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10.1038/cdd.2015.166 http://scihub22266oqcxt.onion/10.1038/cdd.2015.166 C4946884!4946884!26794447     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Differ 2016 ; 23 (7): 1165-74 Nephropedia Template TP {{tp|p=26794447|t=2016. Cardiolipin or MTCH2 can serve as tBID receptors during apoptosis |pdf=|usr=}}{{26794447}} gab.com Text Cardiolipin or MTCH2 can serve as tBID receptors during apoptosis JO: Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=26794447 #FOAvip During apoptosis, proapoptotic BAX and BAK trigger mitochondrial outer membrane (MOM) permeabilization by a mechanism that is not yet fully understood. BH3-only proteins such as tBID, together with lipids of the MOM, are thought to play a key role in BAX and BAK activation. In particular, cardiolipin (CL) has been shown to stimulate tBID-induced BAX activation in vitro. However, it is still unclear whether this process also relies on CL in the cell, or whether it is more dependent on MTCH2, a proposed receptor for tBID present in the MOM. To address this issue, we deleted both alleles of cardiolipin synthase in human HCT116 cells by homologous recombination, which resulted in a complete absence of CL. The CL-deficient cells were fully viable in glucose but displayed impaired oxidative phosphorylation and an inability to grow in galactose. Using these cells, we found that CL was not required for either tBID-induced BAX activation, or for apoptosis in response to treatment with TRAIL. Downregulation of MTCH2 in HCT116 cells also failed to prevent recruitment of tBID to mitochondria in apoptotic conditions. However, when both CL and MTCH2 were depleted, a significant reduction in tBID recruitment was observed, suggesting that in HCT116 cells, CL and MTCH2 can have redundant functions in this process. Twit Text FOAVip Cardiolipin or MTCH2 can serve as tBID receptors during apoptosis ????Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=26794447 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26794447 #FOAvip English Wikipedia <ref>{{Cite pmid|26794447}}</ref> Cardiolipin or MTCH2 can serve as tBID receptors during apoptosis #MMPMID26794447 Raemy E; Montessuit S; Pierredon S; van Kampen AH; Vaz FM; Martinou JC Cell Death Differ 2016[Jul]; 23 (7): 1165-74 PMID26794447show ga During apoptosis, proapoptotic BAX and BAK trigger mitochondrial outer membrane (MOM) permeabilization by a mechanism that is not yet fully understood. BH3-only proteins such as tBID, together with lipids of the MOM, are thought to play a key role in BAX and BAK activation. In particular, cardiolipin (CL) has been shown to stimulate tBID-induced BAX activation in vitro. However, it is still unclear whether this process also relies on CL in the cell, or whether it is more dependent on MTCH2, a proposed receptor for tBID present in the MOM. To address this issue, we deleted both alleles of cardiolipin synthase in human HCT116 cells by homologous recombination, which resulted in a complete absence of CL. The CL-deficient cells were fully viable in glucose but displayed impaired oxidative phosphorylation and an inability to grow in galactose. Using these cells, we found that CL was not required for either tBID-induced BAX activation, or for apoptosis in response to treatment with TRAIL. Downregulation of MTCH2 in HCT116 cells also failed to prevent recruitment of tBID to mitochondria in apoptotic conditions. However, when both CL and MTCH2 were depleted, a significant reduction in tBID recruitment was observed, suggesting that in HCT116 cells, CL and MTCH2 can have redundant functions in this process. äCardiolipin or MTCH2 can serve as tBID receptors during apoptosis (epmc).pdf DeepDyve Pubget Overpricing