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Validated All-in-One™ qPCR Primer for APAF1(NM_181861.2) Search again
By 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
This gene encodes a cytoplasmic protein that initiates apoptosis. This protein contains several copies of the WD-40 domain, a caspase recruitment domain (CARD), and an ATPase domain (NB-ARC). Upon binding cytochrome c and dATP, this protein forms an oligomeric apoptosome. The apoptosome binds and cleaves caspase 9 preproprotein, releasing its mature, activated form. Activated caspase 9 stimulates the subsequent caspase cascade that commits the cell to apoptosis. Alternative splicing results in several transcript variants encoding different isoforms. [provided by RefSeq].
Gene References into function
- Apaf1 WD40 repeat domains form propellar-like structures that are important for procaspase 9 binding to the CARD domain.
- lack of role in caspase-9 activation in Sendai virus-infected cells
- APAF-1 is under transcriptional regulation of E2F-1 and initiates a caspase cascade
- Data show that the trace amount of cytochrome c present in neutrophils is both necessary and sufficient for apoptotic protease-activating factor 1 (Apaf-1)-dependent caspase activation in these cells.
- function of Apaf-1 is not only to oligomerize procaspase-9 but also to maintain the interaction of the caspase-9 protease domain after processing
- alternatively spliced APAF-1-ALT is a molecule that is deficient and impeded for mediating apoptosis and may contribute to the resistance to DNA damage-induced treatment observed in LNCaP
- Bcl-XL directly binds to the ATPase domain of Apaf-1.
- AMF regulates expression of Apaf-1 and caspase-9 genes via a complex signaling pathway and indirectly regulates formation of the apoptosome.
- the cytochrome c-Apaf-1-procaspase-9 complex functions in the caspase amplification rather than in its initiation
- the functional apoptosome complex in apoptotic cells consists primarily of Apaf-1 and processed caspase-9
- Loss of APAF-1 expression can be considered an indicator of malignant transformation in melanoma.
- Allelic imbalance of 12q22-23 associated with APAF-1 locus correlates with poor disease outcome in cutaneous melanoma
- Apaf-1 proteolytic degradation does not significantly abrogate either the apoptotic morphology or the cleavage of canonical targets.
- Apaf-1 expression is significantly reduced in human melanoma and Apaf-1 may serve as a therapeutic target in melanoma.
- results suggest that APAF-1 gene haploinsufficiency caused by AI increases with tumor progression, and relates to hepatic metastasis
- Limiting Apaf-1 activity may alleviate both pathological protein aggregation and neuronal cell death in HD.
- there is an inverse correlation between Apaf-1 expression and pathologic stage of melanoma
- noncytosolic localization of Apaf-1 may constitute a novel mechanism of chemoresistance in B lymphoma
- Protein kinase A regulates caspase-9 activation by Apaf-1 downstream of cytochrome c
- Apaf-1 expression in 15 melanoma cell lines
- Apaf-1 levels vary in melanoma
- Loss of Apaf-1 expression may represent a marker of aggressive tumor behavior since it correlates significantly with the occurrence of lymph node metastasis in cervical cancer.
- Methylation silencing is a mechanism of the inactivation of APAF1 in acute leukemia.
- Using different cell lines of neuronal origin and modulating the expression of both mutant SOD1s and Apaf1, we show that the removal of Apaf1 prevents cells death.
- No coorelation between apaf-1 expression in melanoma and malignancy
- The depression-associated alleles thus have a common phenotype that is distinct from that of non-associated variants
- Apaf-1 gene structure and function and its role in apoptotic machinery. Involvement in melanoma progression and chemoresistance, as well as clinico-pathological relevance of these findings in treatment of this deadly disease. Review.
- poor prognosis was observed in patients with loss of APAF-1 expression and additional p53 mutation; thus, loss of APAF-1 may become relevant when additional core apoptosis signaling components are disrupted
- These results suggest that Apaf-1 expression may become a prognostic marker for progress of human cutaneous melanoma and further support the notion that loss of Apaf-1 may be an important contributory factor in the development of the disease.
- progression of UV-induced apoptosis requires IRES-mediated translation of Apaf-1 to ensure continuous levels of Apaf-1 despite an overall suppression of protein synthesis
- The promoter hypermethylation of APAF-1 is a marker of aggressive renal cell carcinoma and provides independent prognostic information on disease outcome.
- Methylation of APAF-1 is associated with bladder and kidney cancer
- Data support a model in which Apaf-1 is necessary for the cleavage or activation of all procaspases and the promotion of mitochondrial apoptotic events induced by genotoxic drugs.
- mRNA elevation of apaf1 during blast crisis indicates an involvement in chronic myelogenous leukemia disease progression.
- APAF-1 methylation is related to transcriptional activity of EZH2 expression in early-stage tumor disease of the bladder.
- Fas receptor and Apaf-1 were down-regulated in stage III colorectal cancer cell line.
- The expression of Apaf-1 gene is low in gastric cancer tissues. Methylation of Apaf-1 gene promoter and LOH in domain of 12q22-23 are the main reasons for the expression and altered expression of Apaf-1 gene.
- Reduced expression of Apaf-1 is associated with colorectal adenocarcinoma
- These findings suggest that the efflux of K(+) is prerequisite not only for the formation of the apoptosome but also for the downstream apoptotic signal-transduction pathways.
- These data point to a role for Apaf-1 as a bona fide tumor suppressor.
- Apaf-1 has a role in regulating cytochrome c induction of apoptosis in brain tumors but not in normal neural tissues
- Frameshift mutation at mononucleotide repeat in Apaf-1 is rare in gastric carcinomas.
- PHAPI, CAS, and Hsp70 function together to accelerate nucleotide exchange on Apaf-1 and prevent inactive Apaf-1/cytochrome c aggregation.
- The methylation profile observed demonstrates a substantial role of the APAF-1 gene in urogenital tumorigenesis.
- it has been shown that only the isoforms with the extra WD-40 repeat region activate procaspase-9, it suggests that low procaspase-9 activation may also be involved in the deregulation of apoptosis and chemotherapy resistance in acute myeloid leukemia.
- Frequent HDAC2 mutations are found in MSI tumors and HDAC2 plays a major role in mediating apoptotic response to HDAC inhibitors through direct regulation of APAF1.
