signaling proteins including IRAK-1 and -4, TRAF-6, which in turn leads to the activation of target kinases and transcription factors responsible for bactericidal and pro-inflammatory response of macrophages. The aim of these studies was a detailed clarification of the role of Mtb cholesterol oxidase as a virulence factor affecting the TLR2 signaling pathway in human macrophages. As human macrophages the THP-1 differentiated cells were applied. The virulent wild-type Mtb strain (H37Rv), its mutant lacking a functional copy of gene encoding cholesterol oxidase (∆choD), as well as complimented strain (∆choD–choD) were used. We tested the impact of Mtb strains on the expression of TLR2-depended signaling proteins (mRNA level, cytosolic level and phosphorylation status). The cytokine and bactericidal response of THP-1 derived macrophages infected with Mtb strains in relation to TLR2 signaling pathway dependence was also determined. We found that during the 24-hours of infection process the wild-type and complemented Mtb significantly reduced the cytosolic level and phosphorylation status of IRAK-4 and TRAF-6 proteins in macrophages, that was not observed in the case of ΔchoD mutant. Decreasement of TLR2-dependent signaling proteins, induced by wild-type Mtb, was not dependent on the activity of proteasome. Blocking of TLR2 expression, before infection, effectively prevented the induced by wild-type strain reduction of cytosolic level and phosphorylation of IRAK-4. None of the strains affected the surface expression of TLR2. The mRNA level of IRAK-4 and TRAF-6 genes were significantly increased in macrophages 24 hours post-infection with either of tested strains. However, the impact of wild-type Mtb strain on both examined genes was significantly stronger than its ΔchoD mutant. We also found that wild-type strain stimulated macrophages to release high amount of immunosuppressive IL-10, accompanied by low amount of pro-inflammatory IL-8 and bactericidal nitric oxide in comparison to mutant lacking cholesterol oxidase. The influence of wild-type Mtb on this type of macrophages' response strongly dependent on fully active IRAK-1 and IRAK-4 signaling proteins. In conclusion, Mtb using cholesterol oxidase causes the over-activation of TLR2 signaling proteins leading to the reduction of their cytosolic level and activity resulting in the modulation of macrophages response to allow its intracellular survival. Supported by grant: 2014/15/B/NZ6/01565, National Science Center, Poland <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mycobacterium%20tuberculosis" title="Mycobacterium tuberculosis">Mycobacterium tuberculosis</a>, <a href="https://publications.waset.org/abstracts/search?q=cholesterol%20oxidase" title=" cholesterol oxidase"> cholesterol oxidase</a>, <a href="https://publications.waset.org/abstracts/search?q=macrophages" title=" macrophages"> macrophages</a>, <a href="https://publications.waset.org/abstracts/search?q=TLR2-dependent%20signaling%20pathway" title=" TLR2-dependent signaling pathway"> TLR2-dependent signaling pathway</a> </p> <a href="https://publications.waset.org/abstracts/80872/the-role-of-cholesterol-oxidase-of-mycobacterium-tuberculosis-in-the-down-regulation-of-tlr2-signaling-pathway-in-human-macrophages-during-infection-process" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/80872.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">419</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">950</span> Role of Sulforaphane on Alleviating Duchenne Muscular Dystrophy(DMD) through Activation of Nrf2</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Sulforaphane (SFN) possesses powerful chemo-preventive effects and plays a crucial role on oxidative stress and inflammatory. In our recent study, SFN treatment could relieve muscular dystrophy in mdx mice by activating Nrf2 (NF-E2 related factor 2). Moreover, our findings indicated that SFN-activated Nrf2 alleviated muscle inflammation in dystrophin-deficient mdx mice through suppressing NF-κB signaling pathway. Collectively, SFN-induced Nrf2 molecular pathway might be a promising approach for treatment of the patients with Duchenne muscular dystrophy. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sulforaphane" title="sulforaphane">sulforaphane</a>, <a href="https://publications.waset.org/abstracts/search?q=Duchenne%20muscular%20dystrophy" title=" Duchenne muscular dystrophy"> Duchenne muscular dystrophy</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title=" fibrosis"> fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a> </p> <a href="https://publications.waset.org/abstracts/41533/role-of-sulforaphane-on-alleviating-duchenne-muscular-dystrophydmd-through-activation-of-nrf2" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41533.