Phospho-Chk1 (Ser317) Rabbit anti-Human, Polyclonal, Bethyl Laboratories

Description

• The recommended shelf life for this product is 1 year from date of receipt
• Application Note: For IHC, epitope retrieval with citrate buffer pH 6.0 is recommended for FFPE tissue sections
• CHK1 (CHEK1) is a kinase that phosphorylates cdc25, an important phosphatase in cell cycle control, particularly for entry into mitosis
• CHK1 can also phosphorylate p53 at Ser20 in vitro
• Cell cycle events are regulated by the sequential activation and deactivation of cyclin dependent kinases (Cdks) and by proteolysis of cyclins
• CHK1 is involved in these processes as regulators of Cdks
• CHK1 function as an essential component in the G2 DNA damage checkpoint by phosphorylating Cdc25C in response to DNA damage
• Phosphorylation inhibits Cdc25C activity, thereby blocking mitosis
• Cdc25A, Cdc25B and Cdc25C protein tyrosine phosphatases function as mitotic activators by dephosphorylating Cdc2 p34 on regulatory tyrosine residues
• CHK1 can phosphorylate Wee 1 in vitro, providing evidence that the hyperphosphorylated form of Wee 1, seen in cells delayed by CHK1 overexpression, is due to phosphorylation by CHK1
• CHK1 is phosphorylated on Serine 345 (S345) in response to UV, IR and hydroxyurea (HU)
• CHK1 plays an essential role in the mammalian DNA damage checkpoint, embryonic development and tumor suppression
• Further, CHK1 is a key mediator in the DNA damage-induced checkpoint network
• CHK1 is an evolutionarily conserved protein kinase that functions to ensure genomic integrity upon genotoxic stress
• When the G2 or S checkpoint is abrogated by the inhibition of CHK1, p53-deficient cancer cells undergo mitotic catastrophe and eventually apoptosis, whereas normal cells are still arrested in the G1 phase
• Thus, CHK1 inhibitors can preferentially potentiate the efficacy of DNA damaging agents in cancer cells, and Chk1 is an attractive therapeutic target for cancer treatment, especially since approximately 50% of all human cancers are p53-deficient.