CASP9

(redirected from Caspase-9)
Also found in: Wikipedia.

CASP9

A gene on chromosome 1p36.21 that encodes a ubiquitous protein belonging to the cysteine-aspartic acid protease (caspase) family which, once activated by proteolytic processing, plays a central role in the execution phase of cell apoptosis. CASP9 is an initiator-type caspase, which is activated by, and interacts with, upstream adaptor molecules through CARD and DED protein–protein interaction domains; it is processed by APAF1, an early step in the caspase activation cascade. It is highly expressed in the heart.
Mentioned in ?
References in periodicals archive ?
This apoptosis was prevented by the non-specific caspase inhibitor z-VAD-fmk, and by the selective caspase-9 inhibitor z-LEHD-fmk.
Studies have indicated that Caspase-8 in external pathway and Caspase-9 in internal pathway act as crucial caspases.
Apoptosis is classically signalled by two major apoptotic pathways (12) (Figure 2): the extrinsic pathway (also called the death receptor caspase-8 mediated pathway) and the intrinsic pathway (also called mitochondria-initiated caspase-9 pathway).
As a consequence, cleaved caspase-9 and cleaved caspase-7 levels were significantly downregulated, indicating negative regulation of apoptosis by COC extract.
The findings provide the first example of a protein factor regulating the expression of the protein caspase-9, a main player in apoptosis, or programmed cell death.
This procaspase-9 comes and activates caspase-9 and simultaneously this activates procaspase-3 and then activates caspase-3.
2+] toxicity interfered with inhibitors of cellular signaling pathways, such as ERK and c-jun N-terminal kinase, and with caspase inhibitors, especially inhibitors of caspase-9 and caspase-3.
For the test, sub-confluent NHEK were irradiated with ssUV to induce the intrinsic apoptotic pathway, as determined by the activation of the initiator caspase-9 in a dose-dependent manner.
Although the intrinsic pathway involves early activation of caspase-9, and the extrinsic pathway is mediated through caspase-8, both lead to activation of the "executioner" caspase-3 and a variety of proteases and endonucleases.
The poster presentation and a corresponding abstract from the conference were entitled "GCS-100, A Selective Galectin-3 Mediated CLL Therapy Induces Angiogenic and AKT1 Inhibition With Caspase-9 Activation.
Its effect on cellular morphology, cell cycle arrest, DNA fragmentation and expression levels of caspase-3, caspase-8 and caspase-9 were also determined.
Moreover, crocetin inhibited the enzymatic activity of caspase-9 in a cell-free system.

Full browser ?