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data-work-id="116910670"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/116910670/Supplementary_Data_from_Mechanisms_of_Ascorbate_Induced_Cytotoxicity_in_Pancreatic_Cancer"><img alt="Research paper thumbnail of Supplementary Data from Mechanisms of Ascorbate-Induced Cytotoxicity in Pancreatic Cancer" class="work-thumbnail" src="https://attachments.academia-assets.com/112908854/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/116910670/Supplementary_Data_from_Mechanisms_of_Ascorbate_Induced_Cytotoxicity_in_Pancreatic_Cancer">Supplementary Data from Mechanisms of Ascorbate-Induced Cytotoxicity in Pancreatic Cancer</a></div><div class="wp-workCard_item 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Cytotoxicity in Pancreatic Cancer","translated_title":"","metadata":{"grobid_abstract":"Supplemental Figure 1. Ascorbate increases H 2 O 2 generation in cell culture medium. H 2 O 2 was measured by oxygen electrode. A. H 2 O 2 increased as a function of ascorbate concentration. Ascorbate (0.1, 5.0, and 10.0 mM) increased H 2 O 2 (20, 167, and 217 μM, respectively). B. H 2 O 2 increased as a function of time. Ascorbate (1 mM) increased H 2 O 2 concentrations to over 50 μM after 60 min of incubation. Supplemental Figure 2. Ascorbate-induced cytotoxicity is a non-caspase mediated cell death. A. Minimal change is seen in PARP cleavage in either a dose-dependent or timedependent manner following treatment with ascorbate. MIA PaCa-2 cells were treated with ascorbate (1-5 mM for 1 h) or with ascorbate (5 mM for 1 h). Cells were harvested up to 24 h and equal amounts of protein were separated on 15% SDS-PAGE and immunoblotted. The 116 kDa band represents intact PARP and the 85 kDa band represents the cleaved PARP. Data represent results from three separate experiments. B. Necrotic cells increased over time following ascorbate (5 mM). Annexin/propidium iodide staining measured by flow cytometry demonstrates an initial increase in the apoptotic fraction of cells one hour after ascorbate treatment. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="116910669"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/116910669/Tumor_necrosis_factor_related_apoptosis_inducing_ligand_mediated_activation_of_mitochondria_associated_nuclear_factor_kappaB_in_prostatic_carcinoma_cell_lines"><img alt="Research paper thumbnail of Tumor necrosis factor-related apoptosis-inducing ligand-mediated activation of mitochondria-associated nuclear factor-kappaB in prostatic carcinoma cell lines" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/116910669/Tumor_necrosis_factor_related_apoptosis_inducing_ligand_mediated_activation_of_mitochondria_associated_nuclear_factor_kappaB_in_prostatic_carcinoma_cell_lines">Tumor necrosis factor-related apoptosis-inducing ligand-mediated activation of mitochondria-associated nuclear factor-kappaB in prostatic carcinoma cell lines</a></div><div class="wp-workCard_item"><span>PubMed</span><span>, Oct 1, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">It has been suggested that some nuclear transcription factors may participate in the regulation o...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">It has been suggested that some nuclear transcription factors may participate in the regulation of mitochondrial functions through transcriptional control of mitochondrial DNA. Very little is known about the response of transcription factors within mitochondria to the activation of death receptors. Recent publications indicate that nuclear factor-kappaB (NF-kappaB) is localized in mitochondria of mammalian cells. Because of the critical role of mitochondria in the execution of many apoptotic pathways, we suggest that NF-kappaB-dependent mechanisms operating at the level of mitochondria contribute to its role in regulating death receptor signaling. We have found NF-kappaB p65 and p50 subunits with DNA binding activity in the mitochondria of prostatic carcinoma cell lines. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) affects DNA binding activity of mitochondria-associated NF-kappaB but does not change the amount of p65 in mitochondria, which suggests activation of mitochondrial NF-kappaB without additional translocation of NF-kappaB subunits to mitochondria. We have also shown that TRAIL decreases mitochondrial genome encoded mRNA levels and inhibition of NF-kappaB prevents this decrease. TRAIL effects on mitochondrial NF-kappaB-DNA binding and mitochondrial genome encoded mRNA levels also depend on Bcl-2 overexpression. In addition, transcription factor activator protein-1 with DNA binding activity is also found in mitochondria of prostatic carcinoma cells and TRAIL treatment affects this binding. In summary, NF-kappaB is found in mitochondria of prostatic carcinoma cells, where it is thought to regulate mitochondria genome encoded mRNA levels in response to TRAIL treatment.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="116910669"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="116910669"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 116910669; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=116910669]").text(description); $(".js-view-count[data-work-id=116910669]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 116910669; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='116910669']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 116910669, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=116910669]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":116910669,"title":"Tumor necrosis factor-related apoptosis-inducing ligand-mediated activation of mitochondria-associated nuclear factor-kappaB in prostatic carcinoma cell lines","translated_title":"","metadata":{"abstract":"It has been suggested that some nuclear transcription factors may participate in the regulation of mitochondrial functions through transcriptional control of mitochondrial DNA. Very little is known about the response of transcription factors within mitochondria to the activation of death receptors. Recent publications indicate that nuclear factor-kappaB (NF-kappaB) is localized in mitochondria of mammalian cells. Because of the critical role of mitochondria in the execution of many apoptotic pathways, we suggest that NF-kappaB-dependent mechanisms operating at the level of mitochondria contribute to its role in regulating death receptor signaling. We have found NF-kappaB p65 and p50 subunits with DNA binding activity in the mitochondria of prostatic carcinoma cell lines. