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All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

Phospho-ATM (Ser1981) (D25E5) Rabbit Antibody

INQUIRY

CAT. NO.: AMA-0303

Target Information
UniProt ID	Q13315

Product Details
Size	100 µL
Reactivity	Human
Host	Rabbit
Source/Isotype	Rabbit IgG
Storage	Store at -20°C. Do not aliquot the antibody.
Purification	Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser1981 of human ATM protein.

Usage
Application	WB
Product Usage Information Dilution	Western Blotting (1:1000)
MW (Target)	350 kDa

Background
ATM (ataxia telangiectasia mutated kinase) is a serine/threonine protein kinase best known for its role in DNA repair signaling in response to DNA double-strand breaks (DSBs). When DSBs occur, the MRE11:RAD50:NBS1 (MRN) sensor complex recruits ATM to sites of DNA damage. ATM then signals to numerous effector proteins, leading to cellular responses including regulation of DNA repair, cell cycle progression, apoptosis, senescence, gene transcription. Along with ATR, DNA-PKcs, SMG1 and mTOR, ATM is a member of the PI3K-like protein kinase (PIKK) family. PIKK family members typically function in response to various types of cellular stress. Substrates of ATM are numerous, and include CHK2, AKT, p53, BRCA1 and DNA-PK. Inactive ATM exists as a homodimer. In response to DSBs, ATM undergoes autophosphorylation in trans at Ser1981, which leads to dissociation of the complex to become an active monomer. Functional DNA repair pathways are important in cellular homeostasis, and defects in these pathways cause genomic instability, which can lead to tumorigenesis. Inactivation of ATM results in ataxia telangiectasia (AT), a neurodegenerative disease characterized by predisposition to cancer.

Background

ATM (ataxia telangiectasia mutated kinase) is a serine/threonine protein kinase best known for its role in DNA repair signaling in response to DNA double-strand breaks (DSBs). When DSBs occur, the MRE11:RAD50:NBS1 (MRN) sensor complex recruits ATM to sites of DNA damage. ATM then signals to numerous effector proteins, leading to cellular responses including regulation of DNA repair, cell cycle progression, apoptosis, senescence, gene transcription. Along with ATR, DNA-PKcs, SMG1 and mTOR, ATM is a member of the PI3K-like protein kinase (PIKK) family. PIKK family members typically function in response to various types of cellular stress. Substrates of ATM are numerous, and include CHK2, AKT, p53, BRCA1 and DNA-PK. Inactive ATM exists as a homodimer. In response to DSBs, ATM undergoes autophosphorylation in trans at Ser1981, which leads to dissociation of the complex to become an active monomer. Functional DNA repair pathways are important in cellular homeostasis, and defects in these pathways cause genomic instability, which can lead to tumorigenesis. Inactivation of ATM results in ataxia telangiectasia (AT), a neurodegenerative disease characterized by predisposition to cancer.

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All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.