Caspase-8 belongs to the family of cysteine proteases that plays a critical role in the regulation of programmed cell death (apoptosis). For example, caspase-8 function is required for proper signaling via the death receptor (extrinsic) pathway. Accordingly, the disturbance of caspase-8 expression or function may contribute to cancer formation and progression. In addition, inactivation of caspa...

In response to overwhelming external stimuli, cells are forced to die in different ways. By default, cells are prone to apoptosis, a programmed cell death through the activation of the caspase cascade. However, this process would be blocked if one of the proteins involved in executing apoptosis was genetically impaired or chemically inhibited, or if the apoptotic machinery was not properly oper...

The Caenorhabditis elegans Bcl-2-like protein CED-9 prevents programmed cell death by antagonizing the Apaf-1-like cell-death activator CED-4. Endogenous CED-9 and CED-4 proteins localized to mitochondria in wild-type embryos, in which most cells survive. By contrast, in embryos in which cells had been induced to die, CED-4 assumed a perinuclear localization. CED-4 translocation induced by the ...

Programmed cell death is critical for normal nervous system development and is regulated by Bcl-2 and Caspase family members. Targeted disruption of bcl-x(L), an antiapoptotic bcl-2 gene family member, causes massive death of immature neurons in the developing nervous system whereas disruption of caspase-9, a proapoptotic caspase gene family member, leads to decreased neuronal apoptosis and neu...

BACKGROUND Programmed necrosis is a form of caspase-independent cell death whose molecular regulation is poorly understood. While tumor necrosis factor-alpha (TNF-α) has been identified as an activator of programmed necrosis, the specific context under which this can happen is unclear. Recently we reported that TNF-α can be expressed by human tumor cells as both a membrane tethered (mTNF-α) and...

Synthetic caspase inhibitors and particularly broad-spectrum caspase inhibitors can prevent cells from death or at least slow down cell death process and abrogate some apoptotic hallmarks [Kitanaka, C., Kuchino, Y., 1999. Caspase-independent programmed cell death with necrotic morphology. Cell Death and Differentiation 6, 508-515]. However, not all synthetic caspase inhibitors diminish cell dea...

We have isolated the recently identified Drosophila caspase DRONC through its interaction with the effector caspase drICE. Ectopic expression of DRONC induces cell death in Schizosaccharomyces pombe, mammalian fibroblasts and the developing Drosophila eye. The caspase inhibitor p35 fails to rescue DRONC-induced cell death in vivo and is not cleaved by DRONC in vitro, making DRONC the first iden...

objective(s):ischemia is described as organs and tissues are destitute of oxygen due to decreased arterial or venous blood flow. many mechanisms play role in cell death happened as a consequence of a new blood flow is needed for both cell regeneration and to clean toxic metabolites during ischemia and later. lung damage induced by ischemia/reperfusion (i/r) is a frequent problem in lung transpl...

The death receptors FAS, TRAIL-Rs and TNFR1 play critical roles in programmed cell death, particularly in the immune system. Upon ligation of death receptors, caspase-8 is activated within the so-called ‘Death Induced Signalling Complex’ (DISC) but the mechanisms that mediate and modulate the activation of caspase-8 are still not fully understood. This is an important issue because caspase-8 is...