Monoclonal Anti-ATM (mouse IgG1 isotype) is derived from the hybridoma MAT3-4G10/8 produced by the fusion of mouse myeloma cells (NSO) and splenocytes from BALB/c mice immunized with a peptide.
Specificity
Monoclonal Anti-ATM antibody reacts specifically with mouse and human ATM.
Immunogen
peptide spanning positions 1967-1988 of mouse ATM containing a cysteine at its NH2 terminus coupled to KLH.
Application
Monoclonal Anti-ATM antibody can be used in immunoblotting , ELISA and immunoprecipitation.
Biochem/physiol Actions
Anti-Ataxia-Telangiectasia Mutated (ATM) is responsible for the activation and stabilization of p53 in response to double-strand break (DSB). ATM phosphorylates p53 directly on Ser15 and concomitantly activates other kinases that phosphorylate the same molecule on additional sites. Furthermore, human homolog of double minute 2 (Hdm2) is phosphorylated by ATM on Ser395 and this phosphorylation inhibits Hdm2-mediated degradation of p53.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Journal of human genetics, 62(5), 581-584 (2017-01-27)
Ataxia-telangiectasia (A-T) is an autosomal recessive chromosome breakage disorder caused by mutations in the ATM gene. Typically, it presents in early childhood with progressive cerebellar dysfunction along with immunodeficiency and oculocutaneous telangiectasia. An increased risk of malignancy is also associated
Phosphorylation of Hdmx mediates its Hdm2- and ATM-dependent degradation in response to DNA damage
Pereg Y, et al.
Proceedings of the National Academy of Sciences of the USA, 102(14), 5056-5061 (2005)
High grade gliomas (HGG) are one of the leading causes of cancer-related deaths in children, and there is increasing evidence that pediatric HGG may harbor distinct molecular characteristics compared to adult tumors. We have sought to clarify the role of
ATM-dependent phosphorylation of Mdm2 on serine 395: role in p53 activation by DNA damage
The kinase ATR is activated by RPA-coated single-stranded DNA generated at aberrant replicative structures and resected double strand breaks. While many hundred candidate ATR substrates have been identified, the essential role of ATR in the replicative stress response has impeded
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