Invitrogen

ATM Recombinant Rabbit Monoclonal Antibody (SI70-01)

Advanced Verification

This Antibody was verified by Knockdown to ensure that the antibody binds to the antigen stated.

1 Reference
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Datasheet
Protocols
Questions & Answers

Product Details

MA5-32063

Applications
Tested Dilution
Publications

Western Blot (WB)

1:1,000
-

Immunohistochemistry (IHC)

-
View 1 publication 1 publication

Immunohistochemistry (Paraffin) (IHC (P))

1:50-1:1,000
-

Immunocytochemistry (ICC/IF)

1:50-1:200
-
Product Specifications

Species Reactivity

Human

Published species

Mouse

Host/Isotype

Rabbit / IgG

Expression System

HEK293 cells

Class

Recombinant Monoclonal

Type

Antibody

Clone

SI70-01

Immunogen

Synthetic peptide within Human ATM aa 1,951-2,000
View immunogen

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

1 mg/mL

Purification

Protein A

Storage buffer

TBS, pH 7.4, with 40% Glycerol, 0.05% BSA

Contains

0.05% sodium azide

Storage conditions

Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.

Shipping conditions

Wet ice

RRID

AB_2809357

Product Specific Information

Recombinant rabbit monoclonal antibodies are produced using in vitro expression systems. The expression systems are developed by cloning in the specific antibody DNA sequences from immunoreactive rabbits. Then, individual clones are screened to select the best candidates for production. The advantages of using recombinant rabbit monoclonal antibodies include: better specificity and sensitivity, lot-to-lot consistency, animal origin-free formulations, and broader immunoreactivity to diverse targets due to larger rabbit immune repertoire.

Target Information

Ataxia-telangiectasia Mutated (ATM) is a protein that belongs to the PI3/PI4 kinase family. Ataxia-telangiectasia is a rare autosomal recessive disorder characterized by progressive neurologic degeneration, immunologic deficiency, and an increased risk of lymphoid cancer. The ATM gene codes for a protein belonging to the phosphoinositide 3-kinase (PI3K) superfamily. ATM phosphorylates proteins instead of lipid and has many downstream targets that act as cell-cycle regulators including: P53, Mdm2, BRCA1, and SMC1. The ATM protein is responsible for repairing double-stranded DNA breaks that occur because of ionizing radiation and other mutagens. The ATM’s C-terminal region has extensive homology to the catalytic domains of phosphatidylinositol 3-kinases (PI3 kinases). Studies have shown that ATM becomes autophosphorylated and upregulated by exposure to ionizing radiation. AT cells are hypersensitive to ionizing radiation, impaired in mediating the inhibition of DNA synthesis and display delays in p53 induction. Further, DNA damage caused by ionizing irradiation activates ATM-kinase, leading to a cascade of kinase reactions that regulate cell cycle, apoptosis, and DNA damage repair. Studies have linked ATM to apoptosis along with Nbs1 and Chk2 in the E2F1 pathway.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.

Bioinformatics

Protein Aliases: A-T mutated; AT mutated; AT mutated protein; Ataxia t; Ataxia telangiectasia mutated; DKFZp781A0353; EC 2.7.1.37; MGC74674; Serine-protein kinase ATM; TEL1, telomere maintenance 1, homolog

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Gene Aliases: AT1; ATA; ATC; ATD; ATDC; ATE; ATM; TEL1; TELO1

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UniProt ID: (Human) Q13315

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Entrez Gene ID: (Human) 472

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Function(s)
DNA binding protein serine/threonine kinase activity DNA-dependent protein kinase activity protein binding ATP binding 1-phosphatidylinositol-3-kinase activity protein complex binding protein dimerization activity protein N-terminus binding non-receptor serine/threonine protein kinase
Process(es)
double-strand break repair via homologous recombination DNA double-strand break processing DNA synthesis involved in DNA repair strand displacement response to hypoxia somitogenesis pre-B cell allelic exclusion DNA replication DNA repair double-strand break repair via nonhomologous end joining protein phosphorylation cellular response to DNA damage stimulus DNA damage induced protein phosphorylation DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest telomere maintenance via telomerase cell cycle arrest mitotic spindle assembly checkpoint reciprocal meiotic recombination signal transduction brain development heart development determination of adult lifespan intrinsic apoptotic signaling pathway in response to DNA damage response to ionizing radiation regulation of autophagy histone phosphorylation peptidyl-serine phosphorylation negative regulation of B cell proliferation positive regulation of telomere maintenance via telomerase positive regulation of histone phosphorylation V(D)J recombination phosphatidylinositol-3-phosphate biosynthetic process peptidyl-serine autophosphorylation lipoprotein catabolic process regulation of apoptotic process positive regulation of apoptotic process positive regulation of DNA damage response, signal transduction by p53 class mediator positive regulation of neuron apoptotic process meiotic telomere clustering protein autophosphorylation oocyte development neuron apoptotic process regulation of telomerase activity histone mRNA catabolic process cellular response to gamma radiation cellular response to X-ray cellular response to nitrosative stress signal transduction involved in mitotic G2 DNA damage checkpoint replicative senescence establishment of RNA localization to telomere establishment of macromolecular complex localization to telomere regulation of cellular response to heat regulation of signal transduction by p53 class mediator negative regulation of TORC1 signaling negative regulation of telomere capping positive regulation of telomere maintenance via telomere lengthening positive regulation of telomerase catalytic core complex assembly
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