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ATM [p Ser1981] Antibody (10H11.E12) [DyLight 405]

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Product Details

Summary
Reactivity Hu, Mu, Rt, Ca(-)Species Glossary
Applications WB, ICC/IF, IHC, IP
Clone
10H11.E12
Clonality
Monoclonal
Host
Mouse
Conjugate
DyLight 405

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ATM [p Ser1981] Antibody (10H11.E12) [DyLight 405] Summary

Immunogen
ATM [p Ser1981] Antibody (10H11.E12) [DyLight 405] was made to a synthetic peptide made to a region surrounding the phosphorylated Serine 1981 of human ATM. [UniProt# Q13315]
Modification
p Ser1981
Localization
Nucleus, cytoplasm.
Isotype
IgG1 Kappa
Clonality
Monoclonal
Host
Mouse
Gene
ATM
Purity
Protein G purified
Innovator's Reward
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Applications/Dilutions

Dilutions
  • Immunocytochemistry/ Immunofluorescence
  • Immunohistochemistry
  • Immunohistochemistry-Paraffin
  • Immunoprecipitation
  • Western Blot
Application Notes
Optimal dilution of this antibody should be experimentally determined.
Theoretical MW
351 kDa.
Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.

Packaging, Storage & Formulations

Storage
Store at 4C in the dark.
Buffer
50mM Sodium Borate
Preservative
0.05% Sodium Azide
Purity
Protein G purified

Notes



DyLight (R) is a trademark of Thermo Fisher Scientific Inc. and its subsidiaries.

Alternate Names for ATM [p Ser1981] Antibody (10H11.E12) [DyLight 405]

  • AT mutated
  • A-T mutated
  • AT1
  • ATA
  • ataxia telangiectasia mutated (includes complementation groups A, C and D)
  • ataxia telangiectasia mutated
  • ATC
  • ATD
  • ATDC
  • ATE
  • ATM serine/threonine kinase
  • ATM
  • DKFZp781A0353
  • EC 2.7.11.1
  • MGC74674
  • serine-protein kinase ATM
  • TEL1
  • TEL1, telomere maintenance 1, homolog
  • TELO1
  • TPLL

Background

ATM (ataxia telangiectasia mutated kinase) is the master regulator of the DNA double-strand break (DSB) repair pathway. This ubiquitously expressed serine/threonine protein kinase belongs to the PI3K-like family of proteins and responds to DSBs caused by oxidative and other genotoxic stresses (1). In addition to regulating the DNA damage response, ATM participates in vesicle and protein transport, T-cell development, gonads/neurological function, pre-B cell allelic exclusion, cell cycle control, and acts as a tumor suppressor (2,3). Defects in ATM are associated with ataxia telangiectasia (AT), T-cell acute lymphoblastic leukemia (TALL), T-prolymphocytic leukemia (TPLL), and B-cell non-Hodgkin lymphomas (BNHL) including mantle cell lymphoma (MCL) and B-cell chronic lymphocytic leukemia (BCLL) (4).

The theoretical molecular weight of ATM is 350 kDa and it has 3 main domains: a FAT (focal adhesion targeting) domain (aa 1960-2566), a PI-3/PI-4 kinase catalytic domain (aa 2712-2962), and a C-terminal FAT domain (aa 3024-3056). ATM exists as a dimer or tetramer in its inactive state. Upon sensing DNA damage, the MRE11-RAD50-NBS1 (MRN) complex recruits ATM. The intricate process of ATM activation involves acetylation by KAT5/TIP60, autophosphorylation at Ser-1981, and dissociation into catalytically active monomers (5). Following activation, ATM phosphorylates multiple substrates such as p53/TP53 and Chk2 involved in DNA repair, checkpoint signaling, and the apoptosis pathway.

References

1. Paull TT. (2015) Mechanisms of ATM Activation. Annu Rev Biochem. 84:711-38. PMID: 25580527

2. Chaudhary MW and Al-Baradie RS. (2014) Ataxia-telangiectasia: future prospects. Appl Clin Genet. 7:159-167. PMID: 25258552

3. Stagni V, Cirotti C, and Barila D. (2018) Ataxia-Telangiectasia Mutated Kinase in the Control of Oxidative Stress, Mitochondria, and Autophagy in Cancer: A Maestro With a Large Orchestra. Front Oncol. 8:73. PMID: 29616191

4. Gumy-Pause F, Wacker P, and Sappino AP. (2004) ATM gene and lymphoid malignancies. Leukemia. 18(2):238-42. PMID: 14628072

5. Adamowicz M. (2018) Breaking up with ATM. J Immunol Sci. 2(1):26-31. PMID: 29652413

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

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Product General Protocols

Find general support by application which include: protocols, troubleshooting, illustrated assays, videos and webinars.

Video Protocols

WB Video Protocol
ICC/IF Video Protocol

FAQs for ATM Antibody (NB100-306V). (Showing 1 - 1 of 1 FAQ).

  1. What is the theoretical molecular weight for your ATM antibodies?
    • The theoretical molecular weight for our ATM antibodies is 351 kDa.

Secondary Antibodies

 

Isotype Controls

Additional ATM Products

Research Areas for ATM Antibody (NB100-306V)

Find related products by research area.

Blogs on ATM.

Further unraveling the role of gamma H2AX in DNA damage response
Our genome experiences a moderate amount of DNA damage in our cells on a daily basis.  This DNA damage can be in response to external environmental factors, or be a result of our internal metabolic processes going awry.  While normal rates of DNA ...  Read full blog post.

The recent relationship of BRCA1 and 53BP1
The p53-binding protein 1 (53BP1) is a DNA damage response factor, which is recruited to nuclear structures at the site of DNA damage.  DNA double-strand breaks (DSBs) are mutations that are detrimental to cell viability and genome stability, and m...  Read full blog post.

Application Highlight: Recent uses of TERF2 in immunofluorescence (IF)
Telomeres are a region of repeat nucleotide sequences located at the end of chromosomes to protect our DNA from becoming damaged via end-to-end fusion.  TERF2, or telomeric-repeat binding factor 2, is important for telomere integrity and aids in th...  Read full blog post.

ATM - detecting and responding to DNA damage
Ataxia telangiectasia mutated (ATM) is essential for the maintenance of genomic stability. ATM is a 370 kDa serine-threonine kinase that is constitutively expressed in various tissues. Although primarily nuclear, ATM is also found at lower levels ...  Read full blog post.

53BP1 - a marker for DNA Double Strand Break
53BP1 (p53 binding protein 1) was originally thought to be an enhancer for p53 transcriptional, but later studies have demonstrated that it is actually a substrate for ataxia telangiectasia mutated (ATM). 53BP1 is a classic late DNA damage response...  Read full blog post.

53BP1 - DNA damage is no fun
The 53BP1 (p53 binding protein 1) was initially believed to be a p53 transcriptional enhancing partner, but it has now been established as an ataxia telangiectasia mutated (ATM) substrate. As a late DNA damage response (DDR) marker, 53BP1 appears duri...  Read full blog post.

ATM and DSB Repair in Cancer
Ataxia Telangiectasia Mutated (ATM) is a serine/threonine protein kinase that is the master regulator of the DNA double-strand break (DSB) repair pathway. ATM is a key part of the cell cycle machinery that activates checkpoint signaling in response to...  Read full blog post.

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Bioinformatics

Gene Symbol ATM