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Description

ASCIZ is a transcription factor that interacts with the potent kinase ATM and regulates its activity and stability. ATM is best known for its role as an apical activator of the DNA damage response in the face of DNA double-strand breaks (DSBs). Following induction of DSBs, ATM mobilizes one of the most extensive signaling networks that responds to specific stimuli and modifies directly or indirectly a broad range of targets. ASCIZ plays a crucial role in cell survival and RAD51 foci formation in response to methylating DNA damage as well. ASCIZ is also critical in development. Knockouts are lethal at E16 and show severe organ developmental defects, including a complete absence of lungs similar to mutants in Wnt2-2b/ß,-catenin and FGF10/FGFR2b signaling pathways. Thus, ASCIZ has dual functions as an efficiency factor for DNA base damage repair as well as a key transcriptional regulator of early lung development. ASCIZ is localized to the nucleus in discrete foci during G1 and is ubiquitously expressed in normal and cancerous tissues.