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You are here:Home » Antibodies » Abs to Protein Kinases » Anti -ATM (Ataxia Telangiectasia Mutated, ATA, AT Complementation Group A, ATC, ATD, ATE)

Anti -ATM (Ataxia Telangiectasia Mutated, ATA, AT Complementation Group A, ATC, ATD, ATE)

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Specifications

Clone Host Grade Applications
Polyclonal Rabbit Serum B
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.
Catalog #A4000-25C
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.
ApplicationsWestern Blotting: 1:500-1:1000
Optimal working dilutions to be determined by researcher.
Clone TypePolyclonal
IsotypeIgG
HostRabbit
SourceHuman
ConcentrationNot determined
FormSupplied as a liquid with 0.1% sodium azide.
PuritySerum
ImmunogenRecombinant human ATM fragment (amino acids 1391-1693).
SpecificityRecognizes the human ATM protein, a 350kD polypeptide that is the product of the ATM gene. Species Crossreactivity: Rodent, primate
Important NoteThis product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications without the expressed written authorization of United States Biological.


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