ELISA/assay

Human Ataxia Telangiectasia Mutated ELISA Kit

MBS721915

48-Strip-Wells

470 USD

ELISA Kit

Human Ataxia Telangiectasia Mutated ELISA Kit

Ataxia Telangiectasia Mutated

ATM; Serine-protein kinase ATM; serine-protein kinase ATM; AT mutated; A-T mutated; ataxia telangiectasia mutated; TEL1, telomere maintenance 1, homolog; ATM serine/threonine kinase; Ataxia telangiectasia mutated; A-T mutated

ATM

ATM; ATM; AT1; ATA; ATC; ATD; ATE; ATDC; TEL1; TELO1; A-T mutated

ATM_HUMAN

Human

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 0.1 ng/mL.

Highest Standards: 10ng/mL. Concentration of Standards: Concentration of Standards: 0,0.5,1.0,2.5,5.0,10ng/mL

For samples: Serum, plasma, cell culture supernatants, body fluid and tissue homogenate. INTENDED USE This ATM ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human ATM. This ELISA kit for research use only, not for therapeutic or diagnostic applications! . PRINCIPLE OF THE ASSAY ATM ELISA kit applies the quantitative sandwich enzyme immunoassay technique. The microtiter plate has been pre-coated with a monoclonal antibody specific for ATM. Standards or samples are then added to the microtiter plate wells and ATM if present, will bind to the antibody pre-coated wells. In order to quantitatively determine the amount of ATM present in the sample, a standardized preparation of horseradish peroxidase (HRP)-conjugated polyclonal antibody, specific for ATM are added to each well to “sandwich” the ATM immobilized on the plate. The microtiter plate undergoes incubation, and then the wells are thoroughly washed to remove all unbound components. Next, substrate solutions are added to each well. The enzyme (HRP) and substrate are allowed to react over a short incubation period. Only those wells that contain ATM and enzyme-conjugated antibody will exhibit a change in color. The enzyme-substrate reaction is terminated by addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The ATM concentration in each sample is interpolated from this standard curve.

2304971

AAB65827.1

350,687 Da

ATM Mediated Phosphorylation Of Repair Proteins Pathway (105865); ATM Mediated Response To DNA Double-strand Break Pathway (105864); Apoptosis Pathway (83060); Apoptosis Pathway (470); Autodegradation Of The E3 Ubiquitin Ligase COP1 Pathway (160939); BARD1 Signaling Events Pathway (137959); BRCA1-associated Genome Surveillance Complex (BASC) Pathway (413428); BRCA1-associated Genome Surveillance Complex (BASC) Pathway (890555); Canonical NF-kappaB Pathway (138030); Cell Cycle Pathway (530733)

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, Aug 2010]

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: DNA repair, damage; Protein kinase, atypical; Tumor suppressor; EC 2.7.11.1; Protein kinase, Ser/Thr (non-receptor); Kinase, protein; 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; DNA damage induced protein phosphorylation; positive regulation of apoptosis; protein amino acid autophosphorylation; heart development; pre-B cell allelic exclusion; negative regulation of B cell proliferation; signal transduction; DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest; protein amino acid phosphorylation; double-strand break repair; positive regulation of neuron apoptosis; mitotic cell cycle spindle assembly checkpoint; cell cycle arrest; telomere maintenance; somitogenesis; V(D)J recombination; DNA repair; double-strand break repair via homologous recombination; peptidyl-serine phosphorylation; neuron apoptosis; DNA damage response, signal transduction resulting in induction of apoptosis; meiotic recombination; response to hypoxia; response to ionizing radiation; brain development; positive regulation of DNA damage response, signal transduction by p53 class mediator; response to DNA damage stimulus; oocyte development. Disease: Ataxia-telangiectasia; Breast Cancer

48-Strip-Wells

470 USD

96-Strip-Wells

675