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) affects DNA binding activity of mitochondria-associated NF-kappaB but does not change the amount of p65 in mitochondria, which suggests activation of mitochondrial NF-kappaB without additional translocation of NF-kappaB subunits to mitochondria. We have also shown that TRAIL decreases mitochondrial genome encoded mRNA levels and inhibition of NF-kappaB prevents this decrease. TRAIL effects on mitochondrial NF-kappaB-DNA binding and mitochondrial genome encoded mRNA levels also depend on Bcl-2 overexpression. In addition, transcription factor activator protein-1 with DNA binding activity is also found in mitochondria of prostatic carcinoma cells and TRAIL treatment affects this binding. In summary, NF-kappaB is found in mitochondria of prostatic carcinoma cells, where it is thought to regulate mitochondria genome encoded mRNA levels in response to TRAIL treatment.","publication_date":{"day":1,"month":10,"year":2004,"errors":{}},"publication_name":"PubMed"},"translated_abstract":"It has been suggested that some nuclear transcription factors may participate in the regulation of mitochondrial functions through transcriptional control of mitochondrial DNA. Very little is known about the response of transcription factors within mitochondria to the activation of death receptors. Recent publications indicate that nuclear factor-kappaB (NF-kappaB) is localized in mitochondria of mammalian cells. Because of the critical role of mitochondria in the execution of many apoptotic pathways, we suggest that NF-kappaB-dependent mechanisms operating at the level of mitochondria contribute to its role in regulating death receptor signaling. We have found NF-kappaB p65 and p50 subunits with DNA binding activity in the mitochondria of prostatic carcinoma cell lines. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) affects DNA binding activity of mitochondria-associated NF-kappaB but does not change the amount of p65 in mitochondria, which suggests activation of mitochondrial NF-kappaB without additional translocation of NF-kappaB subunits to mitochondria. 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Quantitative RT-PCR showing effective silencing of Rb1 mRNA by Rb1 shRNAs in RABL6A kn...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Figure S4. Quantitative RT-PCR showing effective silencing of Rb1 mRNA by Rb1 shRNAs in RABL6A knockdown cells.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="116910666"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="116910666"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 116910666; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=116910666]").text(description); $(".js-view-count[data-work-id=116910666]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 116910666; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='116910666']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 116910666, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=116910666]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":116910666,"title":"Figure S4 from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner","translated_title":"","metadata":{"abstract":"Figure S4. 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Cohen)" class="work-thumbnail" src="https://attachments.academia-assets.com/112908867/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/116910665/Tumor_Necrosis_Factor_Related_Apoptosis_Inducing_Ligand_Mediated_Activation_of_Mitochondria_Associated_Nuclear_Factor_%CE%BA_B_in_Prostatic_Carcinoma_Cell_Lines_1_1_NIH_grant_CA93870_M_B_Cohen_">Tumor Necrosis Factor − Related Apoptosis-Inducing Ligand − Mediated Activation of Mitochondria-Associated Nuclear Factor- κ B in Prostatic Carcinoma Cell Lines 1 1 NIH grant CA93870 (M.B. Cohen)</a></div><div class="wp-workCard_item"><span>Molecular Cancer Research</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1aed5764a2ead78e69d683cc98a449e5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":112908867,"asset_id":116910665,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/112908867/download_file?st=MTczMjcwMTg0MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="116910665"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="116910665"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 116910665; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=116910665]").text(description); $(".js-view-count[data-work-id=116910665]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 116910665; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='116910665']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 116910665, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "1aed5764a2ead78e69d683cc98a449e5" } } $('.js-work-strip[data-work-id=116910665]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":116910665,"title":"Tumor Necrosis Factor − Related Apoptosis-Inducing Ligand − Mediated Activation of Mitochondria-Associated Nuclear Factor- κ B in Prostatic Carcinoma Cell Lines 1 1 NIH grant CA93870 (M.B. 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Quantitative RT-PCR showing RABL6A depletion does not affect p21 mRNA expression</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="106421528"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="106421528"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 106421528; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=106421528]").text(description); $(".js-view-count[data-work-id=106421528]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 106421528; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='106421528']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 106421528, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=106421528]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":106421528,"title":"Figure S3 from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner","translated_title":"","metadata":{"abstract":"Figure S3. 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Representative IPA mechanistic network for signaling regulators predicted to contribut...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Figure S2. Representative IPA mechanistic network for signaling regulators predicted to contribute to the RABL6A knockdown phenotype.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="106421526"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="106421526"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 106421526; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=106421526]").text(description); $(".js-view-count[data-work-id=106421526]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 106421526; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='106421526']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 106421526, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=106421526]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":106421526,"title":"Figure S2 from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner","translated_title":"","metadata":{"abstract":"Figure S2. 