Rabbit anti-Human, Mouse ATM Polyclonal Antibody | anti-ATM antibody

ATM, phosphorylated (Ser1981) (Serine-protein Kinase ATM, Ataxia Telangiectasia Mutated, A-T Mutated)

Cat. Num. AAA626375

• Gene Names: ATM; AT1; ATA; ATC; ATD; ATE; ATDC; TEL1; TELO1; MGC74674; DKFZp781A0353
• Reactivity: Human, Mouse
• Applications: ELISA, Immunohistochemistry
• Purity: Affinity Purified; Purified by immunoaffinity chromatography.
• Synonyms: ATM; Polyclonal Antibody; phosphorylated (Ser1981) (Serine-protein Kinase ATM; Ataxia Telangiectasia Mutated; A-T Mutated); Anti -ATM; anti-ATM antibody

• Host: Rabbit
• Reactivity: Human, Mouse
• Clonality: Polyclonal
• Isotype: IgG
• Specificity: Recognizes human ATM when phosphorylated at serine 1981. Species Cross-Reactivity: mouse.
• Purity/Purification: Affinity Purified; Purified by immunoaffinity chromatography.
• Form/Format: Supplied as a liquid in PBS (without Mg2+ and Ca2+), pH 7.4, 150mM sodium chloride, 0.02% sodium azide, 50% glycerol.

• Applicable Applications for anti-ATM antibody: ELISA (EL/EIA), Immunohistochemistry (IHC)
• Application Notes: Suitable for use in Immunohistochemistry.; Dilution: Immunohistochemistry: 1:50-1:100
• Immunogen: Synthetic phosphopeptide corresponding to human ATM around the phosphorylation site of serine 1981 (E-G-SP-Q-S).
• Preparation and Storage: May be stored at 4 degree C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20 degree C. Aliquots are stable for at least 12 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Related Product Information for anti-ATM antibody

Ataxia-telangiectasia (A-T) is a recessive childhood disease caused by mutations in the ATM (AT-mutated) gene. Symptoms include neurological abnormalities that cause unsteady posture, dilated blood vessels, infertility, radiation sensitivity, immune deficiencies and lymphoid malignancies. It appears that the diverse defects seen in ATM null mammals are manifestations of disparate signal transduction defects. The ATM protein is related to a family of proteins through a C-terminal phoshatidylinositol 3-kinase (PI3-kinase) domain. ATM also shares sequence homology with portions of the yeast RAD3 gene. The main role of ATM appears to be induction of a DNA-damage control pathway in response to genotoxic insults, such as ionizing radiation or anti-tumor medications and the programmed DNA breaks of meiosis. Ataxia telangiectasia mutated kinase (ATM) and ataxia telangiectasia and Rad3-related kinase (ATR) are related kinases that regulate cell cycle checkpoints and DNA repair. ATM activates p53, increasing the p21Cip1 levels, thus blocking activation of cdk2. That results in Rb hypophosphorylation and blockage of the G1/S transition. Separately, ATM also phosphorylates and activates Chk1, which phosphorylates cdc25C, preventing it from phosphorylating the inhibitory phosphotyrosine residue on cdc2/cdk1, thus preventiing the G2/M transition. The identified substrates for ATM are p53, p95/NBS1, MDM2, Chk2, BRCA1, CtIP, 4E-BP1 and Chk1. The essential requirement for the substrates of ATM/ATR is S*/T*Q. Hydrophobic amino acids at positions -3 and -1, and negatively charged amino acids at position +1 are positive determinants for substrate recognition by these kinases. Positively charged residues surrounding the S/TQ are negative determinants for substrate phosphorylation. The complex phenotype of AT cells suggests that it must have other cellular substrates as well. In order to better understand the kinase and identify substrates for ATM and the related kinase ATR, we have antibodies that recognize phosphorylated serine or threonine in S*/T*Q motifs. As shown by ELISA, Phospho-(Ser/Thr) ATM/ATR Substrate Antibody is specific for phosphorylated ATM/ATR substrates.

