Anti-XAF1 / XIAP associated factor 1

0.5mg/ml if reconstituted with 0.2ml sterile DI water. XAF1, also called XIAP-associated factor 1, antagonizes the anti-caspase activity of XIAP and may be important in mediating apoptosis resistance in cancer cells. By genomic sequence analysis, the XAF1 gene contains 7 exons spanning 18 kb. Southern blot analysis suggested that XAF1 is a single-copy gene. The XAF1 gene is mapped on 17p13.1. Fluorescence microscopy demonstrated nuclear expression of XAF1, in contrast to the cytoplasmic expression of XIAP. Functional analysis indicated that XAF1 reverses the XIAP-mediated inhibition of CASP3 and its protection against apoptosis. Northern blot analysis detected wide expression of 3.9-, 4.5-, 6.0-, and 7.0-kb XAF1 transcripts, with highest levels in heart and ovary and lowest levels in brain and testis. Antisense experiments determined that loss of XAF1 expression enhances resistance to apoptosis. Alteration in XAF1 and XIAP RNA expression levels may lead to increased apoptotic resistance and proliferation due to unregulated XIAP function in cancer cells. Protein function: Seems to function as a negative regulator of members of the IAP (inhibitor of apoptosis protein) family. Inhibits anti-caspase activity of BIRC4. Induces cleavage and inactivation of BIRC4 independent of caspase activation. Mediates TNF-alpha-induced apoptosis and is involved in apoptosis in trophoblast cells. May inhibit BIRC4 indirectly by activating the mitochondrial apoptosis pathway. After translocation to mitochondria, promotes translocation of BAX to mitochondria and cytochrome c release from mitochondria. Seems to promote the redistribution of BIRC4 from the cytoplasm to the nucleus, probably independent of BIRC4 inactivation which seems to occur in the cytoplasm. The BIRC4-XAF1 complex mediates down-regulation of BIRC5/survivin, the process requires the E3 ligase activity of BIRC4. Seems to be involved in cellular sensitivity to the proapoptotic actions of TRAIL. May be a tumor suppressor by mediating apoptosis resistance of cancer cells. [The UniProt Consortium]