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10.1128/MCB.01091-14 http://scihub22266oqcxt.onion/10.1128/MCB.01091-14 C4333088!4333088 !25561470     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25561470 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mol+Cell+Biol 2015 ; 35 (6 ): 956-76 Nephropedia Template TP {{tp|p=25561470 |t=2015. Regulation of the transcription factor EB-PGC1? axis by beclin-1 controls mitochondrial quality and cardiomyocyte death under stress |pdf=|usr=}}{{25561470 }} gab.com Text Regulation of the transcription factor EB-PGC1 axis by beclin-1 controls mitochondrial quality and cardiomyocyte death under stress JO: Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=25561470 #FOAvip In cardiac ischemia-reperfusion injury, reactive oxygen species (ROS) generation and upregulation of the hypoxia-inducible protein BNIP3 result in mitochondrial permeabilization, but impairment in autophagic removal of damaged mitochondria provokes programmed cardiomyocyte death. BNIP3 expression and ROS generation result in upregulation of beclin-1, a protein associated with transcriptional suppression of autophagy-lysosome proteins and reduced activation of transcription factor EB (TFEB), a master regulator of the autophagy-lysosome machinery. Partial beclin-1 knockdown transcriptionally stimulates lysosome biogenesis and autophagy via mTOR inhibition and activation of TFEB, enhancing removal of depolarized mitochondria. TFEB activation concomitantly stimulates mitochondrial biogenesis via PGC1? induction to restore normally polarized mitochondria and attenuate BNIP3- and hypoxia-reoxygenation-induced cell death. Conversely, overexpression of beclin-1 activates mTOR to inhibit TFEB, resulting in declines in lysosome numbers and suppression of PGC1? transcription. Importantly, knockdown of endogenous TFEB or PGC1? results in a complete or partial loss, respectively, of the cytoprotective effects of partial beclin-1 knockdown, indicating a critical role for both mitochondrial autophagy and biogenesis in ensuring cellular viability. These studies uncover a transcriptional feedback loop for beclin-1-mediated regulation of TFEB activation and implicate a central role for TFEB in coordinating mitochondrial autophagy with biogenesis to restore normally polarized mitochondria and prevent ischemia-reperfusion-induced cardiomyocyte death. Twit Text FOAVip Regulation of the transcription factor EB-PGC1 axis by beclin-1 controls mitochondrial quality and cardiomyocyte death under stress ????Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=25561470 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25561470 #FOAvip English Wikipedia <ref>{{Cite pmid|25561470 }}</ref> Regulation of the transcription factor EB-PGC1? axis by beclin-1 controls mitochondrial quality and cardiomyocyte death under stress #MMPMID25561470 Ma X ; Liu H ; Murphy JT ; Foyil SR ; Godar RJ ; Abuirqeba H ; Weinheimer CJ ; Barger PM ; Diwan A Mol Cell Biol 2015[Mar]; 35 (6 ): 956-76 PMID25561470 show ga In cardiac ischemia-reperfusion injury, reactive oxygen species (ROS) generation and upregulation of the hypoxia-inducible protein BNIP3 result in mitochondrial permeabilization, but impairment in autophagic removal of damaged mitochondria provokes programmed cardiomyocyte death. BNIP3 expression and ROS generation result in upregulation of beclin-1, a protein associated with transcriptional suppression of autophagy-lysosome proteins and reduced activation of transcription factor EB (TFEB), a master regulator of the autophagy-lysosome machinery. Partial beclin-1 knockdown transcriptionally stimulates lysosome biogenesis and autophagy via mTOR inhibition and activation of TFEB, enhancing removal of depolarized mitochondria. TFEB activation concomitantly stimulates mitochondrial biogenesis via PGC1? induction to restore normally polarized mitochondria and attenuate BNIP3- and hypoxia-reoxygenation-induced cell death. Conversely, overexpression of beclin-1 activates mTOR to inhibit TFEB, resulting in declines in lysosome numbers and suppression of PGC1? transcription. Importantly, knockdown of endogenous TFEB or PGC1? results in a complete or partial loss, respectively, of the cytoprotective effects of partial beclin-1 knockdown, indicating a critical role for both mitochondrial autophagy and biogenesis in ensuring cellular viability. These studies uncover a transcriptional feedback loop for beclin-1-mediated regulation of TFEB activation and implicate a central role for TFEB in coordinating mitochondrial autophagy with biogenesis to restore normally polarized mitochondria and prevent ischemia-reperfusion-induced cardiomyocyte death. |Animals [MESH] |Apoptosis Regulatory Proteins/genetics/*metabolism [MESH] |Autophagy/genetics [MESH] |Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics/*metabolism [MESH] |Cell Death/*genetics [MESH] |Cells, Cultured [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Lysosomes/genetics/metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mitochondria/genetics/*metabolism [MESH] |Myocytes, Cardiac/*metabolism [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Reperfusion Injury/genetics/metabolism [MESH] |Stress, Physiological/*genetics [MESH] |Transcription Factors/genetics/*metabolism [MESH]Regulation of the transcription factor EB-PGC1? axis by beclin-1 contr(epmc).pdf DeepDyve Pubget Overpricing