Thermo Fisher Scientific Phospho-ATM (Ser1981) Monoclonal Antibody (10H11.E12)

Applications

Tested Dilution

Publications

Western Blot (WB)

1:1,000

View 2 publications 2 publications

Immunohistochemistry (Paraffin) (IHC (P))

1:200

View 1 publication 1 publication

Immunocytochemistry (ICC/IF)

1:1,000

-

Immunoprecipitation (IP)

1:10-1:500

-

Product Specifications

Species Reactivity

Human, Mouse, Rat

Published species

Human

Host/Isotype

Mouse / IgG1, kappa

Class

Monoclonal

Type

Antibody

Clone

10H11.E12

Immunogen

A synthetic peptide with a phosphorylated serine (1981).

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

1 mg/mL

Purification

Protein G

Storage buffer

PBS

Contains

0.05% sodium azide

Storage conditions

-20° C, Avoid Freeze/Thaw Cycles

Shipping conditions

Wet ice

RRID

AB_2062982

Product Specific Information

This antibody does not react with canine samples.

Suggested positive control: Irradiated normal human fibroblasts.

No reactivity against un-irradiated cell extracts.

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.