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List of differentially regulated genes caused by RABL6A knockdown (KD), relative to con...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Table S1. List of differentially regulated genes caused by RABL6A knockdown (KD), relative to control (CON), in BON-1 PNET cells.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="106421524"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="106421524"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 106421524; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=106421524]").text(description); $(".js-view-count[data-work-id=106421524]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 106421524; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='106421524']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 106421524, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=106421524]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":106421524,"title":"Table S1 from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner","translated_title":"","metadata":{"abstract":"Table S1. 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Cohen)" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/100064636/Tumor_Necrosis_Factor_Related_Apoptosis_Inducing_Ligand_Mediated_Activation_of_Mitochondria_Associated_Nuclear_Factor_%CE%BAB_in_Prostatic_Carcinoma_Cell_Lines11NIH_grant_CA93870_M_B_Cohen_">Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Mediated Activation of Mitochondria-Associated Nuclear Factor-κB in Prostatic Carcinoma Cell Lines11NIH grant CA93870 (M.B. Cohen)</a></div><div class="wp-workCard_item"><span>Molecular Cancer Research</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">It has been suggested that some nuclear transcription factors may participate in the regulation o...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">It has been suggested that some nuclear transcription factors may participate in the regulation of mitochondrial functions through transcriptional control of mitochondrial DNA. Very little is known about the response of transcription factors within mitochondria to the activation of death receptors. Recent publications indicate that nuclear factor-κB (NF-κB) is localized in mitochondria of mammalian cells. Because of the critical role of mitochondria in the execution of many apoptotic pathways, we suggest that NF-κB-dependent mechanisms operating at the level of mitochondria contribute to its role in regulating death receptor signaling. We have found NF-κB p65 and p50 subunits with DNA binding activity in the mitochondria of prostatic carcinoma cell lines. Tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) affects DNA binding activity of mitochondria-associated NF-κB but does not change the amount of p65 in mitochondria, which suggests activation of mitochondrial NF-κB w...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100064636"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100064636"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100064636; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=100064636]").text(description); $(".js-view-count[data-work-id=100064636]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 100064636; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='100064636']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 100064636, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=100064636]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":100064636,"title":"Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Mediated Activation of Mitochondria-Associated Nuclear Factor-κB in Prostatic Carcinoma Cell Lines11NIH grant CA93870 (M.B. 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Cohen)" class="work-thumbnail" src="https://attachments.academia-assets.com/100988655/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/100064634/Tumor_Necrosis_Factor_Related_Apoptosis_Inducing_Ligand_Mediated_Activation_of_Mitochondria_Associated_Nuclear_Factor_%CE%BAB_in_Prostatic_Carcinoma_Cell_Lines11NIH_grant_CA93870_M_B_Cohen_">Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Mediated Activation of Mitochondria-Associated Nuclear Factor-κB in Prostatic Carcinoma Cell Lines11NIH grant CA93870 (M.B. Cohen)</a></div><div class="wp-workCard_item"><span>Molecular Cancer Research</span><span>, Oct 1, 2004</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9205a8aa10e4208bcb9be9b1f5cce157" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":100988655,"asset_id":100064634,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/100988655/download_file?st=MTczMjcwMTg0MSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100064634"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100064634"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100064634; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=100064634]").text(description); $(".js-view-count[data-work-id=100064634]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 100064634; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='100064634']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 100064634, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "9205a8aa10e4208bcb9be9b1f5cce157" } } $('.js-work-strip[data-work-id=100064634]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":100064634,"title":"Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Mediated Activation of Mitochondria-Associated Nuclear Factor-κB in Prostatic Carcinoma Cell Lines11NIH grant CA93870 (M.B. Cohen)","translated_title":"","metadata":{"grobid_abstract":"It has been suggested that some nuclear transcription factors may participate in the regulation of mitochondrial functions through transcriptional control of mitochondrial DNA. Very little is known about the response of transcription factors within mitochondria to the activation of death receptors. Recent publications indicate that nuclear factor-KB (NF-KB) is localized in mitochondria of mammalian cells. Because of the critical role of mitochondria in the execution of many apoptotic pathways, we suggest that NF-KB-dependent mechanisms operating at the level of mitochondria contribute to its role in regulating death receptor signaling. We have found NF-KB p65 and p50 subunits with DNA binding activity in the mitochondria of prostatic carcinoma cell lines. