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Mouse Monoclonal Atm antibody [5C5] (STJ97855)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, ELISA
Recommended dilution: WB 1:500-1:2000; ELISA 1:10000
Recommended protocols: check protocols
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Check alternative names for the antibodyExpand
ATM antibody,|A-T mutated antibody|A-T mutated homolog antibody|AT mutated antibody|AT1 antibody|ATA antibody|Ataxia telangiectasia mutated antibody|Ataxia telangiectasia mutated gene antibody|Ataxia telangiectasia mutated homolog (human) antibody|Ataxia telangiectasia mutated homolog antibody|ATC antibody|ATD antibody|ATDC antibody|ATE antibody|ATM antibody|ATM serine/threonine kinase antibody|ATM_HUMAN antibody|DKFZp781A0353 antibody|MGC74674 antibody|OTTHUMP00000232981 antibody|Serine protein kinase ATM antibody|Serine-protein kinase ATM antibody|Serine/threonine-protein kinase ATM antibody|Tefu antibody|TEL1 antibody|TEL1, telomere maintenance 1, homolog antibody|TELO1 antibody|Telomere fusion protein antibody|Phospho anti-ATM (S1981) antibody [EP1890Y] (ab81292)
SCBT cat No: sc-73615|sc-135663|sc-23921|sc-23922|sc-53173|sc-377293|sc-7230|sc-28881|sc-7129|sc-373834|
Atm Monoclonal Antibody
|Catalogue No.|| |
Atm Monoclonal Antibody detects endogenous levels of Atm protein.
Purified recombinant fragment of human Atm expressed in E Coli
|Recommended dilution|| |
WB 1:500-1:2000; ELISA 1:10000
Atm Antibody was tube-contained. Ascitic fluid containing 0.03% sodium azide.
Atm Antibody was purified using affinity purification.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
Serine-protein kinase ATM antibody, Ataxia telangiectasia mutated antibody, A-T mutated antibody
|Protein names|| |
Serine-protein kinase ATM , Ataxia telangiectasia mutated , A-T mutated
|Protein 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. / ATP + a protein = ADP + a phosphoprotein. / Inhibited by wortmannin.
|Protein tissue specificity|| |
Found in pancreas, kidney, skeletal muscle, liver, lung, placenta, brain, heart, spleen, thymus, testis, ovary, small intestine, colon and leukocytes.
|Involvement in disease|| |
Ataxia telangiectasia (AT) [MIM:208900]: 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. Patients have a strong predisposition to cancer; about 30% of patients develop tumors, particularly lymphomas and leukemias. Cells from affected individuals are highly sensitive to damage by ionizing radiation and resistant to inhibition of DNA synthesis following irradiation. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Note: Defects in ATM 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. The clinical course is highly aggressive, with poor response to chemotherapy and short survival time. TPLL occurs both in adults as a sporadic disease and in younger AT patients. .; Note: Defects in ATM contribute to B-cell non-Hodgkin lymphomas (BNHL), including mantle cell lymphoma (MCL). .; Note: Defects in ATM contribute to B-cell chronic lymphocytic leukemia (BCLL). BCLL is the commonest form of leukemia in the elderly. It is characterized by the accumulation of mature CD5+ B-lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure. .
|Protein sequence and domain|| |
The FATC domain is required for interaction with KAT5. / Belongs to the PI3/PI4-kinase family. ATM subfamily. / Contains 1 FAT domain. / Contains 1 FATC domain. / Contains 1 PI3K/PI4K domain.
|Protein post-translational modifications|| |
Phosphorylated by NUAK1/ARK5. Autophosphorylation on Ser-367, Ser-1893, Ser-1981 correlates with DNA damage-mediated activation of the kinase. / Acetylation, on DNA damage, is required for activation of the kinase activity, dimer-monomer transition, and subsequent autophosphorylation on Ser-1981. Acetylated in vitro by KAT5/TIP60.
|Protein cellular localization|| |
Nucleus / Cytoplasmic vesicle
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St John’s Laboratory Ltd.
|Product type|| |
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