What is the function of caspase-9?

What is the function of caspase-9?

Caspase-9 is a member of caspase family of cysteine proteases that have been implicated in apoptosis and cytokine processing. When cells receive apoptotic stimuli, mitochondria releases cytochrome c which then binds to Apaf-1, the mammalian Ced-4 homologue, together with dATP. The resultant complex … Caspase-9 Int J Biochem Cell Biol.

What should I avoid while using caspase-9 antibody?

* Avoid repeated exposure to skin. Caspase-9 Antibody detects endogenous levels of full length caspase-9 (47 kDa) and large fragments of caspase-9. The antibody does not recognize other caspases.

What happens if caspase-9 is low?

Low amounts of caspase-9 leads to cancer and neurodegenerative diseases like Alzheimer’s disease. Further alterations at single-nucleotide polymorphism (SNP) levels and whole gene levels of caspase-9 can cause germ-line mutations linked to non-Hodgkin’s lymphoma.

What is the PMID for caspase-9?

PMID 9390557. S2CID 14321446. Pan G, O’Rourke K, Dixit VM (March 1998). “Caspase-9, Bcl-XL, and Apaf-1 form a ternary complex”. The Journal of Biological Chemistry. 273 (10): 5841–5. doi: 10.1074/jbc.273.10.5841.

Active caspase-9 works as an initiating caspase by cleaving, thus activating downstream executioner caspases, initiating apoptosis. Once activated, caspase-9 goes on to cleave caspase-3, -6, and -7, initiating the caspase cascade as they cleave several other cellular targets.

Which caspase enzymes is the part of mitochondrial pathway?

As the initiator caspase component of the apoptosome complex, caspase-9 is activated downstream of mitochondrial cytochrome c release and thus has a crucial role in activating effector caspases in response to a variety of death stimuli.

What happens when caspase is cleaved?

Cleavage. Once appropriately dimerised, the Caspases cleave at inter domain linker regions, forming a large and small subunit. This cleavage allows the active-site loops to take up a conformation favourable for enzymatic activity.

What happens to mitochondria after cell death?

Mitochondria regulate caspase activation and cell death through an event termed mitochondrial outer membrane permeabilization (MOMP); this leads to the release of various mitochondrial intermembrane space proteins that activate caspases, resulting in apoptosis.

What is caspase-independent cell death?

We define caspase-independent cell death (CICD) as death that ensues when a signal that normally induces apoptosis fails to activate caspases. These include upstream signalling pathways that are critical for both forms of death such as mitochondrial outer membrane permeabilization (MOMP).

Does cytochrome c activate caspase-9?

Caspase-9 is activated in a cytochrome c-independent manner early during TNFalpha-induced apoptosis in murine cells. Cell Death Differ.

What triggers caspase-9 release from mitochondria?

Caspase-9 is released from isolated mitochondria on treatment with Ca 2+ or Bax, stimuli implicated in ischemic neuronal cell death that are known to induce cyto-c release from mitochondria. In neuronal cell culture models, apoptosis-inducing agents trigger translocation of caspase-9 from mitochondria to the nucleus, which is inhibitable by Bcl-2.

What is caspase-9?

As the most intensively studied initiator caspase, caspase-9 is a key player in the intrinsic or mitochondrial pathway which is involved in various stimuli, including chemotherapies, stress agents and radiation.

Does caspase-9 enter the nucleus in ischemia-damaged neurons?

In these cells, the mitochondria concentrated around the nucleus, but caspase-9 remained associated with these organelles and did not enter the nucleus, as determined by two-color confocal immunofluorescence microscopic analysis of Mitotracker-stained cells (Fig. 5 i – l ). In Vivo Release of Caspase-9 from Mitochondria in Ischemia-Damaged Neurons.

What is the relationship between caspase-9 activation and apoptosis in carcinoma?

Failure of Activation of Caspase-9 Induces a Higher Threshold for Apoptosis and Cisplatin Resistance in Testicular Cancer. Cancer Research. 2003;63:513–21. [PubMed] [Google Scholar]