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) affects DNA binding activity of mitochondria-associated NF-KB but does not change the amount of p65 in mitochondria, which suggests activation of mitochondrial NF-KB without additional translocation of NF-KB subunits to mitochondria. We have also shown that TRAIL decreases mitochondrial genome encoded mRNA levels and inhibition of NF-KB prevents this decrease. TRAIL effects on mitochondrial NF-KB-DNA binding and mitochondrial genome encoded mRNA levels also depend on Bcl-2 overexpression. In addition, transcription factor activator protein-1 with DNA binding activity is also found in mitochondria of prostatic carcinoma cells and TRAIL treatment affects this binding. In summary, NF-KB is found in mitochondria of prostatic carcinoma cells, where it is thought to regulate mitochondria genome encoded mRNA levels in response to TRAIL treatment. 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Ascorbate increases H 2 O 2 generation in cell culture medium. H 2 O 2 was measured by oxygen electrode. A. H 2 O 2 increased as a function of ascorbate concentration. Ascorbate (0.1, 5.0, and 10.0 mM) increased H 2 O 2 (20, 167, and 217 μM, respectively). B. H 2 O 2 increased as a function of time. Ascorbate (1 mM) increased H 2 O 2 concentrations to over 50 μM after 60 min of incubation. Supplemental Figure 2. Ascorbate-induced cytotoxicity is a non-caspase mediated cell death. A. Minimal change is seen in PARP cleavage in either a dose-dependent or timedependent manner following treatment with ascorbate. MIA PaCa-2 cells were treated with ascorbate (1-5 mM for 1 h) or with ascorbate (5 mM for 1 h). Cells were harvested up to 24 h and equal amounts of protein were separated on 15% SDS-PAGE and immunoblotted. The 116 kDa band represents intact PARP and the 85 kDa band represents the cleaved PARP. Data represent results from three separate experiments. B. Necrotic cells increased over time following ascorbate (5 mM). Annexin/propidium iodide staining measured by flow cytometry demonstrates an initial increase in the apoptotic fraction of cells one hour after ascorbate treatment. However, the necrotic fraction of cells increased in a time-dependent manner following treatment with ascorbate.","publication_date":{"day":31,"month":3,"year":2023,"errors":{}},"grobid_abstract_attachment_id":112908854},"translated_abstract":null,"internal_url":"https://www.academia.edu/116910670/Supplementary_Data_from_Mechanisms_of_Ascorbate_Induced_Cytotoxicity_in_Pancreatic_Cancer","translated_internal_url":"","created_at":"2024-03-31T13:38:53.912-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":94918209,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":112908854,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/112908854/thumbnails/1.jpg","file_name":"10780432ccr091713-sup-supplementary_data.pdf","download_url":"https://www.academia.edu/attachments/112908854/download_file?st=MTczMjcwMTg0Miw4LjIyMi4yMDguMTQ2&st=MTczMjcwMTg0MCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Supplementary_Data_from_Mechanisms_of_As.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/112908854/10780432ccr091713-sup-supplementary_data-libre.pdf?1711917674=\u0026response-content-disposition=attachment%3B+filename%3DSupplementary_Data_from_Mechanisms_of_As.pdf\u0026Expires=1732705439\u0026Signature=OJlcOaNDdcKUdHmoCi0rOgyoG7PnBHR36okyEk7GCKEuyWfjmwmWThqnPbbL0~CjW93YaVrlHkaOjCjCa8tMNofYe6OBc9~~HppJV6E1xfFNv9~3Bqtcg1DxH74BlJnioi-Kow~ekjFJ6a3RMk27vYd-0bTqpAoAoDMmOnIIgo8vf7jtaPmzU~UOSxlKO6A74xQ7EeJCqojky0tVR0qwMK573yQI~vJJCKnXgo0OWdqr5KYRaWlOn4nx-Vei2pXE7St62VyFohM7pBwamB1a4fyMqCWGbll0ux-JuvO2l~4Eg3YYcRR1zZB-1~5ysdkxaHxjdwk-wbzqG4ndBxeS8w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Supplementary_Data_from_Mechanisms_of_Ascorbate_Induced_Cytotoxicity_in_Pancreatic_Cancer","translated_slug":"","page_count":3,"language":"en","content_type":"Work","owner":{"id":94918209,"first_name":"Agshin","middle_initials":null,"last_name":"Taghiyev","page_name":"AgshinTaghiyev","domain_name":"independent","created_at":"2018-10-11T07:04:06.359-07:00","display_name":"Agshin Taghiyev","url":"https://independent.academia.edu/AgshinTaghiyev"},"attachments":[{"id":112908854,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/112908854/thumbnails/1.jpg","file_name":"10780432ccr091713-sup-supplementary_data.pdf","download_url":"https://www.academia.edu/attachments/112908854/download_file?st=MTczMjcwMTg0Miw4LjIyMi4yMDguMTQ2&st=MTczMjcwMTg0MCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Supplementary_Data_from_Mechanisms_of_As.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/112908854/10780432ccr091713-sup-supplementary_data-libre.pdf?1711917674=\u0026response-content-disposition=attachment%3B+filename%3DSupplementary_Data_from_Mechanisms_of_As.pdf\u0026Expires=1732705439\u0026Signature=OJlcOaNDdcKUdHmoCi0rOgyoG7PnBHR36okyEk7GCKEuyWfjmwmWThqnPbbL0~CjW93YaVrlHkaOjCjCa8tMNofYe6OBc9~~HppJV6E1xfFNv9~3Bqtcg1DxH74BlJnioi-Kow~ekjFJ6a3RMk27vYd-0bTqpAoAoDMmOnIIgo8vf7jtaPmzU~UOSxlKO6A74xQ7EeJCqojky0tVR0qwMK573yQI~vJJCKnXgo0OWdqr5KYRaWlOn4nx-Vei2pXE7St62VyFohM7pBwamB1a4fyMqCWGbll0ux-JuvO2l~4Eg3YYcRR1zZB-1~5ysdkxaHxjdwk-wbzqG4ndBxeS8w__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":112908855,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/112908855/thumbnails/1.jpg","file_name":"10780432ccr091713-sup-supplementary_data.pdf","download_url":"https://www.academia.edu/attachments/112908855/download_file","bulk_download_file_name":"Supplementary_Data_from_Mechanisms_of_As.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/112908855/10780432ccr091713-sup-supplementary_data-libre.pdf?1711917673=\u0026response-content-disposition=attachment%3B+filename%3DSupplementary_Data_from_Mechanisms_of_As.pdf\u0026Expires=1732705439\u0026Signature=SQzG2PwPnNdnx3G~~wClfYXnfCDDEEv3PFRyYCXzjh1FoRS~cEyQj6GFoaVKI0tbGNHfWf2-h-LnQy0uV-~fQyArmzea73ST4f4PSpzrRki40XQs0IXxgQbRXP2ORgJmCSqpfMjEP8rJu5uQxaXZbLY4buu5qdCyWQxww~k9wzSLB1ddaJ-kj8-hz2JuXBa71MQ4X5Ox97mXIyeO6cRC8QvKd7HHlxxVo3Yp497DH7f4QBEkJFlXgCsGq-RCzaJd5upwrqPmZqqVybQuXxi2yCvzcpRufIv0Ths1Dg31y2EQ06kSmt20~-4LcqrU2a6IIs1IUAhgzgxIbOnmgsu76g__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":22050,"name":"Cytotoxicity","url":"https://www.academia.edu/Documents/in/Cytotoxicity"},{"id":26623,"name":"Pancreatic Cancer","url":"https://www.academia.edu/Documents/in/Pancreatic_Cancer"}],"urls":[{"id":40747510,"url":"https://aacr.figshare.com/articles/journal_contribution/Supplementary_Data_from_Mechanisms_of_Ascorbate-Induced_Cytotoxicity_in_Pancreatic_Cancer/22440258/1/files/39891120.