Anti-XAF1: Rabbit X-Linked Inhibitor of Apoptosis-Associated Factor 1 Antibody

Several regulatory pathways of XAF1 expression have been reported. In addition to hypermethylation of XAF1 promoter, it has been demonstrated that heat shock factor 1 negatively while interferon regulatory factor-1 and STAT1 positively modulated XAF1 transcription.³ These facts implicated that XAF1 might play important role in multiple cellular events such as growth, apoptosis and stress response. Cell division or proliferation is well controlled by some key checkpoint proteins. In normal cells, G2/M checkpoint, which is usually activated by DNA damage, involves a complex network of genes involved in cell cycle arrest, DNA repair and apoptosis. Checkpoint kinase 1 (Chk1) and Chk2 are two checkpoint proteins during G2–M transition and both can phosphorylate Cdc25C to create a binding site for 14-3-3 proteins, which in turn sequester Cdc25C in the cytoplasm, preventing Cdc25 from activating Cdc2–cyclin B complex in the nucleus. Some tumor suppressor has been reported to be able to interact with and modulate the function of Chks. It was showed that XAF1 protein expression was G2/M phase dependent. It interacted with and activated Chk1 and modulated G2/M checkpoint. Overexpression of XAF1 induced cell cycle arrest at G2/M phase and resulted in mitotic catastrophe. Thus XAF1 acts as a novel cell cycle modulator and plays important role in carcinogenesis.⁴