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10.1016/j.devcel.2015.04.021 http://scihub22266oqcxt.onion/10.1016/j.devcel.2015.04.021 C4509618!4509618!26028220     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Dev+Cell 2015 ; 33 (5): 507-21 Nephropedia Template TP {{tp|p=26028220|t=2015. HIF1? represses cell stress pathways to allow proliferation of hypoxic fetal cardiomyocytes |pdf=|usr=}}{{26028220}} gab.com Text HIF1 represses cell stress pathways to allow proliferation of hypoxic fetal cardiomyocytes JO: Dev Cell http://www.kidney.de/pget.php?&tw=1&pmid=26028220 #FOAvip Transcriptional mediators of cell stress pathways, including HIF1?, ATF4, and p53, are key to normal development and play critical roles in disease, including ischemia and cancer. Despite their importance, mechanisms by which pathways mediated by these transcription factors interact with each other are not fully understood. In addressing the controversial role of HIF1? in cardiomyocytes (CMs) during heart development, we have discovered a mid-gestational requirement for HIF1? for proliferation of hypoxic CMs, involving metabolic switching and a complex interplay between HIF1?, ATF4 and p53. Loss of HIF1? resulted in activation of ATF4 and p53, the latter inhibiting CM proliferation. Bioinformatic and biochemical analyses revealed unexpected mechanisms by which HIF1? intersects with ATF4 and p53 pathways. Our results highlight previously undescribed roles of HIF1? and interactions between major cell stress pathways that could be targeted to enhance proliferation of CMs in ischemia, and may have relevance to other diseases, including cancer. Twit Text FOAVip HIF1 represses cell stress pathways to allow proliferation of hypoxic fetal cardiomyocytes ????Dev Cell http://www.kidney.de/pget.php?&tw=1&pmid=26028220 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26028220 #FOAvip English Wikipedia <ref>{{Cite pmid|26028220}}</ref> HIF1? represses cell stress pathways to allow proliferation of hypoxic fetal cardiomyocytes #MMPMID26028220 Guimarães-Camboa N; Stowe J; Aneas I; Sakabe N; Cattaneo P; Henderson L; Kilberg MS; Johnson RS; Chen J; McCulloch AD; Nobrega MA; Evans SM; Zambon AC Dev Cell 2015[Jun]; 33 (5): 507-21 PMID26028220show ga Transcriptional mediators of cell stress pathways, including HIF1?, ATF4, and p53, are key to normal development and play critical roles in disease, including ischemia and cancer. Despite their importance, mechanisms by which pathways mediated by these transcription factors interact with each other are not fully understood. In addressing the controversial role of HIF1? in cardiomyocytes (CMs) during heart development, we have discovered a mid-gestational requirement for HIF1? for proliferation of hypoxic CMs, involving metabolic switching and a complex interplay between HIF1?, ATF4 and p53. Loss of HIF1? resulted in activation of ATF4 and p53, the latter inhibiting CM proliferation. Bioinformatic and biochemical analyses revealed unexpected mechanisms by which HIF1? intersects with ATF4 and p53 pathways. Our results highlight previously undescribed roles of HIF1? and interactions between major cell stress pathways that could be targeted to enhance proliferation of CMs in ischemia, and may have relevance to other diseases, including cancer. äHIF1? represses cell stress pathways to allow proliferation of hypoxic(epmc).pdf DeepDyve Pubget Overpricing