|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for XAF1(NM_017523.5) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
X-linked inhibitor of apoptosis (XIAP; MIM 300079) is a potent member of the IAP family. All members of this family possess baculoviral IAP (BIR) repeats, cysteine-rich domains of approximately 80 amino acids that bind and inhibit caspases (e.g., CASP3; MIM 600636). XIAP has 3 BIR domains and a C-terminal RING zinc finger that possesses E3 ubiquitin ligase (see MIM 601623) activity. XAF1 antagonizes the anticaspase activity of XIAP and may be important in mediating apoptosis resistance in cancer cells (Liston et al., 2001 [PubMed 11175744]).[supplied by OMIM].
Gene References into function
- XAF1 augments TRAIL-induced apoptosis
- Epigenetic silencing of XAF1 by aberrant promoter methylation may contribute to the malignant progression of human gastric tumors.
- XAF1 expression in melanoma tissues was significantly reduced compared with benign melanocytic nevi
- endogenous stress pressure in cancer cells sustained the high level expression of HSF1 and subsequently suppressed XAF1 expression, implicating the synergized effect of two anti-apoptotic protein families in cytoprotection under stress circumstances
- The ratio of XAF1(A) and XAF1C mRNA expression differs amongst the cell lines tested, suggesting differential mRNA stabilities and/or the existence of tissue- or cell type-specific splicing regulation.
- alternative splicing of XAF1 mRNA leads to formation of truncated XAF1 protein, which likely affects its functional interaction with XIAP, and consequently, contributes to pathogenesis of prostate cancers by disrupting balance of apoptosis machinery
- Gene expression incresed in multiple sclerosis patients treated with interferon-beta.
- siRNA to XAF1 inhibited IFN-induced apoptosis; conversely, overexpression of XAF1 overcame resistance to apoptosis induction by IFN-beta.
- Epigenetic alteration of XAF1 is frequent in human urogenital cancers and may contribute to the malignant progression of tumors by rendering tumor cells a survival advantage partially through the attenuated p53 response.
- Down-regulation of XAF1 in association with hypermethylation was detected in 3 of 4 human gastric cancer cell lines and 6 of 8 colon cancer cell lines.
- Our study provides evidence that XAF1 is a crucial interferon-stimulated gene (ISG) mediator of IFN-induced sensitization to TRAIL in cancer.
- Low XAF1 mRNA expression levels relate to an unfavorable clinical course in renal cell carcinoma.
- An increased expression ratio of XIAP to XAF1 in combination with a disturbed expression of the XAF1 splice variants could be shown in gastric adenocarcinomas.
- Genetic and epigenetic alteration of XAF1 is a common event in colorectal tumorigenesis and contributes to the malignant tumor progression by providing survival advantages for tumor cells under various stress conditions.
- XAF1 mediates Survivin down-regulation through a complex containing XIAP, supporting dual roles for XAF1 in apoptosis
- Induction of XAF1 by IFNbeta was mediated by the transcription regulator Stat1 through the ISRE site within the promoter region of XAF1 gene in colon cancer.
- Interferon gamma induces XAF1 and Noxa expression and potentiates apoptosis by STAT3 activation
- CBP is a novel binding partner of XAF1, and the interaction between XAF1 and CBP and their functional consequence were mediated by adaptor-related protein complex 1.
- Promoter hypermethylation and down regulation of XAF1 is associated with liver tumor recurrence after liver transplantation.
- These data suggest that a down-regulation of Smac/DIABLO and HtrA2 is implicated in the development and progression of TGCT, whereas overexpression of XAF1 in TGCT might contribute to their extraordinary sensitivity to chemotherapy.
- JNK1 stimulated and mediated the effects of IFN and TNF-alpha on XAF1 expression through transcriptional regulation by induction of IRF-1.