missing translation for 'onlineSavingsMsg'
Learn More

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

Product Code. 15587566

  • £213.00 / 100µg
Estimated Shipment: 28-05-2024
to see stock.

Please to purchase this item. Need a web account? Register with us today!


Description

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

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
Product Suggestions

Product Suggestions

Videos
SDS
Documents

Documents

Certificates
Special Offers

Special Offers

For Research Use Only.