mortality/aging
N |
• mice exhibit normal mortality in response to polymicrobial septic shock following cecal ligation and perforation
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immune system
N |
• mice exhibit normal T cell, macrophage and neutrophil development
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• macrophages are resistant to LPS and pan-caspase inhibitor N-benzyloxycarbonyl-valyl-alanyl-aspartic-acid (O-methyl)-fluoromethylketone (zVAD)- or oxidized low-density lipoprotein (oxLDL) and zVAD-induced necroptosis compared with wild-type cells
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cellular
• macrophages are resistant to LPS and pan-caspase inhibitor N-benzyloxycarbonyl-valyl-alanyl-aspartic-acid (O-methyl)-fluoromethylketone (zVAD)- or oxidized low-density lipoprotein (oxLDL) and zVAD-induced necroptosis compared with wild-type cells
• mouse embryonic fibroblasts exhibit resistance to TNF, cycloheximide (CHX) and zVAD-induced cell death compared with wild-type cells
• however, mouse embryonic fibroblasts exhibit normal cell death induced by TNF and CHX; TNF and Smac mimetic (SmacM); TRAIL and CHX; TRAIL, CHX and zVAD; etoposide or staurosporine (STS)
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homeostasis/metabolism
• mice are protected from cerulean-induced acute pancreatitis compared with wild-type mice
• however, mice exhibit normal mortality in response to polymicrobial septic shock following cecal ligation and perforation
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hematopoietic system
• macrophages are resistant to LPS and pan-caspase inhibitor N-benzyloxycarbonyl-valyl-alanyl-aspartic-acid (O-methyl)-fluoromethylketone (zVAD)- or oxidized low-density lipoprotein (oxLDL) and zVAD-induced necroptosis compared with wild-type cells
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