Checkpoint Rad proteins function early in the DNA damage signaling cascade to arrest cell cycle progression in response to DNA damage (1). There is a direct regulatory linkage between Rad17 and the checkpoint kinases, ATM and ATR (2). Rad17 has been reported to be a phosphorylation substrate of ATR and is critical for ATR-mediated checkpoint signaling and cell survival. Phosphorylation of Rad17 by ATR is important for genomic stability and restraint of S phase but is not essential for cell survival (3).
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