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Polyclonal Anti-ATM

Cat no: PA1784


Supplier: Boster Immunoleader
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Rabbit IgG polyclonal antibody for Serine-protein kinase ATM (ATM) detection. Tested with WB in Human;Mouse;Rat.
Catalogue number: PA1784
Price: $200.00
Reactivities: Human, Mouse, Rat
Applications: Western Blot
Size: 100ug/vial
Gene: ATM
Swiss prot: Q13315
Form: Lyophilized
Format: Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg Thimerosal, 0.05mg NaN3.
Storage temp: At -20 degree C for one year. After reconstitution, at 4 degree C for one month. It can also be aliquotted and stored frozen at -20 degree C for a longer time.Avoid repeated freezing and thawing.
Scientific background: ATM(ataxia telangiectasia mutated),also known as TEL1 or TELO1, is a serine/threonine protein kinase that is recruited and activated by DNA double-strand breaks. The ATM protein is a member of the phosphatidylinositol 3-kinase family of proteins that respond to DNA damage by phosphorylating key substrates involved in DNA repair and/or cell cycle control. Linkage analysis of ataxia-telangiectasia led to mapping of the ATM gene to chromosome 11q22.3. Using an antiserum developed to a peptide corresponding to the deduced amino acid sequence of ATM, the ATM protein is a single, high molecular weight protein predominantly confined to the nucleus of human fibroblasts, although it is present in both nuclear and microsomal fractions from human lymphoblast cells and peripheral blood lymphocytes. Overexpression of ATM cDNA in AT cells enhanced their survival after radiation exposure, decreased radiation-induced chromosome aberrations, reduced radioresistant DNA synthesis, and partially corrected defective cell cycle checkpoints and induction of stress-activated protein kinase. ATM has an essential role in the reconstitutive capacity of hematopoietic stem cells but is not as important for the proliferation or differentiation of progenitors, in a telomere-independent manner. ATM functions directly in the repair of chromosomal DNA double-stranded breaks by maintaining DNA ends in repair complexes generated during lymphocyte gene assembly.
References: 1. Allen, D. M., van Praag, H., Ray, J., Weaver, Z., Winrow, C. J., Carter, T. A., Braquet, R., Harrington, E., Ried, T., Brown, K. D., Gage, F. H., Barlow, C. Ataxia telangiectasia mutated is essential during adult neurogenesis. Genes Dev. 15: 554-566, 2001. 2. Bakkenist, C. J., Kastan, M. B. DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation.Nature 421: 499-506, 2003. 3. Chong, M. J., Murray, M. R., Gosink, E. C., Russell, H. R. C., Srinivasan, A., Kapsetaki, M., Korsmeyer, S. J., McKinnon, P. J. Atm and Bax cooperate in ionizing radiation-induced apoptosis in the central nervous system. Proc. Nat. Acad. Sci. 97: 889-894, 2000
Additional info: A synthetic peptide corresponding to a sequence at the N-terminal of human ATM, different from the related rat and mouse sequences by two amino acids.