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10.1128/MCB.00067-16 http://scihub22266oqcxt.onion/10.1128/MCB.00067-16 C4907096!4907096 !27090638     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27090638 &cmd=llinks): Failed to open stream: HTTP request failed! 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Parallel Regulation of von Hippel-Lindau Disease by pVHL-Mediated Degradation of B-Myb and Hypoxia-Inducible Factor ? |pdf=|usr=}}{{27090638 }} gab.com Text Parallel Regulation of von Hippel-Lindau Disease by pVHL-Mediated Degradation of B-Myb and Hypoxia-Inducible Factor JO: Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27090638 #FOAvip pVHL, the protein product of the von Hippel-Lindau (VHL) tumor suppressor gene, is a ubiquitin ligase that targets hypoxia-inducible factor ? (HIF-?) for proteasomal degradation. Although HIF-? activation is necessary for VHL disease pathogenesis, constitutive activation of HIF-? alone did not induce renal clear cell carcinomas and pheochromocytomas in mice, suggesting the involvement of an HIF-?-independent pathway in VHL pathogenesis. Here, we show that the transcription factor B-Myb is a pVHL substrate that is degraded via the ubiquitin-proteasome pathway and that vascular endothelial growth factor (VEGF)- and/or platelet-derived growth factor (PDGF)-dependent tyrosine 15 phosphorylation of B-Myb prevents its degradation. Mice injected with B-Myb knockdown 786-O cells developed dramatically larger tumors than those bearing control cell tumors. Microarray screening of B-Myb-regulated genes showed that the expression of HIF-?-dependent genes was not affected by B-Myb knockdown, indicating that B-Myb prevents HIF-?-dependent tumorigenesis through an HIF-?-independent pathway. These data indicate that the regulation of B-Myb by pVHL plays a critical role in VHL disease. Twit Text FOAVip Parallel Regulation of von Hippel-Lindau Disease by pVHL-Mediated Degradation of B-Myb and Hypoxia-Inducible Factor ????Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27090638 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27090638 #FOAvip English Wikipedia <ref>{{Cite pmid|27090638 }}</ref> Parallel Regulation of von Hippel-Lindau Disease by pVHL-Mediated Degradation of B-Myb and Hypoxia-Inducible Factor ? #MMPMID27090638 Okumura F ; Uematsu K ; Byrne SD ; Hirano M ; Joo-Okumura A ; Nishikimi A ; Shuin T ; Fukui Y ; Nakatsukasa K ; Kamura T Mol Cell Biol 2016[Jun]; 36 (12 ): 1803-17 PMID27090638 show ga pVHL, the protein product of the von Hippel-Lindau (VHL) tumor suppressor gene, is a ubiquitin ligase that targets hypoxia-inducible factor ? (HIF-?) for proteasomal degradation. Although HIF-? activation is necessary for VHL disease pathogenesis, constitutive activation of HIF-? alone did not induce renal clear cell carcinomas and pheochromocytomas in mice, suggesting the involvement of an HIF-?-independent pathway in VHL pathogenesis. Here, we show that the transcription factor B-Myb is a pVHL substrate that is degraded via the ubiquitin-proteasome pathway and that vascular endothelial growth factor (VEGF)- and/or platelet-derived growth factor (PDGF)-dependent tyrosine 15 phosphorylation of B-Myb prevents its degradation. Mice injected with B-Myb knockdown 786-O cells developed dramatically larger tumors than those bearing control cell tumors. Microarray screening of B-Myb-regulated genes showed that the expression of HIF-?-dependent genes was not affected by B-Myb knockdown, indicating that B-Myb prevents HIF-?-dependent tumorigenesis through an HIF-?-independent pathway. These data indicate that the regulation of B-Myb by pVHL plays a critical role in VHL disease. |Animals [MESH] |Basic Helix-Loop-Helix Transcription Factors/*metabolism [MESH] |Cell Cycle Proteins/*genetics/*metabolism [MESH] |Cell Line, Tumor [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Gene Knockdown Techniques [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Mice [MESH] |Neoplasm Transplantation [MESH] |Phosphorylation [MESH] |Proteasome Endopeptidase Complex/metabolism [MESH] |Proteolysis [MESH] |Signal Transduction [MESH] |Trans-Activators/*genetics/*metabolism [MESH] |Tyrosine/*metabolism [MESH] |Ubiquitin/metabolism [MESH] |Von Hippel-Lindau Tumor Suppressor Protein/*metabolism [MESH]Parallel Regulation of von Hippel-Lindau Disease by pVHL-Mediated Degr(epmc).pdf DeepDyve Pubget Overpricing