RIP1-dependent and independent effects of necrostatin-1 in necrosis and T cell activation.

Interestingly, we found that ROS was not only required for AMPK-autophagy activation, it was also important for salinomycin-induced apoptosis and cell death .Thus

Pim-1 kinase inhibits the activation of reporter gene expression in Elk-1 and c-Fos reporting systems but not the endogenous gene expression: an artifact of the reporter gene assay

Knockdown of the taurine transporter (TAUT) or treatment with the ERK-specific inhibitor PD98059 (10 μM) blocked the activation of ERK induced by taurine (1 0 mM) and abolished

In the process of apoptosis, cell death is induced by the activation of a genetically and biochemically regulated cell death system, involving the participation of

does not increase cell proliferation or cell death but rather that the increases in cell proliferation and cell death are due to the increases in pilocarpine seizure severity

In addition to a role for Fyn kinase in IL-4- mediated B cell and T cell activation [38,39], we recently showed that Fyn is required for IgE-induced STAT5 activation in mast

Importantly, the activation of the caspase cascade and caspase-8-mediated RIP1 cleavage in TNF a -stimulated TAK1 deficient cells is not sufficient to prevent RIP1-dependent

Though the main apoptosis pathway in both cell lines was found to be through caspase-8 activation, caspase-9 was also activated in MDA-MB-231 cells but suppressed in MCF-7 cells..