05-740
Anti-phospho-ATM (Ser1981) Antibody, clone 10H11.E12
clone 10H11.E12, Upstate®, from mouse
Synonym(s):
A-T, mutated, AT mutated, TEL1, telomere maintenance 1, homolog, ataxia telangiectasia mutated, ataxia telangiectasia mutated (includes complementation groups A, C and D), ataxia telangiectasia mutated protein, human phosphatidylinositol 3-kinase homolog
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
antibody form
purified antibody
antibody product type
primary antibodies
clone
10H11.E12, monoclonal
species reactivity
mouse, human
packaging
antibody small pack of 25 μg
manufacturer/tradename
Upstate®
technique(s)
immunocytochemistry: suitable
immunofluorescence: suitable
immunoprecipitation (IP): suitable
western blot: suitable
isotype
IgG1κ
NCBI accession no.
UniProt accession no.
shipped in
ambient
target post-translational modification
phosphorylation (pSer1981)
Gene Information
human ... ATM(472)
General description
Ataxia telangiectasia mutated kinase (ATM) and ataxia telangiectasia and Rad3-related kinase (ATR) are related kinases that regulate cell cycle checkpoints and DNA repair. Mutation in the ATM gene results in the autosomal recessive disease ataxia telangiectasia (AT). The identified substrates for ATM are p53, p95/NBS1, MDM2, Chk2, BRCA1, CtIP, 4E-BP1 and Chk1. The essential requirement for the substrates of ATM/ATR is S/TQ. Hydrophobic amino acids at positions -3 and -1, and negatively charged amino acids at position +1 are positive determinants for substrate recognition by these kinases. Positively charged residues surrounding the S/TQ are negative determinants for substrate phosphorylation. The complex phenotype of cells derived from patients with AT suggests that ATM has additional cellular substrates. In unirradiated cells, ATM is present as an inactive homodimer or multimer. Double-stranded breaks in DNA caused by ionizing radiation cause rapid ATM kinase activation through dissociation of this complex and ATM autophosphorylation at Ser1981.
Specificity
Predicted to cross-react with rat based on sequence homology
This antibody recognizes ATM, Mr ~370 kDa. A non-specific protein was also detected, Mr ~ >400 kDa.
Immunogen
KLH-conjugated, synthetic peptide corresponding to amino acids 1974-1988 (SLAFEEG[pS]QSTTISS) of human ATM. The immunizing sequence has 11/12 identical amino acids in mouse and rat.
Application
Immunoprecipitation:
Phosphorylated ATM was immunoprecipitated from irradiated HeLa cells (Figure A, lanes 3 and 4).
Immunocytochemistry:
Foci are detected in irradiated human and mouse fibroblasts. Determined by an independent laboratory.
Phosphorylated ATM was immunoprecipitated from irradiated HeLa cells (Figure A, lanes 3 and 4).
Immunocytochemistry:
Foci are detected in irradiated human and mouse fibroblasts. Determined by an independent laboratory.
Research Category
Epigenetics & Nuclear Function
Epigenetics & Nuclear Function
Research Sub Category
Cell Cycle, DNA Replication & Repair
Cell Cycle, DNA Replication & Repair
Use Anti-phospho-ATM (Ser1981) Antibody, clone 10H11.E12 (Mouse Monoclonal Antibody) validated in ICC, IF, IP, WB to detect phospho-ATM (Ser1981) also known as A-T mutated.
Quality
Routinely evaluated by immunoblot on in crude lysates from irradiated HeLa cells.
Western Blot Analysis:
0.5 µg/mL of this lot detected phosphorylated ATM in crude lysates from irradiated HeLa cells.
Western Blot Analysis:
0.5 µg/mL of this lot detected phosphorylated ATM in crude lysates from irradiated HeLa cells.
Target description
~370 kDa
Physical form
Format: Purified
Protein G Purified
Protein G purified mouse IgG in 0.014 M phosphate buffer, pH 7.6, with 0.175 M NaCl, 0.07 % Sodium Azide and 30% glycerol. Liquid at -20°C.
Storage and Stability
Stable for 1 year at -20°C from date of receipt.
Handling Recommendations:
Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance. Note: Variability in freezer temperatures below -20°C may cause glycerol containing solutions to become frozen during storage.
Handling Recommendations:
Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance. Note: Variability in freezer temperatures below -20°C may cause glycerol containing solutions to become frozen during storage.
Analysis Note
Control
Irradiated HeLa cell lysates
Irradiated HeLa cell lysates
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
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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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Find documentation for the products that you have recently purchased in the Document Library.
DNA repair: Damage alert.
Bartek, Jiri and Lukas, Jiri
Nature, 421, 486-488 (2003)
DNA damage response induced by tobacco smoke in normal human bronchial epithelial and A549 pulmonary adenocarcinoma cells assessed by laser scanning cytometry.
Zhao, Hong, et al.
Cytometry. Part A : the Journal of the International Society For Analytical Cytology, 75, 840-847 (2009)
Fluoroquinolones lower constitutive H2AX and ATM phosphorylation in TK6 lymphoblastoid cells via modulation of the intracellular redox status.
Halicka, H Dorota, et al.
Pharmacological Reports, 61, 711-718 null
Gina Chun et al.
Carcinogenesis, 31(5), 785-793 (2010-01-22)
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Fernanda I Staquicini et al.
The Journal of biological chemistry, 290(12), 7345-7359 (2015-01-28)
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