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cyclase</title> <meta name="description" content="Search results for: glutaminyl cyclase"> <meta name="keywords" content="glutaminyl cyclase"> <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="glutaminyl cyclase"> <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> 8</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: glutaminyl cyclase</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">8</span> Pharmacophore-Based Modeling of a Series of Human Glutaminyl Cyclase Inhibitors to Identify Lead Molecules by Virtual Screening, Molecular Docking and Molecular Dynamics Simulation Study</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ankur%20Chaudhuri">Ankur Chaudhuri</a>, <a href="https://publications.waset.org/abstracts/search?q=Sibani%20Sen%20Chakraborty"> Sibani Sen Chakraborty</a> </p> <p class="card-text"><strong>Abstract:</strong></p> In human, glutaminyl cyclase activity is highly abundant in neuronal and secretory tissues and is preferentially restricted to hypothalamus and pituitary. The N-terminal modification of β-amyloids (Aβs) peptides by the generation of a pyro-glutamyl (pGlu) modified Aβs (pE-Aβs) is an important process in the initiation of the formation of neurotoxic plaques in Alzheimer’s disease (AD). This process is catalyzed by glutaminyl cyclase (QC). The expression of QC is characteristically up-regulated in the early stage of AD, and the hallmark of the inhibition of QC is the prevention of the formation of pE-Aβs and plaques. A computer-aided drug design (CADD) process was employed to give an idea for the designing of potentially active compounds to understand the inhibitory potency against human glutaminyl cyclase (QC). This work elaborates the ligand-based and structure-based pharmacophore exploration of glutaminyl cyclase (QC) by using the known inhibitors. Three dimensional (3D) quantitative structure-activity relationship (QSAR) methods were applied to 154 compounds with known IC50 values. All the inhibitors were divided into two sets, training-set, and test-sets. Generally, training-set was used to build the quantitative pharmacophore model based on the principle of structural diversity, whereas the test-set was employed to evaluate the predictive ability of the pharmacophore hypotheses. A chemical feature-based pharmacophore model was generated from the known 92 training-set compounds by HypoGen module implemented in Discovery Studio 2017 R2 software package. The best hypothesis was selected (Hypo1) based upon the highest correlation coefficient (0.8906), lowest total cost (463.72), and the lowest root mean square deviation (2.24Å) values. The highest correlation coefficient value indicates greater predictive activity of the hypothesis, whereas the lower root mean square deviation signifies a small deviation of experimental activity from the predicted one. The best pharmacophore model (Hypo1) of the candidate inhibitors predicted comprised four features: two hydrogen bond acceptor, one hydrogen bond donor, and one hydrophobic feature. The Hypo1 was validated by several parameters such as test set activity prediction, cost analysis, Fischer's randomization test, leave-one-out method, and heat map of ligand profiler. The predicted features were then used for virtual screening of potential compounds from NCI, ASINEX, Maybridge and Chembridge databases. More than seven million compounds were used for this purpose. The hit compounds were filtered by drug-likeness and pharmacokinetics properties. The selective hits were docked to the high-resolution three-dimensional structure of the target protein glutaminyl cyclase (PDB ID: 2AFU/2AFW) to filter these hits further. To validate the molecular docking results, the most active compound from the dataset was selected as a reference molecule. From the density functional theory (DFT) study, ten molecules were selected based on their highest HOMO (highest occupied molecular orbitals) energy and the lowest bandgap values. Molecular dynamics simulations with explicit solvation systems of the final ten hit compounds revealed that a large number of non-covalent interactions were formed with the binding site of the human glutaminyl cyclase. It was suggested that the hit compounds reported in this study could help in future designing of potent inhibitors as leads against human glutaminyl cyclase. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=glutaminyl%20cyclase" title="glutaminyl cyclase">glutaminyl cyclase</a>, <a href="https://publications.waset.org/abstracts/search?q=hit%20lead" title=" hit lead"> hit lead</a>, <a href="https://publications.waset.org/abstracts/search?q=pharmacophore%20model" title=" pharmacophore model"> pharmacophore model</a>, <a href="https://publications.waset.org/abstracts/search?q=simulation" title=" simulation"> simulation</a> </p> <a href="https://publications.waset.org/abstracts/110703/pharmacophore-based-modeling-of-a-series-of-human-glutaminyl-cyclase-inhibitors-to-identify-lead-molecules-by-virtual-screening-molecular-docking-and-molecular-dynamics-simulation-study" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/110703.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">131</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">7</span> Oxidosqualene Cyclase: A Novel Inhibitor </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Devadrita%20Dey%20Sarkar">Devadrita Dey Sarkar</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Oxidosqualene cyclase is a membrane bound enzyme in which helps in the formation of steroid scaffold in higher organisms. In a highly selective cyclization reaction oxidosqualene cyclase forms LANOSTEROL with seven chiral centres starting from the linear substrate 2,3-oxidosqualene. In humans OSC in cholesterol biosynthesis it represents a target for the discovery of novel anticholesteraemic drugs that could complement the widely used statins. The enzyme oxidosqualene: lanosterol cyclase (OSC) represents a novel target for the treatment of hypercholesterolemia. OSC catalyzes the cyclization of the linear 2,3-monoepoxysqualene to lanosterol, the initial four-ringed sterol intermediate in the cholesterol biosynthetic pathway. OSC also catalyzes the formation of 24(S), 25-epoxycholesterol, a ligand activator of the liver X receptor. Inhibition of OSC reduces cholesterol biosynthesis and selectively enhances 24(S),25-epoxycholesterol synthesis. Through this dual mechanism, OSC inhibition decreases plasma levels of low-density lipoprotein (LDL)-cholesterol and prevents cholesterol deposition within macrophages. The recent crystallization of OSC identifies the mechanism of action for this complex enzyme, setting the stage for the design of OSC inhibitors with improved pharmacological properties for cholesterol lowering and treatment of atherosclerosis. While studying and designing the inhibitor of oxidosqulene cyclase, I worked on the pdb id of 1w6k which was the most worked on pdb id and I used several methods, techniques and softwares to identify and validate the top most molecules which could be acting as an inhibitor for oxidosqualene cyclase. Thus, by partial blockage of this enzyme, both an inhibition of lanosterol and subsequently cholesterol formation as well as a concomitant effect on HMG-CoA reductase can be achieved. Both effects complement each other and lead to an effective control of cholesterol biosynthesis. It is therefore concluded that 2,3-oxidosqualene cyclase plays a crucial role in the regulation of intracellular cholesterol homeostasis. 2,3-Oxidosqualene cyclase inhibitors offer an attractive approach for novel lipid-lowering agents. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=anticholesteraemic" title="anticholesteraemic">anticholesteraemic</a>, <a href="https://publications.waset.org/abstracts/search?q=crystallization" title=" crystallization"> crystallization</a>, <a href="https://publications.waset.org/abstracts/search?q=statins" title=" statins"> statins</a>, <a href="https://publications.waset.org/abstracts/search?q=homeostasis" title=" homeostasis"> homeostasis</a> </p> <a href="https://publications.waset.org/abstracts/23245/oxidosqualene-cyclase-a-novel-inhibitor" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/23245.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">351</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">6</span> Comparative Proteomic Analysis of Rice bri1 Mutant Leaves at Jointing-Booting Stage</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Jiang%20Xu">Jiang Xu</a>, <a href="https://publications.waset.org/abstracts/search?q=Daoping%20Wang"> Daoping Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yinghong%20Pan"> Yinghong Pan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The jointing-booting stage is a critical period of both vegetative growth and reproductive growth in rice. Therefore, the proteomic analysis of the mutant Osbri1, whose corresponding gene OsBRI1 encodes the putative BRs receptor OsBRI1, at jointing-booting stage is very important for understanding the effects of BRs on vegetative and reproductive growth. In this study, the proteomes of leaves from an allelic mutant of the DWARF 61 (D61, OsBRI1) gene, Fn189 (dwarf54, d54) and its wild-type variety T65 (Taichung 65) at jointing-booting stage were analysed by using a Q Exactive plus orbitrap mass spectrometer, and more than 3,100 proteins were identified in each sample. Ontology analysis showed that these proteins distribute in various space of the cells, such as the chloroplast, mitochondrion, and nucleus, they functioned as structural components and/or catalytic enzymes and involved in many physiological processes. Moreover, quantitative analysis displayed that 266 proteins were differentially expressed in two samples, among them, 77 proteins decreased and 189 increased more than two times in Fn189 compared with T65, the proteins whose content decreased in Fn189 including b5-like Heme/Steroid binding domain containing protein, putative retrotransposon protein, putative glutaminyl-tRNA synthetase, and higher content proteins such as mTERF, putative Oligopeptidase homologue, zinc knuckle protein, and so on. A former study founded that the transcription level of a mTERF was up-regulated in the leaves of maize seedling after EBR treatment. In our experiments, it was interesting that one mTERF protein increased, but another mTERF decreased in leaves of Fn189 at jointing-booting stage, which suggested that BRs may have differential regulation mechanisms on the expression of various mTERF proteins. The relationship between other differential proteins with BRs is still unclear, and the effects of BRs on rice protein contents and its regulation mechanisms still need further research. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=bri1%20mutant" title="bri1 mutant">bri1 mutant</a>, <a href="https://publications.waset.org/abstracts/search?q=jointing-booting%20stage" title=" jointing-booting stage"> jointing-booting stage</a>, <a href="https://publications.waset.org/abstracts/search?q=proteomic%20analysis" title=" proteomic analysis"> proteomic analysis</a>, <a href="https://publications.waset.org/abstracts/search?q=rice" title=" rice"> rice</a> </p> <a href="https://publications.waset.org/abstracts/85257/comparative-proteomic-analysis-of-rice-bri1-mutant-leaves-at-jointing-booting-stage" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/85257.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">247</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">5</span> An Inverse Docking Approach for Identifying New Potential Anticancer Targets</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Soujanya%20Pasumarthi">Soujanya Pasumarthi</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Inverse docking is a relatively new technique that has been used to identify potential receptor targets of small molecules. Our docking software package MDock is well suited for such an application as it is both computationally efficient, yet simultaneously shows adequate results in binding affinity predictions and enrichment tests. As a validation study, we present the first stage results of an inverse-docking study which seeks to identify potential direct targets of PRIMA-1. PRIMA-1 is well known for its ability to restore mutant p53's tumor suppressor function, leading to apoptosis in several types of cancer cells. For this reason, we believe that potential direct targets of PRIMA-1 identified in silico should be experimentally screened for their ability to inhibitcancer cell growth. The highest-ranked human protein of our PRIMA-1 docking results is oxidosqualene cyclase (OSC), which is part of the cholesterol synthetic pathway. The results of two followup experiments which treat OSC as a possible anti-cancer target are promising. We show that both PRIMA-1 and Ro 48-8071, a known potent OSC inhibitor, significantly reduce theviability of BT-474 breast cancer cells relative to normal mammary cells. In addition, like PRIMA-1, we find that Ro 48-8071 results in increased binding of mutant p53 to DNA in BT- 474cells (which highly express p53). For the first time, Ro 48-8071 is shown as a potent agent in killing human breast cancer cells. The potential of OSC as a new target for developing anticancer therapies is worth further investigation. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=inverse%20docking" title="inverse docking">inverse docking</a>, <a href="https://publications.waset.org/abstracts/search?q=in%20silico%20screening" title=" in silico screening"> in silico screening</a>, <a href="https://publications.waset.org/abstracts/search?q=protein-ligand%20interactions" title=" protein-ligand interactions"> protein-ligand interactions</a>, <a href="https://publications.waset.org/abstracts/search?q=molecular%20docking" title=" molecular docking "> molecular docking </a> </p> <a href="https://publications.waset.org/abstracts/9217/an-inverse-docking-approach-for-identifying-new-potential-anticancer-targets" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/9217.