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="116910669"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/116910669/Tumor_necrosis_factor_related_apoptosis_inducing_ligand_mediated_activation_of_mitochondria_associated_nuclear_factor_kappaB_in_prostatic_carcinoma_cell_lines"><img alt="Research paper thumbnail of Tumor necrosis factor-related apoptosis-inducing ligand-mediated activation of mitochondria-associated nuclear factor-kappaB in prostatic carcinoma cell lines" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/116910669/Tumor_necrosis_factor_related_apoptosis_inducing_ligand_mediated_activation_of_mitochondria_associated_nuclear_factor_kappaB_in_prostatic_carcinoma_cell_lines">Tumor necrosis factor-related apoptosis-inducing ligand-mediated activation of mitochondria-associated nuclear factor-kappaB in prostatic carcinoma cell lines</a></div><div class="wp-workCard_item"><span>PubMed</span><span>, Oct 1, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">It has been suggested that some nuclear transcription factors may participate in the regulation o...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">It has been suggested that some nuclear transcription factors may participate in the regulation of mitochondrial functions through transcriptional control of mitochondrial DNA. Very little is known about the response of transcription factors within mitochondria to the activation of death receptors. Recent publications indicate that nuclear factor-kappaB (NF-kappaB) is localized in mitochondria of mammalian cells. Because of the critical role of mitochondria in the execution of many apoptotic pathways, we suggest that NF-kappaB-dependent mechanisms operating at the level of mitochondria contribute to its role in regulating death receptor signaling. We have found NF-kappaB p65 and p50 subunits with DNA binding activity in the mitochondria of prostatic carcinoma cell lines. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) affects DNA binding activity of mitochondria-associated NF-kappaB but does not change the amount of p65 in mitochondria, which suggests activation of mitochondrial NF-kappaB without additional translocation of NF-kappaB subunits to mitochondria. We have also shown that TRAIL decreases mitochondrial genome encoded mRNA levels and inhibition of NF-kappaB prevents this decrease. TRAIL effects on mitochondrial NF-kappaB-DNA binding and mitochondrial genome encoded mRNA levels also depend on Bcl-2 overexpression. In addition, transcription factor activator protein-1 with DNA binding activity is also found in mitochondria of prostatic carcinoma cells and TRAIL treatment affects this binding. In summary, NF-kappaB is found in mitochondria of prostatic carcinoma cells, where it is thought to regulate mitochondria genome encoded mRNA levels in response to TRAIL treatment.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="116910669"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="116910669"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 116910669; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=116910669]").text(description); $(".js-view-count[data-work-id=116910669]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 116910669; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='116910669']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 116910669, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=116910669]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":116910669,"title":"Tumor necrosis factor-related apoptosis-inducing ligand-mediated activation of mitochondria-associated nuclear factor-kappaB in prostatic carcinoma cell lines","translated_title":"","metadata":{"abstract":"It has been suggested that some nuclear transcription factors may participate in the regulation of mitochondrial functions through transcriptional control of mitochondrial DNA. Very little is known about the response of transcription factors within mitochondria to the activation of death receptors. Recent publications indicate that nuclear factor-kappaB (NF-kappaB) is localized in mitochondria of mammalian cells. Because of the critical role of mitochondria in the execution of many apoptotic pathways, we suggest that NF-kappaB-dependent mechanisms operating at the level of mitochondria contribute to its role in regulating death receptor signaling. We have found NF-kappaB p65 and p50 subunits with DNA binding activity in the mitochondria of prostatic carcinoma cell lines. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) affects DNA binding activity of mitochondria-associated NF-kappaB but does not change the amount of p65 in mitochondria, which suggests activation of mitochondrial NF-kappaB without additional translocation of NF-kappaB subunits to mitochondria. We have also shown that TRAIL decreases mitochondrial genome encoded mRNA levels and inhibition of NF-kappaB prevents this decrease. TRAIL effects on mitochondrial NF-kappaB-DNA binding and mitochondrial genome encoded mRNA levels also depend on Bcl-2 overexpression. In addition, transcription factor activator protein-1 with DNA binding activity is also found in mitochondria of prostatic carcinoma cells and TRAIL treatment affects this binding. In summary, NF-kappaB is found in mitochondria of prostatic carcinoma cells, where it is thought to regulate mitochondria genome encoded mRNA levels in response to TRAIL treatment.","publication_date":{"day":1,"month":10,"year":2004,"errors":{}},"publication_name":"PubMed"},"translated_abstract":"It has been suggested that some nuclear transcription factors may participate in the regulation of mitochondrial functions through transcriptional control of mitochondrial DNA. Very little is known about the response of transcription factors within mitochondria to the activation of death receptors. Recent publications indicate that nuclear factor-kappaB (NF-kappaB) is localized in mitochondria of mammalian cells. Because of the critical role of mitochondria in the execution of many apoptotic pathways, we suggest that NF-kappaB-dependent mechanisms operating at the level of mitochondria contribute to its role in regulating death receptor signaling. We have found NF-kappaB p65 and p50 subunits with DNA binding activity in the mitochondria of prostatic carcinoma cell lines. