Phospho-ATM (Ser1981) Antibody (YA7490)
(Synonyms: Serine-protein kinase ATM, Ataxia telangiectasia mutated, A-T mutated, ATM)
Based on 1 Customer Validation
Phospho-ATM (Ser1981) Antibody (YA7490) is a Rabbit-derived and non-conjugated IgG, Kappa monoclonal antibody, targeting to Phospho-ATM (Ser1981).
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-P, ICC/IF, IP, ELISA, CHIP, Cut&Tag
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in PBS (pH7.4) containing 50% glycerol, 0.05% Proclin 300, 0.05%BSA
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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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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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IP
IP: Immunoprecipitation
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CHIP
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Cut&Tag
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| Dilution Ratio | 1:10000-1:50000 | 1:200-1:1000 | 1:200-1:1000 | 1:5000-1:20000 | 1:50-1:200 | 1:50-1:100 | 1:50-1:100 |
Product Details
Phospho-ATM (Ser1981) Antibody (YA7490) is a Rabbit-derived and non-conjugated IgG, Kappa monoclonal antibody, targeting to Phospho-ATM (Ser1981).
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Host Rabbit
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Clonality Monoclonal,Recombinant
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 351 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
The exact sequence is proprietary to MCE.
Endogenous
Protein A affinity purified
Non-conjugated
Phosphorylated
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS (pH7.4) containing 50% glycerol, 0.05% Proclin 300, 0.05%BSA
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Shipping
Shipping with blue ice.
Verification Images
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HeLa cells were cultured in 6 cm dishes to approximately 70% confluence and then treated with Etoposide (HY-13629) at concentration of 30 μM for 2 h and 4 h, respectively. Phospho-ATM (Ser1981) protein expression was subsequently analyzed by Western blot. The results demonstrated that Etoposide induced DNA damage in HeLa cells, indicated by phosphorylation of ATM (Ser1981). Primary antibodies used: Phospho-ATM (Ser1981) Antibody (HY-P87805) and GAPDH Antibody (HY-P80954A). -
Western blot analysis was performed on protein extracts (25 μg) from HeLa (lane 2), HeLa (lane 3, Etoposide (HY-13629), 30 μM, 2 hours), and HeLa (lane 4, Etoposide (HY-13629), 30 μM, 4 hours) using Phospho-ATM (Ser1981) antibody. Proteins were transferred onto a 0.45 μm PVDF membrane using the Trans-Blot® Turbo™ system for 13 min. The membrane was then blocked with 5% BSA in TBST (HY-K1025) for 1 h at room temperature. The primary antibody (1:10000) and loading control antibody GAPDH Antibody (HRP) (HY-P80954A) (1:5000) were diluted in 5% BSA in TBST and incubated with the membrane overnight at 4°C. After washing, the membrane of primary antibody was incubated with HRP-conjugated goat anti-rabbit/mouse IgG secondary antibody (HY-P8001/HY-P8004) (1:5000) diluted in 5% nonfat milk in TBST for 1 h at room temperature. Protein bands were visualized using an Ultra High Sensitivity ECL detection kit (HY-K1005). -
Immunocytochemistry analysis of Hela cells labeling Phospho-ATM (Ser1981) With Phospho-ATM (Ser1981) antibody (HY-P87805) at 1/300 dilution. Cells were fixed in 4% paraformaldehyde for 15 minutes at room temperature, permeabilized with 0.1% Triton X-100 in PBS for 15 minutes at room temperature, then blocked with quick block buffer for 10 minutes at room temperature. Cells were then incubated with Phospho-ATM (Ser1981) antibody (HY-P87805) at 1/300 dilution in quick block buffer overnight at 4 ℃. AF488-conjugated Goat Anti-Rabbit IgG H&L(HY-P8002, Green) was used as the secondary antibody at 1/1,000 dilution. PBS instead of the primary antibody was used as the secondary antibody only control. The Nuclear counterstain was DAPI (Blue). -
Immunocytochemistry analysis of Hela cells labeling Phospho-ATM (Ser1981) With Phospho-ATM (Ser1981) antibody (HY-P87805) at 1/500 dilution. Cells were fixed in 4% paraformaldehyde for 15 minutes at room temperature, permeabilized with 0.1% Triton X-100 in PBS for 15 minutes at room temperature, then blocked with quick block buffer for 10 minutes at room temperature. Cells were then incubated with Phospho-ATM (Ser1981) antibody (HY-P87805) at 1/500 dilution in quick block buffer overnight at 4 ℃. AF488-conjugated Goat Anti-Rabbit IgG H&L(HY-P8002, Green) was used as the secondary antibody at 1/1,000 dilution. PBS instead of the primary antibody was used as the secondary antibody only control. The Nuclear counterstain was DAPI (Blue).
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: Found in pancreas, kidney, skeletal muscle, liver, lung, placenta, brain, heart, spleen, thymus, testis, ovary, small intestine, colon and leukocytes
Induction: By ionizing radiation -
Isoforms & Post-Translational Modification
Q13315: 3056 amino acids, molecular weight 350687 Da.
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Subunit
Homodimer (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
Documentation
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Data Sheet (260 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)
References
[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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