Anti-Serine-protein kinase ATM ATM Antibody Picoband®

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. The ATM gene is mapped to chromosome 11q22.3. 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 ly in the repair of chromosomal DNA double-stranded breaks by maintaining DNA ends in repair complexes generated during lymphocyte gene assembly.

Serine/threonine protein kinase which activates checkpoint signaling upon double strand breaks (DSBs), apoptosis and genotoxic stresses such as ionizing ultraviolet A light (UVA), thereby acting as a DNA damage sensor. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates 'Ser-139' of histone variant H2AX/H2AFX at double strand breaks (DSBs), thereby regulating DNA damage response mechanism. Also plays a role in pre-B cell allelic exclusion, a process leading to expression of a single immunoglobulin heavy chain allele to enforce clonality and monospecific recognition by the B-cell antigen receptor (BCR) expressed on individual B-lymphocytes. After the introduction of DNA breaks by the RAG complex on one immunoglobulin allele, acts by mediating a repositioning of the second allele to pericentromeric heterochromatin, preventing accessibility to the RAG complex and recombination of the second allele. Also involved in signal transduction and cell cycle control. May function as a tumor suppressor. Necessary for activation of ABL1 and SAPK. Phosphorylates DYRK2, CHEK2, p53/TP53, FANCD2, NFKBIA, BRCA1, CTIP, nibrin (NBN), TERF1, RAD9 and DCLRE1C. May play a role in vesicle and/or protein transport. Could play a role in T-cell development, gonad and neurological function. Plays a role in replication-dependent histone mRNA degradation. Binds DNA ends. Phosphorylation of DYRK2 in nucleus in response to genotoxic stress prevents its MDM2-mediated ubiquitination and subsequent proteasome degradation. Phosphorylates ATF2 which stimulates its function in DNA damage response. .

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.

Store at -20°C for one year from date of receipt. After reconstitution, at 4°C for one month. It can also be aliquotted and stored frozen at -20°C for six months. Avoid repeated freeze-thaw cycles.