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) affects DNA binding activity of mitochondria-associated NF-kappaB but does not change the amount of p65 in mitochondria, which suggests activation of mitochondrial NF-kappaB without additional translocation of NF-kappaB subunits to mitochondria. We have also shown that TRAIL decreases mitochondrial genome encoded mRNA levels and inhibition of NF-kappaB prevents this decrease. TRAIL effects on mitochondrial NF-kappaB-DNA binding and mitochondrial genome encoded mRNA levels also depend on Bcl-2 overexpression. In addition, transcription factor activator protein-1 with DNA binding activity is also found in mitochondria of prostatic carcinoma cells and TRAIL treatment affects this binding. In summary, NF-kappaB is found in mitochondria of prostatic carcinoma cells, where it is thought to regulate mitochondria genome encoded mRNA levels in response to TRAIL treatment.","internal_url":"https://www.academia.edu/116910669/Tumor_necrosis_factor_related_apoptosis_inducing_ligand_mediated_activation_of_mitochondria_associated_nuclear_factor_kappaB_in_prostatic_carcinoma_cell_lines","translated_internal_url":"","created_at":"2024-03-31T13:38:53.746-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":94918209,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Tumor_necrosis_factor_related_apoptosis_inducing_ligand_mediated_activation_of_mitochondria_associated_nuclear_factor_kappaB_in_prostatic_carcinoma_cell_lines","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":94918209,"first_name":"Agshin","middle_initials":null,"last_name":"Taghiyev","page_name":"AgshinTaghiyev","domain_name":"independent","created_at":"2018-10-11T07:04:06.359-07:00","display_name":"Agshin Taghiyev","url":"https://independent.academia.edu/AgshinTaghiyev"},"attachments":[],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":13827,"name":"Cell Biology","url":"https://www.academia.edu/Documents/in/Cell_Biology"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":63093,"name":"Mitochondrial DNA","url":"https://www.academia.edu/Documents/in/Mitochondrial_DNA"},{"id":98939,"name":"Pubmed","url":"https://www.academia.edu/Documents/in/Pubmed"},{"id":213901,"name":"Transcription Factor","url":"https://www.academia.edu/Documents/in/Transcription_Factor"},{"id":2431818,"name":"Mitochondrion","url":"https://www.academia.edu/Documents/in/Mitochondrion"}],"urls":[{"id":40747509,"url":"https://pubmed.ncbi.nlm.nih.gov/15498932"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="116910668"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/116910668/Tumor_Necrosis_Factor_Related_Apoptosis_Inducing_Ligand_Mediated_Activation_of_Mitochondria_Associated_Nuclear_Factor_%CE%BAB_in_Prostatic_Carcinoma_Cell_Lines"><img alt="Research paper thumbnail of Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Mediated Activation of Mitochondria-Associated Nuclear Factor-κB in Prostatic Carcinoma Cell Lines" class="work-thumbnail" src="https://attachments.academia-assets.com/112908853/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/116910668/Tumor_Necrosis_Factor_Related_Apoptosis_Inducing_Ligand_Mediated_Activation_of_Mitochondria_Associated_Nuclear_Factor_%CE%BAB_in_Prostatic_Carcinoma_Cell_Lines">Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Mediated Activation of Mitochondria-Associated Nuclear Factor-κB in Prostatic Carcinoma Cell Lines</a></div><div class="wp-workCard_item"><span>Molecular Cancer Research</span><span>, Oct 1, 2004</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1563f661a194de7601f694dbf1e3e848" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":112908853,"asset_id":116910668,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/112908853/download_file?st=MTczMjcwMTg0Miw4LjIyMi4yMDguMTQ2&st=MTczMjcwMTg0MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="116910668"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="116910668"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 116910668; 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Very little is known about the response of transcription factors within mitochondria to the activation of death receptors. Recent publications indicate that nuclear factor-KB (NF-KB) is localized in mitochondria of mammalian cells. Because of the critical role of mitochondria in the execution of many apoptotic pathways, we suggest that NF-KB-dependent mechanisms operating at the level of mitochondria contribute to its role in regulating death receptor signaling. We have found NF-KB p65 and p50 subunits with DNA binding activity in the mitochondria of prostatic carcinoma cell lines. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) affects DNA binding activity of mitochondria-associated NF-KB but does not change the amount of p65 in mitochondria, which suggests activation of mitochondrial NF-KB without additional translocation of NF-KB subunits to mitochondria. We have also shown that TRAIL decreases mitochondrial genome encoded mRNA levels and inhibition of NF-KB prevents this decrease. TRAIL effects on mitochondrial NF-KB-DNA binding and mitochondrial genome encoded mRNA levels also depend on Bcl-2 overexpression. In addition, transcription factor activator protein-1 with DNA binding activity is also found in mitochondria of prostatic carcinoma cells and TRAIL treatment affects this binding. In summary, NF-KB is found in mitochondria of prostatic carcinoma cells, where it is thought to regulate mitochondria genome encoded mRNA levels in response to TRAIL treatment. (Mol Cancer Res 2004;2(10):574-84)","publication_date":{"day":1,"month":10,"year":2004,"errors":{}},"publication_name":"Molecular Cancer 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Quantitative RT-PCR showing effective silencing of Rb1 mRNA by Rb1 shRNAs in RABL6A kn...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Figure S4. Quantitative RT-PCR showing effective silencing of Rb1 mRNA by Rb1 shRNAs in RABL6A knockdown cells.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="116910666"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="116910666"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 116910666; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=116910666]").text(description); $(".js-view-count[data-work-id=116910666]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 116910666; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='116910666']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 116910666, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=116910666]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":116910666,"title":"Figure S4 from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner","translated_title":"","metadata":{"abstract":"Figure S4. 