MCh

(redirected from Caspase 9)
Also found in: Medical.
Related to Caspase 9: Caspase 3, APAF3

MCh

abbreviation for
(Education) Master of Surgery
[Latin Magister Chirurgiae]
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References in periodicals archive ?
8 Release of cytochrome c from mitochondria through stress stimuli, induces activation of caspase 9, which in turn leads to activation of caspase 3 enzyme.
The primary antibodies were p53 (monoclonal mouse anti-human p53 protein clone DO-7), Bcl-2 (monoclonal mouse anti-human Bcl-2 oncoprotein clone 124), Caspase 8 (monoclonal mouse anti-human Caspase 8 clone Caspase 8), and Caspase 9 (monoclonal mouse anti-human Caspase 9 clone Caspase 9).
Activation of P53 death signals lead to Caspases activation and thus can induce apoptosis through release of mitochondrial Cytochrome c into the cytoplasm which then facilitates activation of Caspase 9, leading to activation of Caspase 3 and other effector caspases.
The mitochondria participated in the process by stimulating the intrinsic pathway via caspase 9 with a reduction in mitochondrial membrane potential (MMP) and an increase in cytochrome c release.
The former was activated by BPS alone and when combined with estradiol, but caspase 9 was less affected, consistent with an increase in apoptosis.
Apoptosis is initiated in OLG concomitant with a rapid decline in phosphatidylinositol-3 kinase (PI3-K) activity and Bcl-2 mRNA expression, a gradual increase in caspase 3 mRNA, and the eventual release of cytochrome c and activation of caspase 9 [56].
Methods: The cytotoxicity of the compounds was determined using a resazurin reduction assay, whereas the caspase-Glo assay was used to detect the activation of caspases 3/7, caspase 8 and caspase 9 in cells treated with compounds 3.
Compounds 3 arrested the cell cycle between G0/G1 and S phases, strongly induced apoptosis via caspases 3/7, caspase 8, caspase 9 activation and disrupted the MMP in CCRF-CEM cells.
Compounds 2-4 strongly induced apoptosis in CCRF-CEM cells via caspases 3/7, caspase 8 and caspase 9 activation and disruption of MMP.
Since becatamide was a most potent inhibitor of mitochondrial membrane depolarization, the effect of this amide on caspase 9 activity in [H.

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