Human.

Signals originating from damaged DNA activate checkpoint pathways and target the mitotic apparatus via a number a distinct mechanisms. These checkpoints link damage to DNA with the components of the cell cycle through signal transduction systems. In mammals, five genes have been identified as components of DNA damage-induced checkpoint pathways: ATM, p53, p21/WAF1/CIP1, hCHK1, and 14-3-3sigma. When overexpressed in mammalian cells, hRAD17 activates p53 and causes an accumulation of G1 phase cells, suggesting an involvement of the hRAD17 gene in this checkpoint pathway.(1).

Quality control test: Antibody reactive against mammalian transfected lysate.

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The protein encoded by this gene is highly similar to the gene product of Schizosaccharomyces pombe rad17, a cell cycle checkpoint gene required for cell cycle arrest and DNA damage repair in response to DNA damage. This protein shares strong similarity with DNA replication factor C (RFC), and can form a complex with RFCs. This protein binds to chromatin prior to DNA damage and is phosphorylated by the checkpoint kinase ATR following damage. This protein recruits the RAD1-RAD9-HUS1 checkpoint protein complex onto chromatin after DNA damage, which may be required for its phosphorylation. The phosphorylation of this protein is required for the DNA-damage-induced cell cycle G2 arrest, and is thought to be a critical early event during checkpoint signaling in DNA-damaged cells. Eight alternatively spliced transcript variants of this gene, which encode four distinct proteins, have been reported. Two pseudogenes, located on chromosomes 7 and 13, have been identified. [provided by RefSeq]