caspase

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Related to Caspases: apoptosis, cytochrome c, Bcl-2

caspase

[′kas‚pās]
(cell and molecular biology)
Any of a family of intracellular proteins that mediate apoptosis.
References in periodicals archive ?
Our results showed that upon exposure of PTZ the neuronal loss occur by activation of caspase pathway and co treatment of metformin reverse the effect of PTZ induced apoptotic cell death in HCN-2 cell.
Flow cytometry results showed the induction of tiliroside on apoptosis, so the apoptosis mechanism at molecular levels was conducted by the observed expression of tumor suppressor (p53), protein apoptosis (Bcl-2), Caspases 8 and 9 (apoptosis initiator), using immunocytochemistry method.
Then, a homotypic interaction between the N-terminal pyrin domain of NLRP3 and ASC, and subsequently between the caspase activation and recruitment domain of the ASC and pro-caspase-1, will recruit pro-caspase-1 to the high molecular weight complex, leading to its auto-cleavage and activation.
Orrenius, Dual regulation of caspase activity by hydrogen peroxide: implications for apoptosis.
Caspases are activated in a hierarchy order, in which initiator caspases (caspase-8 and -10) function to cleave effector caspases (caspase-3 and -7), the latter in turn degrade a number of intercellular protein substrates and lead to the classical morphological changes of apoptosis (Figures 1 and 2) [5,6].
3], deuterated chloroform; F1TC, fluorescence isothiocyanate; mRNA, messenger ribonucleic acid; PCR, polymerase chain reaction; Bcl-2, B-cell lymphoma 2; Caspases 3, 8 and 9, cysteinyl aspartic acid-protease-3, 8 and 9; Hsp70, heat shock protein 70; CAD, caspase-activated DNAse.
Because caspases are an unexplored yet attractive target to modulate apoptotic cell death in atherosclerosis, we chose to examine the impact of caspase-3 deletion on atherosclerosis by crossbreeding caspase-3 knockout ([Casp3.
Caspases are cysteine proteases that play crucial role in apoptotic cell death.
The researchers determined that Legionella pneumophila bacteria somehow suppress activation of caspases 4 and 5 in human cells but, if the enzymes are added back into immune cells, they set off the same fusion events--those also seen in mice --that will kill the bacteria.
This can result from decreased proliferation or increased cell death, which is why the investigators also looked at caspase 8 and caspase 9.
The extrinsic pathway is triggered when death ligands bind to their respective cell surface death receptors through recruitment of FAS-associated death domain (FADD) protein, procaspase-8 through the formation of a complex that induces cell death and activation of the caspases (caspase-8 and caspase-10).