Detect ATM also known as Ataxia Telangiectasia Mutated with Anti-ATM Antibody, clone AM9 (Mouse Monoclonal Antibody), that has been demonstrated to work in WB.
Research Category Epigenetics & Nuclear Function
Research Sub Category Cell Cycle, DNA Replication & Repair
Quality
routinely evaluated by immunoblot on nuclear extract from Raji cells
Target description
350kDa
Linkage
Replaces: 04-200
Physical form
Ascites
mouse ascites containing 0.05% sodium azide
Storage and Stability
2 years at -20°C
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
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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.
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The ataxia telangiectasia mutated (ATM) protein kinase plays a central role in the cellular response to DNA damage. Loss or inactivation of both copies of the ATM gene (ATM) leads to ataxia telangiectasia, a devastating childhood condition characterized by neurodegeneration
Molecular and cellular biology, 19(7), 5096-5105 (1999-06-22)
A-T (ataxia telangiectasia) individuals frequently display gonadal atrophy, and Atm-/- mice show spermatogenic failure due to arrest at prophase of meiosis I. Chromosomal movements take place during meiotic prophase, with telomeres congregating on the nuclear envelope to transiently form a
Variants of unknown significance (VUS) remain a constant challenge in the diagnosis of hereditary cancer and the counseling of patients with pedigrees suggestive of such a syndrome. In order to assess some of this limitation, several variants in the DNA
Molecular and cellular biology, 19(4), 2828-2834 (1999-03-19)
Microinjection of the restriction endonuclease HaeIII, which causes DNA double-strand breaks with blunt ends, induces nuclear accumulation of p53 protein in normal and xeroderma pigmentosum (XP) primary fibroblasts. In contrast, this induction of p53 accumulation is not observed in ataxia
Characterization of mre11 loss following HSV-1 infection.
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