Phospho-ATM (Ser1981) Antibody [A4J11]

Application: Reactivity: Human

Lane 1: 293 (UV, 4 h), Lane 2: 293

Usage Information

Dilution
WB1:1000

Application
WB

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
350 kDa

Datasheet & SDS

Biological Description

Specificity
Phospho-ATM (Ser1981) Antibody [A4J11] detects endogenous levels of total ATM protein only when it is phosphorylated at Ser1981.

Clone
A4J11

Synonym(s)
Serine-protein kinase ATM; Ataxia telangiectasia mutated (A-T mutated); ATM

Background
Phospho ATM at Ser1981 (ATM S1981ph) is the canonical activation mark of the ataxia telangiectasia mutated (ATM) kinase, a central phosphoinositide 3 kinase related kinase that orchestrates the cellular response to DNA double strand breaks in the PIKK signaling network. In the absence of damage, inactive ATM is predominantly dimeric and held in a closed conformation, but when double strand breaks occur the MRE11–RAD50–NBS1 (MRN) sensor complex recruits ATM to the lesion and promotes acetylation dependent dissociation of the dimer, enabling autophosphorylation at Ser1981 in trans, which stabilizes the active monomeric form and reinforces its retention at the break site through interaction with mediators such as MDC1. Once phosphorylated at Ser1981, ATM propagates a robust signaling cascade by phosphorylating numerous downstream effectors, including histone H2AX at Ser139, CHK2, p53, BRCA1, and DNA repair checkpoint associated proteins, thereby coupling DSB detection to cell cycle arrest, DNA repair, and, when damage is severe, senescence or apoptosis. These ATM S1981ph dependent signals integrate with parallel ATR and DNA PKcs pathways to coordinate G2/M checkpoint enforcement, homologous recombination, non homologous end joining, and transcriptional responses across multiple cell types, making phospho ATM Ser1981 a widely used readout for genotoxic stress and DNA damage signaling in experimental systems. In ataxia telangiectasia, loss of ATM function abolishes Ser1981 phosphorylation and disrupts DSB induced checkpoint activation, leading to extreme radiosensitivity, neurodegeneration, and increased cancer risk, so that ATM S1981ph dependent signaling is ultimately dysregulated in both hereditary DNA repair deficiency and various cancer prone contexts.

Background

Phospho ATM at Ser1981 (ATM S1981ph) is the canonical activation mark of the ataxia telangiectasia mutated (ATM) kinase, a central phosphoinositide 3 kinase related kinase that orchestrates the cellular response to DNA double strand breaks in the PIKK signaling network. In the absence of damage, inactive ATM is predominantly dimeric and held in a closed conformation, but when double strand breaks occur the MRE11–RAD50–NBS1 (MRN) sensor complex recruits ATM to the lesion and promotes acetylation dependent dissociation of the dimer, enabling autophosphorylation at Ser1981 in trans, which stabilizes the active monomeric form and reinforces its retention at the break site through interaction with mediators such as MDC1. Once phosphorylated at Ser1981, ATM propagates a robust signaling cascade by phosphorylating numerous downstream effectors, including histone H2AX at Ser139, CHK2, p53, BRCA1, and DNA repair checkpoint associated proteins, thereby coupling DSB detection to cell cycle arrest, DNA repair, and, when damage is severe, senescence or apoptosis. These ATM S1981ph dependent signals integrate with parallel ATR and DNA PKcs pathways to coordinate G2/M checkpoint enforcement, homologous recombination, non homologous end joining, and transcriptional responses across multiple cell types, making phospho ATM Ser1981 a widely used readout for genotoxic stress and DNA damage signaling in experimental systems. In ataxia telangiectasia, loss of ATM function abolishes Ser1981 phosphorylation and disrupts DSB induced checkpoint activation, leading to extreme radiosensitivity, neurodegeneration, and increased cancer risk, so that ATM S1981ph dependent signaling is ultimately dysregulated in both hereditary DNA repair deficiency and various cancer prone contexts.

References
https://pubmed.ncbi.nlm.nih.gov/20026654/ https://pubmed.ncbi.nlm.nih.gov/17622968/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%