Phospho-ATM (Ser1981) Monoclonal Antibody (10H11.E12), Rockland™

Description

• Store vial at -20°C prior to opening
• Aliquot contents and freeze at -20°C or below for extended storage
• Avoid cycles of freezing and thawing
• Centrifuge product if not completely clear after standing at room temperature
• This product is stable for several weeks at 4°C as an undiluted liquid
• Dilute only prior to immediate use
• Anti-ATM phospho S1981 Monoclonal Antibody is directed against human ATM and is useful in determining its presence in various assays
• This monoclonal anti-ATM antibody recognizes the phosphorylated epitope in native and over-expressed proteins found in various tissues and extracts
• By ELISA reactivity against SLAFEEGSpQSTTISS at a 1:1600 dilution shows an absorbance >3.000; whereas reactivity against SLAFEEGSQSTTISS shows and absorbance of 0.145
• Reactivity is observed against human ATM
• Cross reactivity with ATM from other mammalian sources has not been tested
• The immunogen has 91% sequence homology with mouse ATM
• Ataxia-telangiectasia Mutated (ATM) is a protein that belongs to the PI3/PI4 kinase family
• Ataxia-telangiectasia is a rare autosomal recessive disorder characterized by progressive neurologic degeneration, immunologic deficiency, and an increased risk of lymphoid cancer
• The ATM gene codes for a protein belonging to the phosphoinositide 3-kinase (PI3K) superfamily
• ATM phosphorylates proteins instead of lipid and has many downstream targets that act as cell-cycle regulators including: P53, Mdm2, BRCA1, and SMC1
• The ATM protein is responsible for repairing double-stranded DNA breaks that occur because of ionizing radiation and other mutagens
• The ATM’s C-terminal region has extensive homology to the catalytic domains of phosphatidylinositol 3-kinases (PI3 kinases)
• Studies have shown that ATM becomes autophosphorylated and upregulated by exposure to ionizing radiation
• AT cells are hypersensitive to ionizing radiation, impaired in mediating the inhibition of DNA synthesis and display delays in p53 induction
• Further, DNA damage caused by ionizing irradiation activates ATM-kinase, leading to a cascade of kinase reactions that regulate cell cycle, apoptosis, and DNA damage repair
• Studies have linked ATM to apoptosis along with Nbs1 and Chk2 in the E2F1 pathway.