|Application ||WB, IHC-P, IF, E|
|Other Accession||AAB65827, 2304971|
|Calculated MW||350687 Da|
|Application Notes||ATM antibody can be used for detection of ATM by Western blot at 1 - 2 µg/mL. Antibody can also be used for immunohistochemistry starting at 2.5 µg/mL. For immunofluorescence start at 10 µg/mL.|
|Other Names||ATM Antibody: AT1, ATA, ATC, ATD, ATE, ATDC, TEL1, TELO1, Serine-protein kinase ATM, Ataxia telangiectasia mutated, A-T mutated, ataxia telangiectasia mutated|
|Reconstitution & Storage||ATM antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||ATM Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||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.|
|Cellular Location||Nucleus. Cytoplasmic vesicle. Note=Primarily nuclear. Found also in endocytic vesicles in association with beta-adaptin|
|Tissue Location||Found in pancreas, kidney, skeletal muscle, liver, lung, placenta, brain, heart, spleen, thymus, testis, ovary, small intestine, colon and leukocytes|
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Provided below are standard protocols that you may find useful for product applications.
ATM Antibody: DNA double strand breaks represent a major threat to an organism's genome. Eukaryotic cells have developed mechanisms that sense the presence this damage and initiate suitable responses that can include DNA repair, cell cycle delay, and programmed cell death. The ATM (mutated in Ataxia-Telangiectasia) protein kinase is activated following the formation of DNA double strand breaks, phosphorylating p53 and another kinase CHK2. This initiates a signaling cascade leading to the phosphorylation and inhibition of Cdc25, ultimately preventing cell cycle progression. In some cell types, such as the hemapoietic system, this leads to apoptosis instead of cell cycle arrest. Multiple isoforms of ATM are known to exist.
Cahill D, Connor B, and Carney JP. Mechanisms of eukaryotic DNA double strand break repair. Front. Biosci. 2006 ; 11 :1958-76.
Dasika GK, Lis SC, Zhao S, et al. DNA damage-induced cell cycle checkpoints and DNA strand break repair in development and tumorigenesis. Oncogene 1999; 18:7883-99.
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