|Tested species reactivity||Human, Mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||A fragment of human ATM protein expressed in E.coli. The fragment relates to the C-terminal region (within the last third of the protein sequence).|
|Purification||Antigen affinity chromatography|
|Storage buffer||sodium borate|
|Storage Conditions||4° C, store in dark|
|Tested Applications||Dilution *|
|Western Blot (WB)||1:500-1:1000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
Ataxia-telangiectasia (A-T) is a recessive childhood disease caused by mutations in the ATM (AT-mutated) gene. Symptoms include neurological abnormalities that cause unsteady posture, dilated blood vessels, infertility, radiation sensitivity, immune deficiencies and lymphoid malignancies. It appears that the diverse defects seen in ATM null mammals are manifestations of disparate signal transduction defects.
The ATM protein is related to a family of proteins through a C-terminal phoshatidylinositol 3-kinase (PI3-kinase) domain. Members of the PI3-kinase family of proteins are involved in cell cycle control, DNA replication, recombination and repair. ATM also shares sequence homology with portions of the yeast RAD3 gene. The main role of ATM appears to be induction of a DNA-damage control pathway in response to genotoxic insults, such as ionizing radiation or anti-tumor medications and the programmed DNA breaks of meiosis.
ATM has also been linked to apoptosis along with Nbs1 and Chk2 in the E2F1 pathway. (Rogoff et. al.)
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.