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FLASH GENE
Symbol XIAP contributors: shn/mct - updated : 19-10-2019
HGNC name X-linked inhibitor of apoptosis
HGNC id 592
ASSOCIATED DISORDERS
corresponding disease(s) XLP2
Other morbid association(s)
TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
tumoral     --over  
in hepatocellular carcinoma
tumoral   deletion    
in X-linked lymphoproliferative syndrome, and in patients with low numbers of natural killer T-lymphocytes (NKT cells)
constitutional     --low  
renders cells highly sensitive to oxidative stress
tumoral     --over  
in the majority of non-small cell lung carcinoma, together with the abundant or upregulated expression of HBXIP and BIRC5 suggest that tumours are endowed with resistance against a variety of apoptosis-inducing conditions
tumoral     --over  
overexpression of FOXM1, XIAP, and BIRC5 contributes to the development of drug-resistance and is associated with poor clinical outcome in breast cancer patients
Susceptibility
Variant & Polymorphism
Candidate gene
Marker
Therapy target
SystemTypeDisorderPubmed
cancerdigestiveliver
for gene therapy in hepatocellular carcinoma (inhibition of the NF-kappaB/XIAP signaling pathway might selectively abolish the pro-oncogenic activity of TGF-beta1 in advanced hepatocellular carcinomas without affecting the pro-apoptotic effects of TGF-bet
cancer  
inhibition as a treatment for malignancy
cancerdigestivecolon
targeting CFLAR and BIRC4 may represent a therapeutic strategy for the treatment of colorectal tumors with defects in mitochondrial-regulated apoptosis
cardiovascular  
may be target protein for the prevention of cardiovascular disease
cancer  
potential utilization of XIAP as a target for cancer prevention and therapy
cancerendocrinethyroid
XIAP inhibitor can be therapeutically targeted, either alone or in combination, to induce efficient apoptosis in PTC with overexpression of XIAP
ANIMAL & CELL MODELS
mice deficient in Xiap gene were viable, histopathological analysis did not reveal any differences between IAP-deficient and wild-type mice and any defects in induction of caspase-dependent or -independent apoptosis in cells was found