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10.1074/jbc.272.27.17196 http://scihub22266oqcxt.onion/10.1074/jbc.272.27.17196 9202042!ä!9202042 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 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 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 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biol+Chem 1997 ; 272 (27): 17196-203 Nephropedia Template TP {{tp|p=9202042|t=1997. Phospholipase A2 is necessary for tumor necrosis factor alpha-induced ceramide generation in L929 cells |pdf=|usr=}}{{9202042}} gab.com Text Phospholipase A2 is necessary for tumor necrosis factor alpha-induced ceramide generation in L929 cells JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=9202042 #FOAvip The role of cytosolic phospholipase A2 (cPLA2) in the regulation of ceramide formation was examined in a cell line (L929) responsive to the cytotoxic action of tumor necrosis factor alpha (TNFalpha). In L929 cells, the addition of TNFalpha resulted in the release of arachidonate, which was followed by a prolonged accumulation of ceramide occurring over 5-12 h and reaching 250% over base line. The formation of ceramide was accompanied by the hydrolysis of sphingomyelin and the activation of three distinct sphingomyelinases (neutral Mg2+-dependent, neutral Mg2+-independent, and acidic enzymes). The variant cell line C12, which lacks cPLA2, is resistant to the cytotoxic action of TNFalpha. TNFalpha was able to activate nuclear factor kappaB in both the wild-type L929 cells and the C12 cells. However, TNFalpha was unable to cause the release of arachidonate or the accumulation of ceramide in C12 cells. C6-ceramide overcame the resistance to TNFalpha and caused cell death in C12 cells to a level similar to that in L929 cells. The introduction of the cPLA2 gene into C12 cells resulted in partial restoration of TNFalpha-induced arachidonate release, ceramide accumulation, and cytotoxicity. This study suggests that cPLA2 is a necessary component in the pathways leading to ceramide accumulation and cell death. Twit Text FOAVip Phospholipase A2 is necessary for tumor necrosis factor alpha-induced ceramide generation in L929 cells ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=9202042 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=9202042 #FOAvip English Wikipedia <ref>{{Cite pmid|9202042}}</ref> Phospholipase A2 is necessary for tumor necrosis factor alpha-induced ceramide generation in L929 cells #MMPMID9202042 Jayadev S; Hayter HL; Andrieu N; Gamard CJ; Liu B; Balu R; Hayakawa M; Ito F; Hannun YA J Biol Chem 1997[Jul]; 272 (27): 17196-203 PMID9202042show ga The role of cytosolic phospholipase A2 (cPLA2) in the regulation of ceramide formation was examined in a cell line (L929) responsive to the cytotoxic action of tumor necrosis factor alpha (TNFalpha). In L929 cells, the addition of TNFalpha resulted in the release of arachidonate, which was followed by a prolonged accumulation of ceramide occurring over 5-12 h and reaching 250% over base line. The formation of ceramide was accompanied by the hydrolysis of sphingomyelin and the activation of three distinct sphingomyelinases (neutral Mg2+-dependent, neutral Mg2+-independent, and acidic enzymes). The variant cell line C12, which lacks cPLA2, is resistant to the cytotoxic action of TNFalpha. TNFalpha was able to activate nuclear factor kappaB in both the wild-type L929 cells and the C12 cells. However, TNFalpha was unable to cause the release of arachidonate or the accumulation of ceramide in C12 cells. C6-ceramide overcame the resistance to TNFalpha and caused cell death in C12 cells to a level similar to that in L929 cells. The introduction of the cPLA2 gene into C12 cells resulted in partial restoration of TNFalpha-induced arachidonate release, ceramide accumulation, and cytotoxicity. This study suggests that cPLA2 is a necessary component in the pathways leading to ceramide accumulation and cell death. |Animals[MESH] |Arachidonic Acid/metabolism[MESH] |Cell Division/drug effects[MESH] |Ceramides/*metabolism[MESH] |Cytosol/enzymology[MESH] |Fibroblasts/drug effects/metabolism[MESH] |Kinetics[MESH] |Magnesium/metabolism[MESH] |Mice[MESH] |NF-kappa B/metabolism[MESH] |Phospholipases A/*metabolism[MESH] |Phospholipases A2[MESH] |Sphingomyelins/metabolism[MESH] |Tumor Cells, Cultured[MESH]Phospholipase A2 is necessary for tumor necrosis factor alpha-induced (epmc).pdf DeepDyve Pubget Overpricing