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Phospho-ATM (Ser1981) Monoclonal Antibody (10H11.E12), eBioscience™, Invitrogen™
Mouse Monoclonal Antibody
Brand: Affymetrix eBioscience 14-9046-82
Code : NEW
Additional Details : Weight : 0.09500kg
Description
The phosphatidylinositol kinase (PIK) family members fall into two distinct subgroups. The first subgroup contains proteins such as the PI 3- and PI 4-kinases and the second group comprises the PIK-related kinases. The PIK-related kinases include Atm, DNA-PKCS and FRAP. These proteins have in common a region of homology at their carboxy-termini that is not present in the PI 3- and PI 4-kinases. The Atm gene is mutated in the autosomal recessive disorder ataxia telangiectasia (AT) that is characterized by cerebellar degeneration (ataxia) and the appearance of dilated blood vessels (telangiec-tases) in the conjunctivae of the eyes. AT cells are hypersensitive to ionizing radiation, impaired in mediating the inhibition of DNA synthesis and display delays in p53 induction.
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.Specifications
Phospho-ATM (Ser1981) | |
Monoclonal | |
0.5 mg/mL | |
PBS with 0.09% sodium azide; pH 7.2 | |
Q13315, Q62388 | |
ATM | |
Affinity chromatography | |
RUO | |
11920, 300711, 472 | |
4° C | |
Liquid |
Flow Cytometry, Immunocytochemistry, Immunohistochemistry (Paraffin), Immunoprecipitation, Western Blot | |
10H11.E12 | |
Unconjugated | |
ATM | |
AI256621; AT mutated; A-T mutated; A-T mutated homolog; AT mutated protein; AT1; ATA; Ataxia t; Ataxia telangiectasia gene mutated in human beings; ataxia telangiectasia mutated; Ataxia telangiectasia mutated homolog; ATC; ATD; ATDC; ATE; Atm; ATM (phospho S1981); ATM (pS1981); ATM (pSer1981); ATM phospho S1981; ATM phospho Ser1981; ATM serine/threonine kinase; C030026E19Rik; DKFZp781A0353; EC 2.7.1.37; MGC74674; phospho ATM; phospho S1981 ATM; serine-protein kinase ATM; TEL1; TEL1, telomere maintenance 1, homolog; TELO1 | |
Mouse | |
100 μg | |
Primary | |
Human, Mouse, Rat | |
Antibody | |
IgG1 κ |
For Research Use Only.