catalog number :
MBS2508011
products type :
ELISA Kit
products full name :
Rat ATM (Ataxia Telangiectasia Mutated) ELISA Kit
products short name :
[ATM]
other names :
[ATM; Serine-protein kinase ATM; serine-protein kinase ATM; A-T mutated; AT mutated; TEL1, telomere maintenance 1, homolog; ataxia telangiectasia mutated; ATM serine/threonine kinase; Ataxia telangiectasia mutated; A-T mutated]
products gene name :
[ATM]
other gene names :
[ATM; ATM; AT1; ATA; ATC; ATD; ATE; ATDC; TEL1; TELO1; A-T mutated]
uniprot entry name :
ATM_HUMAN
specificity :
This kit recognizes natural and recombinant Rat ATM. No significant cross-reactivity or interference between Rat ATM and analogues was observed.
storage stability :
Store at 4 degree C.
image1 heading :
Typical Testing Data/Standard Curve (for reference only)
other info1 :
Samples: Serum, Plasma, Biological Fluids. Assay Type: Sandwich. Detection Range: 0.156-10ng/mL. Sensitivity: Min: 0.094ng/mL; Max: 10ng/mL
products description :
Intended Uses: This ELISA kit applies to the in vitro quantitative determination of Rat ATM concentrations in serum, plasma and other biological fluids. Principle of the Assay: This ELISA kit uses Sandwich-ELISA as the method. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to ATM. Standards or samples are added to the appropriate micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for ATM and Avidin-Horseradish Peroxidase (HRP) conjugate is added to each micro plate well successively and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain ATM, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of a sulphuric acid solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm +/- 2 nm. The OD value is proportional to the concentration of ATM. You can calculate the concentration of ATM in the samples by comparing the OD of the samples to the standard curve.
ncbi acc num :
AAB65827.1
ncbi mol weight :
350,687 Da
ncbi pathways :
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)
ncbi summary :
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 summary :
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; EC 2.7.11.1; Kinase, protein; Tumor suppressor; Protein kinase, Ser/Thr (non-receptor); Protein kinase, atypical; 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; heart development; protein amino acid autophosphorylation; 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; 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; brain development; positive regulation of DNA damage response, signal transduction by p53 class mediator; response to ionizing radiation; response to DNA damage stimulus; oocyte development. Disease: Breast Cancer; Ataxia-telangiectasia
size5 :
10x96-Strip-Wells