Title : RIP1-mediated mitochondrial dysfunction and ROS production contributed to tumor necrosis factor alpha-induced L929 cell necroptosis and autophagy.

Pub. Date : 2012 Dec

PMID : 23000518






4 Functional Relationships(s)
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1 Moreover, pan-caspase inhibitor z-VAD-fmk (zVAD) increased RIP1 expression and exacerbated TNFalpha-induced mitochondrial dysfunction and ROS production, indicating that RIP1 led to mitochondrial dysfunction and ROS production. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone receptor (TNFRSF)-interacting serine-threonine kinase 1 Mus musculus
2 Moreover, pan-caspase inhibitor z-VAD-fmk (zVAD) increased RIP1 expression and exacerbated TNFalpha-induced mitochondrial dysfunction and ROS production, indicating that RIP1 led to mitochondrial dysfunction and ROS production. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone receptor (TNFRSF)-interacting serine-threonine kinase 1 Mus musculus
3 Moreover, pan-caspase inhibitor z-VAD-fmk (zVAD) increased RIP1 expression and exacerbated TNFalpha-induced mitochondrial dysfunction and ROS production, indicating that RIP1 led to mitochondrial dysfunction and ROS production. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone receptor (TNFRSF)-interacting serine-threonine kinase 1 Mus musculus
4 Moreover, pan-caspase inhibitor z-VAD-fmk (zVAD) increased RIP1 expression and exacerbated TNFalpha-induced mitochondrial dysfunction and ROS production, indicating that RIP1 led to mitochondrial dysfunction and ROS production. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone receptor (TNFRSF)-interacting serine-threonine kinase 1 Mus musculus