ELISA/assay

Porcine Ataxia Telangiectasia Mutated ELISA Kit

MBS037213

48-Strip-Wells

435 USD

ELISA Kit

Porcine Ataxia Telangiectasia Mutated ELISA Kit

Ataxia Telangiectasia Mutated

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

ATM

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

ATM_HUMAN

Porcine

No significant cross-reactivity or interference between Porcine ATM and analogues was observed.

Store all reagents at 2-8 degree C

Samples: Serum, Plasma, Tissue Homogenate, Feces and Urine. Assay Type: Sandwich. Detection Range: 31.2 pg/ml - 1000 pg/ml. Sensitivity: 5.0 pg/ml.

Intended Uses: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! It is intended to be determinated ATM concentrations in Porcine serum, plasma and other body fluids. Using Purified Porcine ATM antibody to coat Microelisa Stripplate wells to make solid-phase antibody, then add ATM and ATM antibody which has been labeled with HRP to wells, then the reactants become antibody-antigen-antibody-enzyme complex, after washing completely, add TMB substrate solution, TMB substrate becomes blue color under HRP enzyme-catalyzed, reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. The concentration of ATM in the samples is then determined by comparing the O.D. of the samples to the standard curve. Intra-assay Precision: Intra-assay CV (%) is less than 15%. Inter-assay Precision: Inter-assay CV (%) is less than 15%. [CV(%) = SD/mean ×100]

Background: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! It is intended to be determinated ATM concentrations in Porcine serum, plasma and other body fluids. Using Purified Porcine ATM antibody to coat Microelisa Stripplate wells to make solid-phase antibody, then add ATM and ATM antibody which has been labeled with HRP to wells, then the reactants become antibody-antigen-antibody-enzyme complex, after washing completely, add TMB substrate solution, TMB substrate becomes blue color under HRP enzyme-catalyzed, reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. The concentration of ATM in the samples is then determined by comparing the O.D. of the samples to the standard curve.

187951615

AAI37170.1

Q13315

350,714 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); Canonical NF-kappaB Pathway (138030); Cell Cycle Pathway (530733); Cell Cycle Checkpoints Pathway (105739)

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: EC 2.7.11.1; Protein kinase, Ser/Thr (non-receptor); DNA repair, damage; Protein kinase, atypical; Kinase, protein; Tumor suppressor; 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; protein N-terminus binding; DNA-dependent protein kinase activity; 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; protein amino acid phosphorylation; DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest; positive regulation of neuron apoptosis; double-strand break repair; 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; neuron apoptosis; peptidyl-serine phosphorylation; DNA damage response, signal transduction resulting in induction of apoptosis; meiotic recombination; response to hypoxia; brain development; response to ionizing radiation; 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

435 USD

96-Strip-Wells

600