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">214</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">949</span> The Type II Immune Response in Acute and Chronic Pancreatitis Mediated by STAT6 in Murine</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hager%20Elsheikh">Hager Elsheikh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Context: Pancreatitis is a condition characterized by inflammation in the pancreas, which can lead to serious complications if untreated. Both acute and chronic pancreatitis are associated with immune reactions and fibrosis, which further damage the pancreas. The type 2 immune response, primarily driven by alternative activated macrophages (AAMs), plays a significant role in the development of fibrosis. The IL-4/STAT6 pathway is a crucial signaling pathway for the activation of M2 macrophages. Pancreatic fibrosis is induced by dysregulated inflammatory responses and can result in the autodigestion and necrosis of pancreatic acinar cells. Research Aim: The aim of this study is to investigate the impact of STAT6, a crucial molecule in the IL-4/STAT6 pathway, on the severity and development of fibrosis during acute and chronic pancreatitis. The research also aims to understand the influence of the JAK/STAT6 signaling pathway on the balance between fibrosis and regeneration in the presence of different macrophage populations. Methodology: The research utilizes murine models of acute and chronic pancreatitis induced by cerulean injection. Animal models will be employed to study the effect of STAT6 knockout on disease severity and fibrosis. Isolation of acinar cells and cell culture techniques will be used to assess the impact of different macrophage populations on wound healing and regeneration. Various techniques such as PCR, histology, immunofluorescence, and transcriptomics will be employed to analyze the tissues and cells. Findings: The research aims to provide insights into the mechanisms underlying tissue fibrosis and wound healing during acute and chronic pancreatitis. By investigating the influence of the JAK/STAT6 signaling pathway and different macrophage populations, the study aims to understand their impact on tissue fibrosis, disease severity, and pancreatic regeneration. Theoretical Importance: This research contributes to our understanding of the role of specific signaling pathways, macrophage polarization, and the type 2 immune response in pancreatitis. It provides insights into the molecular mechanisms underlying tissue fibrosis and the potential for targeted therapies. Data Collection and Analysis Procedures: Data will be collected through the use of murine models, isolation and culture of acinar cells, and various experimental techniques such as PCR, histology, immunofluorescence, and transcriptomics. Data will be analyzed using appropriate statistical methods and techniques, and the findings will be interpreted in the context of the research objectives. Conclusion: By investigating the mechanisms of tissue fibrosis and wound healing during acute and chronic pancreatitis, this research aims to enhance our understanding of the disease progression and potential therapeutic targets. The findings have theoretical importance in expanding our knowledge of pancreatic fibrosis and the role of macrophage polarization in the context of the type 2 immune response. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=immunity%20in%20chronic%20diseases" title="immunity in chronic diseases">immunity in chronic diseases</a>, <a href="https://publications.waset.org/abstracts/search?q=pancreatitis" title=" pancreatitis"> pancreatitis</a>, <a href="https://publications.waset.org/abstracts/search?q=macrophages" title=" macrophages"> macrophages</a>, <a href="https://publications.waset.org/abstracts/search?q=immune%20response" title=" immune response"> immune response</a> </p> <a href="https://publications.waset.org/abstracts/186332/the-type-ii-immune-response-in-acute-and-chronic-pancreatitis-mediated-by-stat6-in-murine" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/186332.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">33</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">948</span> An in silico Approach for Exploring the Intercellular Communication in Cancer Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=M.%20Cardenas-Garcia">M. Cardenas-Garcia</a>, <a href="https://publications.waset.org/abstracts/search?q=P.%20P.%20Gonzalez-Perez"> P. P. Gonzalez-Perez</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Intercellular communication is a necessary condition for cellular functions and it allows a group of cells to survive as a population. Throughout this interaction, the cells work in a coordinated and collaborative way which facilitates their survival. In the case of cancerous cells, these take advantage of intercellular communication to preserve their malignancy, since through these physical unions they can send signs of malignancy. The Wnt/β-catenin signaling pathway plays an important role in the formation of intercellular communications, being also involved in a large number of cellular processes such as proliferation, differentiation, adhesion, cell survival, and cell death. The modeling and simulation of cellular signaling systems have found valuable support in a wide range