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Cohen)" class="work-thumbnail" src="https://attachments.academia-assets.com/112908867/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/116910665/Tumor_Necrosis_Factor_Related_Apoptosis_Inducing_Ligand_Mediated_Activation_of_Mitochondria_Associated_Nuclear_Factor_%CE%BA_B_in_Prostatic_Carcinoma_Cell_Lines_1_1_NIH_grant_CA93870_M_B_Cohen_">Tumor Necrosis Factor − Related Apoptosis-Inducing Ligand − Mediated Activation of Mitochondria-Associated Nuclear Factor- κ B in Prostatic Carcinoma Cell Lines 1 1 NIH grant CA93870 (M.B. Cohen)</a></div><div class="wp-workCard_item"><span>Molecular Cancer Research</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1aed5764a2ead78e69d683cc98a449e5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":112908867,"asset_id":116910665,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/112908867/download_file?st=MTczMjcwMTg0Miw4LjIyMi4yMDguMTQ2&st=MTczMjcwMTg0MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="116910665"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="116910665"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 116910665; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=116910665]").text(description); $(".js-view-count[data-work-id=116910665]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 116910665; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='116910665']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 116910665, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "1aed5764a2ead78e69d683cc98a449e5" } } $('.js-work-strip[data-work-id=116910665]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":116910665,"title":"Tumor Necrosis Factor − Related Apoptosis-Inducing Ligand − Mediated Activation of Mitochondria-Associated Nuclear Factor- κ B in Prostatic Carcinoma Cell Lines 1 1 NIH grant CA93870 (M.B. Cohen)","translated_title":"","metadata":{"grobid_abstract":"As the most common primary bone neoplasm, osteosarcoma is highly aggressive and represents a high risk to human health. Biological agents, including tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), are considered promising therapeutic strategies for osteosarcoma. The current issue limiting the application of TRAIL gene therapy is that normal cells are also affected due to the lack of tumor selectivity. The present study aimed to employ the miRNA response elements (MREs) of microRNA (miR)-34 and miR-122, which are tumor suppressors, to enable the selective expression of TRAIL by adenoviral vectors in osteosarcoma cells. The results revealed that miR-34 and miR-122 were underexpressed in osteosarcoma tissues, compared with normal tissues. The MREs of miR-34 and miR-122 ensured that the luciferase gene was expressed selectively in osteosarcoma cells. Adenovirus (Ad)-TRAIL-34-122, which expressed TRAIL in an miR-34 and miR-122-regulated manner, selectively expressed TRAIL in the osteosarcoma cells assessed, which was detected using reverse transcription quantitative polymerase chain reaction, immunoblotting and ELISA. Apoptosis and cytotoxicity were also detected in the osteosarcoma cells, compared with the normal cells. Animal experiments further indicated that Ad-TRAIL-34-122 was able to reduce the growth of osteosarcoma xenografts without toxicity to the liver. 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Quantitative PCR measurement of human RABL6A DNA copy number in human PNET patient sam...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Figure S1. Quantitative PCR measurement of human RABL6A DNA copy number in human PNET patient samples.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="106421530"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="106421530"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 106421530; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=106421530]").text(description); $(".js-view-count[data-work-id=106421530]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 106421530; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='106421530']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 106421530, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=106421530]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":106421530,"title":"Figure S1 from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner","translated_title":"","metadata":{"abstract":"Figure S1. 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Quantitative RT-PCR showing RABL6A depletion does not affect p21 mRNA expression</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="106421528"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="106421528"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 106421528; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=106421528]").text(description); $(".js-view-count[data-work-id=106421528]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 106421528; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='106421528']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 106421528, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=106421528]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":106421528,"title":"Figure S3 from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner","translated_title":"","metadata":{"abstract":"Figure S3. 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Representative IPA mechanistic network for signaling regulators predicted to contribut...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Figure S2. Representative IPA mechanistic network for signaling regulators predicted to contribute to the RABL6A knockdown phenotype.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="106421526"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="106421526"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 106421526; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=106421526]").text(description); $(".js-view-count[data-work-id=106421526]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 106421526; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='106421526']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 106421526, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=106421526]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":106421526,"title":"Figure S2 from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner","translated_title":"","metadata":{"abstract":"Figure S2. 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List of differentially regulated genes caused by RABL6A knockdown (KD), relative to con...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Table S1. List of differentially regulated genes caused by RABL6A knockdown (KD), relative to control (CON), in BON-1 PNET cells.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="106421524"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="106421524"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 106421524; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=106421524]").text(description); $(".js-view-count[data-work-id=106421524]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 106421524; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='106421524']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 106421524, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=106421524]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":106421524,"title":"Table S1 from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner","translated_title":"","metadata":{"abstract":"Table S1. 