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10.1074/jbc.273.12.6921 http://scihub22266oqcxt.onion/10.1074/jbc.273.12.6921 9506997!ä!9506997 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biol+Chem 1998 ; 273 (12): 6921-7 Nephropedia Template TP {{tp|p=9506997|t=1998. Ceramide formation leads to caspase-3 activation during hypoxic PC12 cell death Inhibitory effects of Bcl-2 on ceramide formation and caspase-3 activation |pdf=|usr=}}{{9506997}} gab.com Text Ceramide formation leads to caspase-3 activation during hypoxic PC12 cell death Inhibitory effects of Bcl-2 on ceramide formation and caspase-3 activation JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=9506997 #FOAvip PC12 cells undergo apoptosis as well as necrosis following exposure to hypoxia. Following a 6-h hypoxic treatment, a time-dependent increase in intracellular ceramide level was observed with a concurrent decrease in sphingomyelin. It was also shown that the hypoxia-induced ceramide accumulation resulted from activation of neutral magnesium-dependent sphingomyelinase. Comparative kinetic analyses of the neutral sphingomyelinase in the cells under normoxia and hypoxia showed that hypoxia increased Vmax but did not affect Km of the enzyme. In PC12 cells overexpressing Bcl-2 which show strong resistance to hypoxia, sphingomyelin hydrolysis was decreased and activation of neutral sphingomyelinase was reduced. Addition of exogenous C2-ceramide induced cell death and activated caspase-3 as markedly as the hypoxia treatment. On the other hand, in PC12 cells overexpressing Bcl-2, significant decreases in cell death and inhibition of caspase-3 activation were observed after exogenous addition of C2-ceramide. The inhibitors of caspase-3 prevented cell death by either hypoxia or C2-ceramide. These results suggest that ceramide generated by activation of neutral magnesium-dependent sphingomyelinase mediates hypoxic cell death and that Bcl-2 has inhibitory effects on ceramide formation and caspase activation. Twit Text FOAVip Ceramide formation leads to caspase-3 activation during hypoxic PC12 cell death Inhibitory effects of Bcl-2 on ceramide formation and caspase-3 activation ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=9506997 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=9506997 #FOAvip English Wikipedia <ref>{{Cite pmid|9506997}}</ref> Ceramide formation leads to caspase-3 activation during hypoxic PC12 cell death Inhibitory effects of Bcl-2 on ceramide formation and caspase-3 activation #MMPMID9506997 Yoshimura S; Banno Y; Nakashima S; Takenaka K; Sakai H; Nishimura Y; Sakai N; Shimizu S; Eguchi Y; Tsujimoto Y; Nozawa Y J Biol Chem 1998[Mar]; 273 (12): 6921-7 PMID9506997show ga PC12 cells undergo apoptosis as well as necrosis following exposure to hypoxia. Following a 6-h hypoxic treatment, a time-dependent increase in intracellular ceramide level was observed with a concurrent decrease in sphingomyelin. It was also shown that the hypoxia-induced ceramide accumulation resulted from activation of neutral magnesium-dependent sphingomyelinase. Comparative kinetic analyses of the neutral sphingomyelinase in the cells under normoxia and hypoxia showed that hypoxia increased Vmax but did not affect Km of the enzyme. In PC12 cells overexpressing Bcl-2 which show strong resistance to hypoxia, sphingomyelin hydrolysis was decreased and activation of neutral sphingomyelinase was reduced. Addition of exogenous C2-ceramide induced cell death and activated caspase-3 as markedly as the hypoxia treatment. On the other hand, in PC12 cells overexpressing Bcl-2, significant decreases in cell death and inhibition of caspase-3 activation were observed after exogenous addition of C2-ceramide. The inhibitors of caspase-3 prevented cell death by either hypoxia or C2-ceramide. These results suggest that ceramide generated by activation of neutral magnesium-dependent sphingomyelinase mediates hypoxic cell death and that Bcl-2 has inhibitory effects on ceramide formation and caspase activation. |*Apoptosis[MESH] |*Caspases[MESH] |*Cell Hypoxia[MESH] |Animals[MESH] |Caspase 3[MESH] |Ceramides/*biosynthesis/metabolism[MESH] |Cysteine Endopeptidases/*metabolism[MESH] |Cysteine Proteinase Inhibitors/pharmacology[MESH] |Enzyme Activation[MESH] |PC12 Cells[MESH] |Proto-Oncogene Proteins c-bcl-2/genetics[MESH] |Rats[MESH]Ceramide formation leads to caspase-3 activation during hypoxic PC12 c(epmc).pdf DeepDyve Pubget Overpricing