of modeling approaches, which cover a wide spectrum ranging from mathematical models; e.g., ordinary differential equations, statistical methods, and numerical methods– to computational models; e.g., process algebra for modeling behavior and variation in molecular systems. Based on these models, different simulation tools have been developed from mathematical ones to computational ones. Regarding cellular and molecular processes in cancer, its study has also found a valuable support in different simulation tools that, covering a spectrum as mentioned above, have allowed the in silico experimentation of this phenomenon at the cellular and molecular level. In this work, we simulate and explore the complex interaction patterns of intercellular communication in cancer cells using the Cellulat bioinformatics tool, a computational simulation tool developed by us and motivated by two key elements: 1) a biochemically inspired model of self-organizing coordination in tuple spaces, and 2) the Gillespie’s algorithm, a stochastic simulation algorithm typically used to mimic systems of chemical/biochemical reactions in an efficient and accurate way. The main idea behind the Cellulat simulation tool is to provide an in silico experimentation environment that complements and guides in vitro experimentation in intra and intercellular signaling networks. Unlike most of the cell signaling simulation tools, such as E-Cell, BetaWB and Cell Illustrator which provides abstractions to model only intracellular behavior, Cellulat is appropriate for modeling both intracellular signaling and intercellular communication, providing the abstractions required to model –and as a result, simulate– the interaction mechanisms that involve two or more cells, that is essential in the scenario discussed in this work. During the development of this work we made evident the application of our computational simulation tool (Cellulat) for the modeling and simulation of intercellular communication between normal and cancerous cells, and in this way, propose key molecules that may prevent the arrival of malignant signals to the cells that surround the tumor cells. In this manner, we could identify the significant role that has the Wnt/β-catenin signaling pathway in cellular communication, and therefore, in the dissemination of cancer cells. We verified, using in silico experiments, how the inhibition of this signaling pathway prevents that the cells that surround a cancerous cell are transformed. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cancer%20cells" title="cancer cells">cancer cells</a>, <a href="https://publications.waset.org/abstracts/search?q=in%20silico%20approach" title=" in silico approach"> in silico approach</a>, <a href="https://publications.waset.org/abstracts/search?q=intercellular%20communication" title=" intercellular communication"> intercellular communication</a>, <a href="https://publications.waset.org/abstracts/search?q=key%20molecules" title=" key molecules"> key molecules</a>, <a href="https://publications.waset.org/abstracts/search?q=modeling%20and%20simulation" title=" modeling and simulation"> modeling and simulation</a> </p> <a href="https://publications.waset.org/abstracts/83145/an-in-silico-approach-for-exploring-the-intercellular-communication-in-cancer-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/83145.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">249</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">947</span> Identification of Nutrient Sensitive Signaling Pathways via Analysis of O-GlcNAcylation</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Michael%20P.%20Mannino">Michael P. Mannino</a>, <a href="https://publications.waset.org/abstracts/search?q=Gerald%20W.%20Hart"> Gerald W. Hart</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The majority of glucose metabolism proceeds through glycolytic pathways such as glycolysis or pentose phosphate pathway, however, about 5% is shunted through the hexosamine biosynthetic pathway, producing uridine diphosphate N-acetyl glucosamine (UDP-GlcNAc). This precursor can then be incorporated into complex oligosaccharides decorating the cell surface or remain as an intracellular post-translational-modification (PTM) of serine/threonine residues (O-GlcNAcylation, OGN), which has been identified on over 4,000 cytosolic or nuclear proteins. Intracellular OGN has major implications on cellularprocesses, typically by modulating protein localization, protein-protein interactions, protein degradation, and gene expression. Additionally, OGN is known to have an extensive cross-talk with phosphorylation, be in a competitive or cooperative manner. Unlike other PTMs there are only two cycling enzymes that are capable of adding or removing the GlcNAc moiety, O-linked N-aceytl glucosamine Transferase (OGT) and O-linked N-acetyl glucoamidase (OGA), respectively. The activity of OGT has been shown to be sensitive to cellular UDP-GlcNAc levels, even changing substrate affinity. Owing to this and that the concentration of UDP-GlcNAc is