Mouse Ataxia Telangiectasia Mutated (ATM) ELISA Kit | ATM elisa kit
Mouse Ataxia Telangiectasia Mutated (ATM) ELISA Kit
To minimize extra influence on the performance, operation procedures and lab conditions, especially room temperature, air humidity, incubator temperature should be strictly controlled. It is also strongly suggested that the whole assay is performed by the same operator from the beginning to the end.
Principle of the Assay: The microplate provided in this kit has been pre-coated with an antibody specific to ATM. Standards or samples are then added to the appropriate microplate wells with a biotin-conjugated antibody specific to ATM. Next, Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. After TMB substrate solution is added, only those wells that contain ATM, biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450nm +/- 10nm. The concentration of ATM in the samples is then determined by comparing the O.D. of the samples to the standard curve.
NCBI and Uniprot Product Information
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, Aug 2010]
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: EC 2.7.11.1; Protein kinase, Ser/Thr (non-receptor); Kinase, protein; Protein kinase, atypical; Tumor suppressor; 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; 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; 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; 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: Breast Cancer; Ataxia-telangiectasia
Research Articles on ATM
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Product Notes
The Mouse ATM atm (Catalog #AAA2019504) is an ELISA Kit and is intended for research purposes only. The product is available for immediate purchase. The AAA2019504 ELISA Kit recognizes Mouse ATM. It is sometimes possible for the material contained within the vial of "Ataxia Telangiectasia Mutated (ATM), ELISA Kit" to become dispersed throughout the inside of the vial, particularly around the seal of said vial, during shipment and storage. We always suggest centrifuging these vials to consolidate all of the liquid away from the lid and to the bottom of the vial prior to opening. Please be advised that certain products may require dry ice for shipping and that, if this is the case, an additional dry ice fee may also be required.Precautions
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