XIAP

(redirected from X-linked Inhibitor of Apoptosis)
Also found in: Acronyms.

XIAP

A gene on chromosome Xq25 that belongs to the inhibitor of apoptosis (IAP) gene family, which encode negative regulatory proteins that prevent apoptotic cell death. XIAP acts by binding to tumour necrosis-factor receptor-associated factors TRAF1 and TRAF2, inhibits apoptosis induced by menadione—a free radical inducer and IL1-beta converting enzyme—and inhibits cell-death proteases caspase-3 and caspase-7.

Molecular pathology
XIAP mutations cause X-linked lymphoproliferative syndrome.
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Bid: BH3 interacting domain death agonist; cIAP: cellular inhibitor of apoptosis; CJ: cisjasmonic acid; 2DG: 2-deoxy-D-glucose; Glc: glucose; J7: methyl 5-chloro-4,5- didehydrojasmonate; JA: jasmonic acid; NSCLC: nonsmall-cell lung carcinoma; Pgp: P-glycoprotein; MDDHJ: methyl 4,5-didehydro- jasmonate; MDR: multidrug resistance; MMP-14: matrix metalloprotease 14; PARP: poly (ADP-ribose) polymerase; PCNA: proliferating cell nuclear antigen; PTPC: permeabilitytransition pore complex; ROS: reactive oxygen species; S100P: protein SP100; TBrJA: 5,7,9,10-tetrabromo jasmonate; TNFR1: tumor-necrosis factor receptor-1; TRAIL: tumor necrosis factor-(TNF-) related apoptosis-inducing ligand; XIAP: X-linked inhibitor of apoptosis protein.
X-linked inhibitor of apoptosis protein (XIAP) was quantified by Western blotting analysis.
Curcumin plus ATO or lonidamine stimulates typical events of the mitochondrial executioner pathway (Bax and Bid activation, cytochrome c release, X-linked inhibitor of apoptosis downregulation, and caspase-9/-3 activation) and causes mitochondrial transmembrane potential dissipation, which nevertheless represents a late event in the apoptotic response.
Aegera has taken this technology to the clinic with an antisense therapeutic, AEG35156, targeting just one of their IAPs named the X-linked inhibitor of apoptosis (XIAP) protein, a target which inhibits apoptosis using duel mechanisms.
Significant apoptosis was detected in embryonic heart at the time of outflow tract shortening [7], and inhibition of apoptosis using the pan-caspase inhibitor zVAD-fmkor adenoviral mediated expression of X-linked inhibitor of apoptosis protein resulted in excessive outflow tract above the base of the ventricles [8], indicating that apoptosis is required for morphogenesis of the outflow tract myocardial tissue.

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