Phospho-ATM (S1981) Antibody (YA223)
(Synonyms: Serine-protein kinase ATM, Ataxia telangiectasia mutated, A-T mutated, ATM)
Based on 1 Customer Validation
Phospho-ATM (S1981) Antibody (YA223) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Phospho-ATM (S1981).
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, ICC/IF, IHC-P, IP
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Reactivity :
Human
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Formulation:
Supplied in 1*TBS (pH7.4), 0.05% BSA and 40% Glycerol. Preservative: 0.05% Sodium Azide.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
IHC-P
IHC-P: Immunohistochemistry-Paraffin
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IP
IP: Immunoprecipitation
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|---|---|---|---|---|
| Dilution Ratio | 1:500-1:1000 | 1:50-1:200 | 1:50-1:100 | Use at an assay dependent concentration. |
Product Details
Phospho-ATM (S1981) Antibody (YA223) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Phospho-ATM (S1981).
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Host Rabbit
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Clonality Recombinant,Monoclonal
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Species ReactivityHuman
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Observed Molecular WeightObserved band size: 370 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 351 kDa
Synthetic phosphopeptide corresponding to residues surrounding Ser1981 of Human ATM.AA range:1940-1989.
Endogenous
Protein A affinity purified.
Non-conjugated
Phosphorylated
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in 1*TBS (pH7.4), 0.05% BSA and 40% Glycerol. Preservative: 0.05% Sodium Azide.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
ATM is a serine/threonine protein kinase and a crucial nexus for the cellular response to DNA double-stranded breaks[1]. Mechanistically, ATM signals to cell-cycle and DNA-repair components by phosphorylating downstream targets including p53, CHK2, NBS1, and BRCA1[2]. Transcription- and topoisomerase I-induced DNA double-strand breaks also activate ATM in post-mitotic neurons and lymphocytes, linking ATM signaling to transcription-associated genome stress[3]. In disease context, ATM mutations cause ataxia-telangiectasia, which includes neurodegeneration, immune dysfunction, radiosensitivity, and cancer predisposition[1]. Compared with related PIKK isoforms, ATM, ATR, and DNA-PK jointly control the DNA damage response, but ATR and DNA-PK can compensate for ATM absence in ataxia-telangiectasia[4]. DNA-PK differs functionally because DNA-PKcs and Ku are essential for double-strand break repair through non-homologous end joining[5]. For experimental applications, loss or inhibition of ATM activity increases sensitivity to ionizing radiation and chemotherapeutic agents that elicit DNA double-strand breaks[2]. KU55933 sensitized cells to the topoisomerase IIα inhibitor NK314, supporting ATM inhibition as a tool for studying DNA repair-dependent drug response[6].
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Subcellular Localization
Nucleus; Cytoplasmic vesicle; Cytoplasm, cytoskeleton, microtubule organizing center, centrosome; Peroxisome matrix
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Expression
Tissue_specificity:It is found in the pancreas, kidneys, skeletal muscle, liver, lungs, placenta, brain, heart, spleen, thymus, testes, ovaries, small intestine, colon, and white blood cells.
Induction:By ionizing radiation -
Subunit
Homodimer (PubMed:12556884, PubMed:15790808, PubMed:28508083). Dimers or tetramers in inactive state (PubMed:12556884, PubMed:15790808, PubMed:28508083).
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SwissProt ID
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Synonyms
Serine-protein kinase ATM, Ataxia telangiectasia mutated, A-T mutated, ATM
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Research Field
Epigenetics and Nuclear Signaling
Documentation
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Data Sheet (263 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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User Guide for Antibodies (1077 KB)
[1]. McKinnon PJ. ATM and ataxia telangiectasia. EMBO Rep. 2004 Aug;5(8):772-6. doi: 10.1038/sj.embor.7400210. PMID: 15289825; PMCID: PMC1299121. et al. ATM and ataxia telangiectasia. EMBO Rep. 2004 Aug;5(8):772-6. [Content Brief]
[3]. Sordet O, et al. Ataxia telangiectasia mutated activation by transcription- and topoisomerase I-induced DNA double-strand breaks. EMBO Rep. 2009 Aug;10(8):887-93. [Content Brief]
[4]. Schlam-Babayov S, et al. It takes three to the DNA damage response tango. Mol Cell Oncol. 2021 Feb 8;8(2):1881395. [Content Brief]
[5]. Matsumoto Y, et al. DNA-Dependent Protein Kinase Catalytic Subunit: The Sensor for DNA Double-Strand Breaks Structurally and Functionally Related to Ataxia Telangiectasia Mutated. Genes (Basel). 2021 Jul 27;12(8):1143. [Content Brief]
[6]. Guo L, et al. DNA-dependent protein kinase and ataxia telangiectasia mutated (ATM) promote cell survival in response to NK314, a topoisomerase IIα inhibitor. Mol Pharmacol. 2011 Aug;80(2):321-7. [Content Brief]
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