Polyclonal Anti-ATM

Price

200.00 USD

Size

100ug/vial

Reactivities

Hum, Mouse, Rat

Format

Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg Thimerosal, 0.05mg NaN3.

References

1. Allen, D. M., van Praag, H., Ray, J., Weaver, Z., Winrow, C. J., Carter, T. A., Braquet, R., Harrington, \nE., Ried, T., Brown, K. D., Gage, F. H., Barlow, C. Ataxia telangiectasia mutated is essential during \nadult neurogenesis. Genes Dev. 15: 554-566, 2001.\n2. Bakkenist, C. J., Kastan, M. B. DNA damage activates ATM through intermolecular \nautophosphorylation and dimer dissociation.Nature 421: 499-506, 2003.\n3. Chong, M. J., Murray, M. R., Gosink, E. C., Russell, H. R. C., Srinivasan, A., Kapsetaki, M., \nKorsmeyer, S. J., McKinnon, P. J. Atm and Bax cooperate in ionizing radiation-induced apoptosis in \nthe central nervous system. Proc. Nat. Acad. Sci. 97: 889-894, 2000

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 \nkinase that is recruited and activated by DNA double-strand breaks. The ATM protein is a member of \nthe phosphatidylinositol 3-kinase family of proteins that respond to DNA damage by phosphorylating \nkey substrates involved in DNA repair and/or cell cycle control. Linkage analysis of ataxia-telangiectasia \nled to mapping of the ATM gene to chromosome 11q22.3. Using an antiserum developed to a peptide \ncorresponding to the deduced amino acid sequence of ATM, the ATM protein is a single, high molecular \nweight protein predominantly confined to the nucleus of human fibroblasts, although it is present in both \nnuclear and microsomal fractions from human lymphoblast cells and peripheral blood \nlymphocytes. Overexpression of ATM cDNA in AT cells enhanced their survival after radiation exposure, \ndecreased radiation-induced chromosome aberrations, reduced radioresistant DNA synthesis, and \npartially corrected defective cell cycle checkpoints and induction of stress-activated protein \nkinase. ATM has an essential role in the reconstitutive capacity of hematopoietic stem cells but is not \nas important for the proliferation or differentiation of progenitors, in a telomere-independent manner. \nATM functions directly in the repair of chromosomal DNA double-stranded breaks by maintaining DNA \nends in repair complexes generated during lymphocyte gene assembly.