related to the metabolisms of glucose, amino acid, fatty acid, and nucleotides, O-GlcNAc is often referred to as a nutrient sensing rheostat. Indeed OGN is known to regulate several signaling pathways as a result of nutrient levels, such as insulin signaling. Dysregulation of OGN is associated with several disease states such as cancer, diabetes, and neurodegeneration. Improvements in glycomics over the past 10-15 years has significantly increased the OGT substrate pool, suggesting O-GlcNAc’s involvement in a wide variety of signaling pathways. However, O-GlcNAc’s role at the receptor level has only been identified in a case-by-case basis of known pathways. Examining the OGN of the plasma membrane (PM) may better focus our understanding of O-GlcNAc-effected signaling pathways. In this current study, PM fractions were isolated from several cell types via ultracentrifugation, followed by purification and MS/MS analysis in several cell lines. This process was repeated with or without OGT/OGA inhibitors or with increased/decreased glucose levels in media to ascertain the importance of OGN. Various pathways are followed up on in more detailed studies employing methods to localize OGN at the PM specifically. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=GlcNAc" title="GlcNAc">GlcNAc</a>, <a href="https://publications.waset.org/abstracts/search?q=nutrient%20sensitive" title=" nutrient sensitive"> nutrient sensitive</a>, <a href="https://publications.waset.org/abstracts/search?q=post-translational-modification" title=" post-translational-modification"> post-translational-modification</a>, <a href="https://publications.waset.org/abstracts/search?q=receptor" title=" receptor"> receptor</a> </p> <a href="https://publications.waset.org/abstracts/154198/identification-of-nutrient-sensitive-signaling-pathways-via-analysis-of-o-glcnacylation" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/154198.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">112</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">946</span> Characterization of Molecular Targets to Mediate Skin Itch and Inflammation</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Anita%20J%C3%A4ger">Anita Jäger</a>, <a href="https://publications.waset.org/abstracts/search?q=Andrew%20Salazar"> Andrew Salazar</a>, <a href="https://publications.waset.org/abstracts/search?q=J%C3%B6rg%20von%20Hagen"> Jörg von Hagen</a>, <a href="https://publications.waset.org/abstracts/search?q=Harald%20Kolmar"> Harald Kolmar</a> </p> <p class="card-text"><strong>Abstract:</strong></p> In the treatment of individuals with sensitive and psoriatic skin, several inflammation and itch-related molecular and cellular targets have been identified, but many of these have yet to be characterized. In this study, we present two potential targets in the skin that can be linked to the inflammation and itch cycle. 11ßHSD1 is the enzyme responsible for converting inactive cortisone to active cortisol used to transmit signals downstream. The activation of the receptor NK1R correlates with promoting inflammation and the perception of itch and pain in the skin. In this study, both targets have been investigated based on their involvement in inflammation. The role of both identified targets was characterized based on the secretion of inflammation cytokine- IL6, IL-8, and CCL2, as well as phosphorylation and signaling pathways. It was found that treating skin cells with molecules able to inhibit inflammatory pathways results in the reduction of inflammatory signaling molecules secreted by skin cells and increases their proliferative capacity. Therefore, these molecular targets and their associated pathways show therapeutic potential and can be mitigated via small molecules. This research can be used for further studies in inflammation and itch pathways and can help to treat pathological symptoms. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=inflammation" title="inflammation">inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=itch" title=" itch"> itch</a>, <a href="https://publications.waset.org/abstracts/search?q=signaling%20pathway" title=" signaling pathway"> signaling pathway</a>, <a href="https://publications.waset.org/abstracts/search?q=skin" title=" skin"> skin</a> </p> <a href="https://publications.waset.org/abstracts/148393/characterization-of-molecular-targets-to-mediate-skin-itch-and-inflammation" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/148393.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">123</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">945</span> Investigation of Possible Behavioural and Molecular Effects of Mobile Phone Exposure on Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=%C3%87.%20G%C3%B6k%C3%A7ek-Sara%C3%A7">Ç. Gökçek-Saraç</a>, <a href="https://publications.waset.org/abstracts/search?q=%C5%9E.%20%C3%96zen"> Ş. Özen</a>, <a href="https://publications.waset.org/abstracts/search?q=N.