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">446</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">4</span> Anti-Prostate Cancer Effect of GV-1001, a Novel Gonadotropin-Releasing Hormone Receptor Ligand</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ji%20Won%20Kim">Ji Won Kim</a>, <a href="https://publications.waset.org/abstracts/search?q=Moo%20Yeol%20Lee"> Moo Yeol Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=Keon%20Wook%20Kang"> Keon Wook Kang</a> </p> <p class="card-text"><strong>Abstract:</strong></p> GV-1001, 16 amino acid fragment of human telomerase reverse transcriptase catalytic subunit (hTERT), has been developed as an injectable cancer vaccine for many types of solid tumors showing high-level of telomerase activity. In the present study, we evaluated the anti-cancer effect of GV-1001 on androgen-receptor-positive prostate cancer. Two signaling pathways, Gs-adenylate cyclase-cAMP and Gq-IP3-Ca2+ pathways play a central role in GnRH receptor (GnRHR)-mediated activities. We found that leuprolide acetate (LA) mainly acted on Gq-mediated Ca2+ signaling, while GV-1001 preferentially acted on cAMP signaling; and both the effects were counteracted by cetrorelix, a GnRHR antagonist. We further tested whether GV-1001 affects tumor growth of human prostate cancer cells in vivo. Prostate tumor xenografts were established using LNCap, androgen receptor-positive prostate cancer cells, and the nude mice bearing tumors were subcutaneously injected with GV-1001 (0.01, 0.1, 1, 10 microg/kg/day) and LA (0.01 microg/kg/day) for 2 weeks. GV-1001 (1 and 10 microg/kg/day) significantly inhibited tumor growth of LNCap xenografts. Interestingly, mRNA expression of MMP2 and MMP9 was significantly suppressed by GV-1001 injection, but not by LA administration. Boyden chamber assay revealed that GV-1001 potently inhibited cell migration of LNCap. Our finding suggests that GV-1001 as a novel GnRHR ligand, has anti-proliferative and anti-migratory effects on androgen receptor-positive prostate cancer cells. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=GV-1001" title="GV-1001">GV-1001</a>, <a href="https://publications.waset.org/abstracts/search?q=GnRH" title=" GnRH"> GnRH</a>, <a href="https://publications.waset.org/abstracts/search?q=hTERT" title=" hTERT"> hTERT</a>, <a href="https://publications.waset.org/abstracts/search?q=prostate%20cancer" title=" prostate cancer"> prostate cancer</a> </p> <a href="https://publications.waset.org/abstracts/22012/anti-prostate-cancer-effect-of-gv-1001-a-novel-gonadotropin-releasing-hormone-receptor-ligand" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/22012.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">370</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">3</span> The Role of Immunologic Diamonds in Dealing with Mycobacterium Tuberculosis; Responses of Immune Cells in Affliction to the Respiratory Tuberculosis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Seyyed%20Mohammad%20Amin%20Mousavi%20Sagharchi">Seyyed Mohammad Amin Mousavi Sagharchi</a>, <a href="https://publications.waset.org/abstracts/search?q=Elham%20Javanroudi"> Elham Javanroudi</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: Tuberculosis (TB) is a known disease with hidden features caused by Mycobacterium tuberculosis (MTB). This disease, which is one of the 10 deadliest in the world, has caused millions of deaths in recent decades. Furthermore, TB is responsible for infecting about 30% population of world. Like any infection, TB can activate the immune system by locating and colonization in the human body, especially in the alveoli. TB is granulomatosis, so MTB can absorb the host’s immune cells and other cells to form granuloma. Method: Different databases (e.g., PubMed) were recruited to prepare this paper and fulfill our goals to search and find effective papers and investigations. Results: Immune response to MTB is related to T cell killers and contains CD1, CD4, and CD8 T lymphocytes. CD1 lymphocytes can recognize glycolipids, which highly exist in the Mycobacterial fatty cell wall. CD4 lymphocytes and macrophages form granuloma, and it is the main line of immune response to Mycobacteria. On the other hand, CD8 cells have cytolytic function for directly killing MTB by secretion of granulysin. Other functions and secretion to the deal are