84-2132-23　ATM, phosphorylated (S1981) (Ataxia telangiectasia mutated) 100ug　168045

特徴

• ATM, the gene mutated in the hereditary disease ataxia-telangiectasia, codes for a protein kinase that acts as a master regulator of cellular responses to DNA double-strand breaks.
• ATM is normally inactive and the question of how it is activated in the event of DNA damage (due to ionizing radiation for instance) is central to understanding its function.
• ATM protein is now shown to be present in undamaged cells as an inactive dimer.
• Low doses of ionizing radiation, which induce only a few DNA breaks, activate at least half of the total ATM protein present, possibly in response to changes in chromatin structure.
• The ATM gene encodes a 370kD protein that belongs to the phosphoinositide 3-kinase (PI(3)K) superfamily, but which phosphorylates proteins rather than lipids.
• The 350aa kinase domain at the C-terminus of this large protein is the only segment of ATM with an assigned function.
• Exposure of cells to IR triggers ATM kinase activity and this function is required for arrests in G1, S and G2 phases of the cell cycle.
• Several substrates of the ATM kinase participate in these IR-induced cell-cycle arrests.
• These include p53, Mdm2 and Chk2 in the G1 checkpoint; Nbs1, Brca1, FancD2 and SMC1 in the transient IR-induced S-phase arrest; and Brca1 and hRad17 in the G2/M checkpoint.
• Applications:Suitable for use in ELISA and Western Blot.
• Other applications not tested.
• Recommended Dilution:ELISA: 1:2000-1:10,000Western Blot: 1:500-1:2000Optimal dilutions to be determined by the researcher.
• Storage and Stability:May be stored at 4°C for short-term only.
• Aliquot to avoid repeated freezing and thawing.
• Store at -20°C.
• Aliquots are stable for 12 months.
• For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.