|Application ||IHC-P, WB, E|
|Calculated MW||350687 Da|
|Antigen Region||3027-3056 aa|
|Other Names||Serine-protein kinase ATM, Ataxia telangiectasia mutated, A-T mutated, ATM|
|Target/Specificity||This ATM antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 3027~3056 amino acids from the C-terminal region of human ATM.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||ATM Antibody (C-term) 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 is involved in signal transduction, cell cycle control and DNA repair, and may function as a tumor suppressor. It is necessary for activation of ABL1 and SAPK, and phosphorylates p53, NFKBIA, BRCA1, CTIP, NIBRIN (NBS1), TERF1, and RAD9. This protein has potential roles in vesicle and/or protein transport, T-cell development, gonad and neurological function. ATM is also part of the BRCA1-associated genome surveillance complex. ATM is induced by ionizing radiation. Defects in ATM are the cause of ataxia talangiectasia (AT), also known as Louis-Bar syndrome, a rare recessive disorder characterized by progressive cerebellar ataxia, dilation of the blood vessels in the conjunctiva and eyeballs, immunodeficiency, growth retardation and sexual immaturity. About 30% of AT patients develop lymphomas and leukemias. Defects in ATM also contribute to T-cell acute lymphoblastic leukemia (TALL) and T-prolymphocytic leukemia (TPLL). TPLL is characterized by a high white blood cell count, with a predominance of prolymphocytes, marked splenomegaly, lymphadenopathy, skin lesions and serous effusion. Defects in ATM also contribute to B-cell non-Hodgkin's lymphomas, and to B-cell chronic lymphocytic leukemia, a disease characterized by accumulation of mature CD5+ B lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure.
Suzuki, A., et al., J. Biol. Chem. 278(1):48-53 (2003).
Kishi, S., et al., J. Biol. Chem. 276(31):29282-29291 (2001).
Schaffner, C., et al., Proc. Natl. Acad. Sci. U.S.A. 97(6):2773-2778 (2000).
Gatei, M., et al., Nat. Genet. 25(1):115-119 (2000).
Becker-Catania, S.G., et al., Mol. Genet. Metab. 70(2):122-133 (2000).
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