CASP6

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CASP6

A gene on chromosome 4q25 that encodes a so-called effector caspase belonging to the cysteine-aspartic acid protease (caspase) family which, once activated by proteolytic processing, plays a central role in the execution phase of apoptosis. Effector (also called executioner) caspases CASP3, -6 and -7 are responsible for cleaving downstream substrates.
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In previous studies, it has been observed that the apoptotic pathway continues to be active in the epileptogenesis process after the acute phase of events that trigger neuronal cell damage such as SE, that the activity of caspase-3 and caspase-6 is prominent, and that caspase-3, in particular, is active until after one week from the onset of neuronal damage (13).
NLRP1 induces caspase-1 and caspase-6, and this pathway is involved in the progression of AD [103].
Pakavathkumar et al., "Neuronal NLRP1 inflammasome activation of caspase-1 coordinately regulates inflammatory interleukin-1-beta production and axonal degeneration-associated caspase-6 activation," Cell Death & Differentiation, vol.
Since both upstream signalling pathways (intrinsic and extrinsic pathway) converge downstream to activate the final effector caspase mechanism, the activity of caspase-3 and caspase-6 executioner caspases was investigated.
The results illustrated that the apoptotic effects of FAA on MCF-7 cells were via the activation of caspase-8, which led to the activation of the final effector, caspase-6, that finally caused apoptosis.
Other studies have also revealed the importance of caspase-2 and caspase-6 in causing the death of retinal ganglion cells following optic nerve transections [41-43].
Magharious et al., "Involvement of caspase-6 and caspase-8 in neuronal apoptosis and the regenerative failure of injured retinal ganglion cells," The Journal ofNeuroscience, vol.
Trifolin acetate-induced cell death in human leukemia cells is dependent on caspase-6 and activates the MAPK pathway.
In Western blot tests, after electrophoresis, the transferred PVDF membranes were incubated overnight with antibodies against Akt, phosphoAkt (Ser473), GSK-3[beta], and phospho-GSK-3[beta] (Ser9) (Cell Signaling Technology, MA, USA), B-cell lymphoma-2 (Bcl-2), Bax, or cleaved cysteine-dependent aspartate-directed proteases (caspase-3, caspase-6, or caspase-9) (Abcam, CA, USA).
The caspase-3 is cleaved at Asp-28-Ser-29 to generate the mature 17 kD fragment, which may cleave and activate caspase-6, -7, and -9, leading to apoptosis [19].
Executioner caspases (caspase-3, caspase-6, and caspase-7) and upstream effector caspases (caspase-2, caspase-8, caspase-9, and caspase-10) are well known as mediators in AD brains [23].
Cytochrome c promotes the assembly of apoptosome and caspase-9 activation, which activates caspase-3 and -7 followed by caspase-6. The extrinsic (or death receptor) apoptotic pathway is mediated by death receptors and induces caspase-8 activation, which cleaves pro-caspases-3 and -7 and active caspase-3 cleaves pro-caspase-6.
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