Product Categories/Family for anti-ATM antibody

Antibodies; Abs to Protein Kinases

NCBI and Uniprot Product Information

• NCBI GI #: 2304971
• NCBI GeneID: 472
• UniProt Accession #: Q13315; O15429; Q12758; Q16551; Q93007; Q9NP02; Q9UCX7; B2RNX5; Q59GH6; Q68DE6; Q6P7P1; Q8TDS0; Q96QM9
• Molecular Weight: 350,714 Da
• NCBI Official Full Name: ATM
• NCBI Official Synonym Full Names: ataxia telangiectasia mutated
• NCBI Official Symbol: ATM
• NCBI Official Synonym Symbols: AT1; ATA; ATC; ATD; ATE; ATDC; TEL1; TELO1; MGC74674; DKFZp781A0353
• NCBI Protein Information: serine-protein kinase ATM; AT mutated; A-T mutated; OTTHUMP00000232981; TEL1, telomere maintenance 1, homolog
• UniProt Protein Name: Serine-protein kinase ATM
• Protein Family: ATM interactor
• UniProt Gene Name: ATM
• UniProt Entry Name: ATM_HUMAN

NCBI Description

The protein encoded by this gene belongs to the PI3/PI4-kinase family. This protein is an important cell cycle checkpoint kinase that phosphorylates; thus, it functions as a regulator of a wide variety of downstream proteins, including tumor suppressor proteins p53 and BRCA1, checkpoint kinase CHK2, checkpoint proteins RAD17 and RAD9, and DNA repair protein NBS1. This protein and the closely related kinase ATR are thought to be master controllers of cell cycle checkpoint signaling pathways that are required for cell response to DNA damage and for genome stability. Mutations in this gene are associated with ataxia telangiectasia, an autosomal recessive disorder. [provided by RefSeq]

Uniprot Description

ATM: an atypical kinase of the PIKK family. Regulates cell cycle checkpoints and DNA repair . May function as a tumor suppressor. 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. Involved in the activation of ABL1 and SAPK. Binds DNA ends and is part of the BRCA1- associated genome surveillance complex (BASC), which contains BRCA1, MSH2, MSH6, MLH1, ATM, BLM, PMS2 and the RAD50-MRE11-NBN protein complex. This association could be a dynamic process changing throughout the cell cycle and within subnuclear domains. DNA damage promotes association with RAD17. LOF mutations associated with ataxia telangiectasia, causing progressive loss of motor control (ataxia), dilation of superficial blood vessels (telangiectasia), cancer and immune deficiency. Approximately 30% of cases develop tumors, mostly lymphomas and leukemias, due to defects in DNA damage repair. Somatic mutations seen in leukemias and lymphomas.

Protein type: Protein kinase, atypical; Tumor suppressor; Protein kinase, Ser/Thr (non-receptor); Kinase, protein; EC 2.7.11.1; DNA repair, damage; ATYPICAL group; PIKK family

Chromosomal Location of Human Ortholog: 11q22-q23

Cellular Component: nucleoplasm; chromosome, telomeric region; cytoplasmic membrane-bound vesicle; spindle

Molecular Function: protein dimerization activity; protein serine/threonine kinase activity; protein binding; DNA binding; 1-phosphatidylinositol-3-kinase activity; protein complex binding; DNA-dependent protein kinase activity; protein N-terminus binding; histone serine kinase activity; ATP binding

Biological Process: lipoprotein catabolic process; somitogenesis; V(D)J recombination; DNA damage induced protein phosphorylation; positive regulation of apoptosis; heart development; protein amino acid autophosphorylation; pre-B cell allelic exclusion; negative regulation of B cell proliferation; DNA repair; signal transduction; DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest; protein amino acid phosphorylation; double-strand break repair via homologous recombination; peptidyl-serine phosphorylation; neuron apoptosis; DNA damage response, signal transduction resulting in induction of apoptosis; positive regulation of neuron apoptosis; double-strand break repair; meiotic recombination; mitotic cell cycle spindle assembly checkpoint; response to hypoxia; positive regulation of DNA damage response, signal transduction by p53 class mediator; brain development; response to ionizing radiation; cell cycle arrest; response to DNA damage stimulus; telomere maintenance; oocyte development

Disease: Breast Cancer; Ataxia-telangiectasia