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10.1038/s41419-018-0373-8 http://scihub22266oqcxt.onion/10.1038/s41419-018-0373-8 C5833444!5833444 !29463790     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29463790 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell+Death+Dis 2018 ; 9 (3 ): 300 Nephropedia Template TP {{tp|p=29463790 |t=2018. Contribution of TMEM16F to pyroptotic cell death |pdf=|usr=}}{{29463790 }} gab.com Text Contribution of TMEM16F to pyroptotic cell death JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29463790 #FOAvip Pyroptosis is a highly inflammatory form of programmed cell death that is caused by infection with intracellular pathogens and activation of canonical or noncanonical inflammasomes. The purinergic receptor P2X(7) is activated by the noncanonical inflammasome and contributes essentially to pyroptotic cell death. The Ca(2+) activated phospholipid scramblase and ion channel TMEM16F has been shown earlier to control cellular effects downstream of purinergic P2X(7) receptors that ultimately lead to cell death. As pyroptotic cell death is accompanied by an increases in intracellular Ca(2+), we asked whether TMEM16F is activated during pyroptosis. The N-terminal cleavage product of gasdermin D (GD-N) is an executioner of pyroptosis by forming large plasma membrane pores. Expression of GD-N enhanced basal Ca(2+) levels and induced cell death. We observed that GD-N induced cell death in HEK293 and HAP1 cells, which was depending on expression of endogenous TMEM16F. GD-N activated large whole cell currents that were suppressed by knockdown or inhibition of TMEM16F. The results suggest that whole cell currents induced by the pore forming domain of gasdermin-D, are at least in part due to activation of TMEM16F. Knockdown of other TMEM16 paralogues expressed in HAP1 cells suggest TMEM16F as a crucial element during pyroptosis and excluded a role of other TMEM16 proteins. Thus TMEM16F supports pyroptosis and other forms of inflammatory cell death such as ferroptosis. Its potent inhibition by tannic acid may be part of the anti-inflammatory effects of flavonoids. Twit Text FOAVip Contribution of TMEM16F to pyroptotic cell death ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29463790 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29463790 #FOAvip English Wikipedia <ref>{{Cite pmid|29463790 }}</ref> Contribution of TMEM16F to pyroptotic cell death #MMPMID29463790 Ousingsawat J ; Wanitchakool P ; Schreiber R ; Kunzelmann K Cell Death Dis 2018[Feb]; 9 (3 ): 300 PMID29463790 show ga Pyroptosis is a highly inflammatory form of programmed cell death that is caused by infection with intracellular pathogens and activation of canonical or noncanonical inflammasomes. The purinergic receptor P2X(7) is activated by the noncanonical inflammasome and contributes essentially to pyroptotic cell death. The Ca(2+) activated phospholipid scramblase and ion channel TMEM16F has been shown earlier to control cellular effects downstream of purinergic P2X(7) receptors that ultimately lead to cell death. As pyroptotic cell death is accompanied by an increases in intracellular Ca(2+), we asked whether TMEM16F is activated during pyroptosis. The N-terminal cleavage product of gasdermin D (GD-N) is an executioner of pyroptosis by forming large plasma membrane pores. Expression of GD-N enhanced basal Ca(2+) levels and induced cell death. We observed that GD-N induced cell death in HEK293 and HAP1 cells, which was depending on expression of endogenous TMEM16F. GD-N activated large whole cell currents that were suppressed by knockdown or inhibition of TMEM16F. The results suggest that whole cell currents induced by the pore forming domain of gasdermin-D, are at least in part due to activation of TMEM16F. Knockdown of other TMEM16 paralogues expressed in HAP1 cells suggest TMEM16F as a crucial element during pyroptosis and excluded a role of other TMEM16 proteins. Thus TMEM16F supports pyroptosis and other forms of inflammatory cell death such as ferroptosis. Its potent inhibition by tannic acid may be part of the anti-inflammatory effects of flavonoids. |*Pyroptosis [MESH] |Anoctamins/chemistry/genetics/*metabolism [MESH] |Calcium/metabolism [MESH] |Cell Membrane/genetics/metabolism [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Intracellular Signaling Peptides and Proteins [MESH] |Neoplasm Proteins/genetics/metabolism [MESH] |Phosphate-Binding Proteins [MESH] |Protein Domains [MESH]Contribution of TMEM16F to pyroptotic cell death (epmc).pdf DeepDyve Pubget Overpricing