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Effect of RABL6A overexpression on Rb1 and p21 mRNA and protein expression</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="106421522"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="106421522"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 106421522; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=106421522]").text(description); $(".js-view-count[data-work-id=106421522]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 106421522; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='106421522']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 106421522, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=106421522]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":106421522,"title":"Figure S5 from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner","translated_title":"","metadata":{"abstract":"Figure S5. 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="100064636"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/100064636/Tumor_Necrosis_Factor_Related_Apoptosis_Inducing_Ligand_Mediated_Activation_of_Mitochondria_Associated_Nuclear_Factor_%CE%BAB_in_Prostatic_Carcinoma_Cell_Lines11NIH_grant_CA93870_M_B_Cohen_"><img alt="Research paper thumbnail of Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Mediated Activation of Mitochondria-Associated Nuclear Factor-κB in Prostatic Carcinoma Cell Lines11NIH grant CA93870 (M.B. Cohen)" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/100064636/Tumor_Necrosis_Factor_Related_Apoptosis_Inducing_Ligand_Mediated_Activation_of_Mitochondria_Associated_Nuclear_Factor_%CE%BAB_in_Prostatic_Carcinoma_Cell_Lines11NIH_grant_CA93870_M_B_Cohen_">Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Mediated Activation of Mitochondria-Associated Nuclear Factor-κB in Prostatic Carcinoma Cell Lines11NIH grant CA93870 (M.B. Cohen)</a></div><div class="wp-workCard_item"><span>Molecular Cancer Research</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">It has been suggested that some nuclear transcription factors may participate in the regulation o...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">It has been suggested that some nuclear transcription factors may participate in the regulation of mitochondrial functions through transcriptional control of mitochondrial DNA. Very little is known about the response of transcription factors within mitochondria to the activation of death receptors. Recent publications indicate that nuclear factor-κB (NF-κB) is localized in mitochondria of mammalian cells. Because of the critical role of mitochondria in the execution of many apoptotic pathways, we suggest that NF-κB-dependent mechanisms operating at the level of mitochondria contribute to its role in regulating death receptor signaling. We have found NF-κB p65 and p50 subunits with DNA binding activity in the mitochondria of prostatic carcinoma cell lines. 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Cohen)" class="work-thumbnail" src="https://attachments.academia-assets.com/100988655/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/100064634/Tumor_Necrosis_Factor_Related_Apoptosis_Inducing_Ligand_Mediated_Activation_of_Mitochondria_Associated_Nuclear_Factor_%CE%BAB_in_Prostatic_Carcinoma_Cell_Lines11NIH_grant_CA93870_M_B_Cohen_">Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Mediated Activation of Mitochondria-Associated Nuclear Factor-κB in Prostatic Carcinoma Cell Lines11NIH grant CA93870 (M.B. Cohen)</a></div><div class="wp-workCard_item"><span>Molecular Cancer Research</span><span>, Oct 1, 2004</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9205a8aa10e4208bcb9be9b1f5cce157" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":100988655,"asset_id":100064634,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/100988655/download_file?st=MTczMjcwMTg0Miw4LjIyMi4yMDguMTQ2&st=MTczMjcwMTg0MSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100064634"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100064634"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100064634; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=100064634]").text(description); $(".js-view-count[data-work-id=100064634]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 100064634; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='100064634']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 100064634, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "9205a8aa10e4208bcb9be9b1f5cce157" } } $('.js-work-strip[data-work-id=100064634]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":100064634,"title":"Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Mediated Activation of Mitochondria-Associated Nuclear Factor-κB in Prostatic Carcinoma Cell Lines11NIH grant CA93870 (M.B. Cohen)","translated_title":"","metadata":{"grobid_abstract":"It has been suggested that some nuclear transcription factors may participate in the regulation of mitochondrial functions through transcriptional control of mitochondrial DNA. Very little is known about the response of transcription factors within mitochondria to the activation of death receptors. Recent publications indicate that nuclear factor-KB (NF-KB) is localized in mitochondria of mammalian cells. Because of the critical role of mitochondria in the execution of many apoptotic pathways, we suggest that NF-KB-dependent mechanisms operating at the level of mitochondria contribute to its role in regulating death receptor signaling. We have found NF-KB p65 and p50 subunits with DNA binding activity in the mitochondria of prostatic carcinoma cell lines. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) affects DNA binding activity of mitochondria-associated NF-KB but does not change the amount of p65 in mitochondria, which suggests activation of mitochondrial NF-KB without additional translocation of NF-KB subunits to mitochondria. We have also shown that TRAIL decreases mitochondrial genome encoded mRNA levels and inhibition of NF-KB prevents this decrease. TRAIL effects on mitochondrial NF-KB-DNA binding and mitochondrial genome encoded mRNA levels also depend on Bcl-2 overexpression. In addition, transcription factor activator protein-1 with DNA binding activity is also found in mitochondria of prostatic carcinoma cells and TRAIL treatment affects this binding. In summary, NF-KB is found in mitochondria of prostatic carcinoma cells, where it is thought to regulate mitochondria genome encoded mRNA levels in response to TRAIL treatment. 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