interleukin-12 (IL-12) by induction of expression interferon-γ (INF-γ) for macrophages activation and creating a granuloma, and tumor necrosis factor (TNF) by promoting macrophage phagolysosomal fusion. Conclusion: Immune cells in battle with MTB are macrophages, dendritic cells (DCs), neutrophils, and natural killer (NK) cells. These immune cells can recognize the Mycobacterium by various receptors, including Toll-like receptors (TLRs), Nod-like receptors (NLRs), and C-type lectin receptors (CLRs) located in the cell surface. In human alveoli exist about 50 dendritic macrophages, which have close communication with other immune cells in the circulating system and epithelial cells to deal with Mycobacteria. Against immune cells, MTB handles some factors (e.g., cordfactor, O-Ag, lipoarabinomannan, sulfatides, and adenylate cyclase) and practical functions (e.g., inhibition of macrophages). <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=immune%20responses" title=" immune responses"> immune responses</a>, <a href="https://publications.waset.org/abstracts/search?q=immunological%20mechanisms" title=" immunological mechanisms"> immunological mechanisms</a>, <a href="https://publications.waset.org/abstracts/search?q=respiratory%20tuberculosis" title=" respiratory tuberculosis"> respiratory tuberculosis</a> </p> <a href="https://publications.waset.org/abstracts/165031/the-role-of-immunologic-diamonds-in-dealing-with-mycobacterium-tuberculosis-responses-of-immune-cells-in-affliction-to-the-respiratory-tuberculosis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/165031.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">109</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">2</span> Inheritance, Stability, and Validation of Provitamin a Markers in Striga Hermonthica-Resistant Maize</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Fiston%20Masudi%20Tambwe">Fiston Masudi Tambwe</a>, <a href="https://publications.waset.org/abstracts/search?q=Lwanga%20Charles"> Lwanga Charles</a>, <a href="https://publications.waset.org/abstracts/search?q=Arfang%20Badji"> Arfang Badji</a>, <a href="https://publications.waset.org/abstracts/search?q=Unzimai%20Innocent"> Unzimai Innocent</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The development of maize varieties combining Provitamin A (PVA), high yield, and Striga resistance is an effective and affordable strategy to contribute to food security in sub-Saharan Africa, where maize is a staple food crop. There has been limited research on introgressing PVA genes into Striga-resistant maize genotypes. The objectives of this study were to: i) determine the mode of gene action controlling PVA carotenoid accumulation in Striga-resistant maize, ii) identify Striga-resistant maize hybrids with high PVA content and stable yield, and iii) validate the presence of PVA functional markers in offspring. Six elite, Striga-resistant inbred females were crossed with six high-PVA inbred males in a North Carolina Design II and their offspring were evaluated in four environments, following a 5x8 alpha lattice design with four hybrid checks. Results revealed that both additive and non-additive gene action control carotenoid accumulation in the present study, with a predominance of non-additive gene effects for PVA. Hybrids STR1004xCLHP0352 and STR1004xCLHP0046 - identified as Striga-resistant because they supported fewer Striga plants – were the highest-yielding genotypes with a moderate PVA concentration of 5.48 and 5.77 µg/g, respectively. However, those two hybrids were not stable in terms of yield across all environments. Hybrid STR1007xCLHP0046, however, supported fewer Striga plants, had a yield of 4.52 T/ha, a PVA concentration of 4.52 µg/g, and was also stable. Gel-based marker systems of CrtRB1 and LCYE were used to screen the hybrids and favorable alleles of CrtRB1 primers were detected in 20 hybrids, confirming good levels of PVA carotenoids. Hybrids with favorable alleles of LCYE had the highest concentration of non-PVA carotenoids. These findings will contribute to the development of high-yielding PVA-rich maize varieties in Uganda. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=gene%20action" title="gene action">gene action</a>, <a href="https://publications.waset.org/abstracts/search?q=stability" title=" stability"> stability</a>, <a href="https://publications.waset.org/abstracts/search?q=striga%20resistance" title=" striga resistance"> striga resistance</a>, <a href="https://publications.waset.org/abstracts/search?q=provitamin%20A%20markers" title=" provitamin A markers"> provitamin A markers</a>, <a href="https://publications.waset.org/abstracts/search?q=beta-carotene%20hydroxylase%201" title=" beta-carotene hydroxylase 1"> beta-carotene hydroxylase 1</a>, <a href="https://publications.waset.org/abstracts/search?q=CrtRB1" title=" CrtRB1"> CrtRB1</a>, <a href="https://publications.waset.org/abstracts/search?q=beta-carotene" title=" beta-carotene"> beta-carotene</a>, <a href="https://publications.waset.org/abstracts/search?q=beta-cryptoxanthin" title=" beta-cryptoxanthin"> beta-cryptoxanthin</a>, <a href="https://publications.waset.org/abstracts/search?q=lycopene%20epsilon%20cyclase" title=" lycopene epsilon cyclase"> lycopene epsilon cyclase</a>, <a href="https://publications.waset.org/abstracts/search?q=LCYE" title=" LCYE"> LCYE</a> </p> <a href="https://publications.waset.org/abstracts/168070/inheritance-stability-and-validation-of-provitamin-a-markers-in-striga-hermonthica-resistant-maize" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/168070.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">70</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">1</span> Capability of a Single Antigen to Induce Both Protective and Disease Enhancing Antibody: An Obstacle in the Creation of Vaccines and Passive Immunotherapies</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Parul%20Kulshreshtha">Parul Kulshreshtha</a>, <a href="https://publications.waset.org/abstracts/search?q=Subrata%20Sinha"> Subrata Sinha</a>, <a href="https://publications.waset.org/abstracts/search?q=Rakesh%20Bhatnagar"> Rakesh Bhatnagar</a> </p> <p class="card-text"><strong>Abstract:</strong></p> This study was conducted by taking B. anthracis as a model pathogen. On infecting a host, B. anthracis secretes three proteins, namely, protective antigen (PA, 83kDa), edema factor (EF, 89 kDa) and lethal factor (LF, 90 kDa). These three proteins are the components of two anthrax toxins. PA binds to the cell surface receptors, namely, tumor endothelial marker (TEM) 8 and capillary morphogenesis protein (CMG) 2. TEM8 and CMG2 interact with LDL-receptor related protein (LRP) 6 for endocytosis of EF and LF. On entering the cell, EF acts as a calmodulin-dependent adenylate cyclase that causes a prolonged increase of cytosolic cyclic adenosine monophosphate (cAMP). LF is a metalloprotease that cleaves most isoforms of mitogen-activated protein kinase kinases (MAPKK/MEK) close to their N-terminus. By secreting these two toxins, B.anthracis ascertains death of the host. Once the systemic levels of the toxins rise, antibiotics alone cannot save the host. Therefore, toxin-specific inhibitors have to be developed. In this wake, monoclonal antibodies have been developed for the neutralization of toxic effects of anthrax toxins. We created hybridomas by using spleen of mice that were actively immunized with rLFn (recombinant N-terminal domain of lethal factor of B. anthracis) to obtain anti-toxin antibodies. Later on, separate group of mice were immunized with rLFn to obtain a polyclonal control for passive immunization studies of monoclonal antibodies. This led to the identification of one cohort of rLFn-immunized mice that harboured disease-enhancing polyclonal antibodies. At the same time, the monoclonal antibodies from all the hybridomas were being tested. Two hybridomas secreted monoclonal antibodies (H8 and H10) that were cross-reactive with EF (edema factor) and LF (lethal factor), while the other two hybridomas secreted LF-specific antibodies (H7 and H11). The protective efficacy of H7, H8, H10 and H11 was investigated. H7, H8 and H10 were found to be protective. H11 was found to have disease enhancing characteristics in-vitro and in mouse model of challenge with B. anthracis. In this study the disease enhancing character of H11 monoclonal antibody and anti-rLFn polyclonal sera was investigated. Combination of H11 with protective monoclonal antibodies (H8 and H10) reduced its disease enhancing nature both in-vitro and in-vivo. But combination of H11 with LETscFv (an scFv with VH and VL identical to H10 but lacking Fc region) could not abrogate the disease-enhancing character of H11 mAb. Therefore it was concluded that for suppression of disease enhancement, Fc portion was absolutely essential for interaction of H10 with H11. Our study indicates that the protective potential of an antibody depends equally on its idiotype/ antigen specificity and its isotype. A number of monoclonal and engineered antibodies are being explored as immunotherapeutics but it is absolutely essential to characterize each one for their individual and combined protective potential. Although new in the sphere of toxin-based diseases, it is extremely important to characterize the disease-enhancing nature of polyclonal as well as monoclonal antibodies. This is because several anti-viral therapeutics and vaccines have failed in the face of this phenomenon. The passive –immunotherapy thus needs to be well formulated to avoid any contraindications. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=immunotherapy" title="immunotherapy">immunotherapy</a>, <a href="https://publications.waset.org/abstracts/search?q=polyclonal" title=" polyclonal"> polyclonal</a>, <a href="https://publications.waset.org/abstracts/search?q=monoclonal" title=" monoclonal"> monoclonal</a>, <a href="https://publications.waset.org/abstracts/search?q=antibody-dependent%20disease%20enhancement" title=" antibody-dependent disease enhancement"> antibody-dependent disease enhancement</a> </p> <a href="https://publications.waset.org/abstracts/41365/capability-of-a-single-antigen-to-induce-both-protective-and-disease-enhancing-antibody-an-obstacle-in-the-creation-of-vaccines-and-passive-immunotherapies" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41365.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">386</span> </span> </div> </div> </div> </main> <footer> <div id="infolinks" class="pt-3 pb-2"> <div class="container"> <div style="background-color:#f5f5f5;" class="p-3"> <div class="row"> <div class="col-md-2"> <ul class="list-unstyled"> About <li><a href="https://waset.org/page/support">About Us</a></li> <li><a href="https://waset.org/page/support#legal-information">Legal</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/WASET-16th-foundational-anniversary.pdf">WASET celebrates its 16th foundational anniversary</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Account <li><a href="https://waset.org/profile">My Account</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Explore <li><a href="https://waset.org/disciplines">Disciplines</a></li> <li><a href="https://waset.org/conferences">Conferences</a></li> <li><a href="https://waset.org/conference-programs">Conference Program</a></li> <li><a href="https://waset.org/committees">Committees</a></li> <li><a href="https://publications.waset.org">Publications</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Research <li><a href="https://publications.waset.org/abstracts">Abstracts</a></li> <li><a href="https://publications.waset.org">Periodicals</a></li> <li><a href="https://publications.waset.org/archive">Archive</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Open Science <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Science-Philosophy.pdf">Open Science Philosophy</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Science-Award.pdf">Open Science Award</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Society-Open-Science-and-Open-Innovation.pdf">Open Innovation</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Postdoctoral-Fellowship-Award.pdf">Postdoctoral Fellowship Award</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Scholarly-Research-Review.pdf">Scholarly Research Review</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Support <li><a href="https://waset.org/page/support">Support</a></li> <li><a href="https://waset.org/profile/messages/create">Contact Us</a></li> <li><a href="https://waset.org/profile/messages/create">Report Abuse</a></li> </ul> </div> </div> </div> </div> </div> <div class="container text-center"> <hr style="margin-top:0;margin-bottom:.3rem;"> <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank" class="text-muted small">Creative Commons Attribution 4.0 International License</a> <div id="copy" class="mt-2">© 2024 World Academy of Science, Engineering and Technology</div> </div> </footer> <a href="javascript:" id="return-to-top"><i class="fas fa-arrow-up"></i></a> <div class="modal" id="modal-template"> <div class="modal-dialog"> <div class="modal-content"> <div class="row m-0 mt-1"> <div class="col-md-12"> <button type="button" class="close" data-dismiss="modal" aria-label="Close"><span aria-hidden="true">×</span></button> </div> </div> <div class="modal-body"></div> </div> </div> </div> <script src="https://cdn.waset.org/static/plugins/jquery-3.3.1.min.js"></script> <script src="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/js/bootstrap.bundle.min.js"></script> <script src="https://cdn.waset.org/static/js/site.js?v=150220211556"></script> <script> jQuery(document).ready(function() { /*jQuery.get("https://publications.waset.org/xhr/user-menu", function (response) { jQuery('#mainNavMenu').append(response); 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