%20Derin"> N. Derin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The N-methyl-D-aspartate (NMDA)-dependent pathway is the major intracellular signaling pathway implemented in both short- and long-term memory formation in the hippocampus which is the most studied brain structure because of its well documented role in learning and memory. However, little is known about the effects of RF-EMR exposure on NMDA receptor signaling pathway including activation of protein kinases, notably Ca<sup>2+</sup>/calmodulin-dependent protein kinase II alpha (CaMKIIα). The aim of the present study was to investigate the effects of acute and chronic 900 MHz RF-EMR exposure on both passive avoidance behaviour and hippocampal levels of CaMKIIα and its phosphorylated form (pCaMKIIα). Rats were divided into the following groups: Sham rats, and rats exposed to 900 MHz RF-EMR for 2 h/day for 1 week (acute group) or 10 weeks (chronic group), respectively. Passive avoidance task was used as a behavioural method. The hippocampal levels of selected kinases were measured using Western Blotting technique. The results of passive avoidance task showed that both acute and chronic exposure to 900 MHz RF-EMR can impair passive avoidance behaviour with minor effects on chronic group of rats. The analysis of western blot data of selected protein kinases demonstrated that hippocampal levels of CaMKIIα and pCaMKIIα were significantly higher in chronic group of rats as compared to acute groups. Taken together, these findings demonstrated that different duration times (1 week vs 10 weeks) of 900 MHz RF-EMR exposure have different effects on both passive avoidance behaviour of rats and hippocampal levels of selected protein kinases. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hippocampus" title="hippocampus">hippocampus</a>, <a href="https://publications.waset.org/abstracts/search?q=protein%20kinase" title=" protein kinase"> protein kinase</a>, <a href="https://publications.waset.org/abstracts/search?q=rat" title=" rat"> rat</a>, <a href="https://publications.waset.org/abstracts/search?q=RF-EMR" title=" RF-EMR"> RF-EMR</a> </p> <a href="https://publications.waset.org/abstracts/68567/investigation-of-possible-behavioural-and-molecular-effects-of-mobile-phone-exposure-on-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/68567.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">255</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">944</span> Analysis of Osmotin as Transcription Factor/Cell Signaling Modulator Using Bioinformatic Tools</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Usha%20Kiran">Usha Kiran</a>, <a href="https://publications.waset.org/abstracts/search?q=M.%20Z.%20Abdin"> M. Z. Abdin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Osmotin is an abundant cationic multifunctional protein discovered in cells of tobacco (Nicotiana tabacum L. var Wisconsin 38) adapted to an environment of low osmotic potential. It provides plants protection from pathogens, hence placed in the PRP family of proteins. The osmotin induced proline accumulation has been reported in plants including transgenic tomato and strawberry conferring tolerance against both biotic and abiotic stresses. The exact mechanism of induction of proline by osmotin is however, not known till date. These observations have led us to hypothesize that osmotin induced proline accumulation could be due to its involvement as transcription factor and/or cell signal pathway modulator in proline biosynthesis. The present investigation was therefore, undertaken to analyze the osmotin protein as transcription factor /cell signalling modulator using bioinformatics tools. The results of available online DNA binding motif search programs revealed that osmotin does not contain DNA-binding motifs. The alignment results of osmotin protein with the protein sequence from DATF showed the homology in the range of 0-20%, suggesting that it might not contain a DNA binding motif. Further to find unique DNA-binding domain, the superimposition of osmotin 3D structure on modeled Arabidopsis transcription factors using Chimera also suggested absence of the same. We, however, found evidence implicating osmotin in cell signaling. With these results, we concluded that osmotin is not a transcription factor but regulating proline biosynthesis and accumulation through cell signaling during abiotic stresses. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=osmotin" title="osmotin">osmotin</a>, <a href="https://publications.waset.org/abstracts/search?q=cell%20signaling%20modulator" title=" cell signaling modulator"> cell signaling modulator</a>, <a href="https://publications.waset.org/abstracts/search?q=bioinformatic%20tools" title=" bioinformatic tools"> bioinformatic tools</a>, <a href="https://publications.waset.org/abstracts/search?q=protein" title=" protein "> protein </a> </p> <a href="https://publications.waset.org/abstracts/8485/analysis-of-osmotin-as-transcription-factorcell-signaling-modulator-using-bioinformatic-tools" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/8485.pdf" target="_blank" class="btn 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