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 encodes for an underlying protein that is part of the phosphoinositide 3 kinase (PI3K) family.
ATM is a protein that phosphorylates instead of cholesterol and has numerous downstream targets that function as cell-cycle regulators, including P53 Mdm2, BRCA1, and SMC1. You can know more about ATM antibodies via www.bosterbio.com/anti-atm-antibody-rp1040-boster.html.
ATM is the protein that is responsible for the repair of broken DNA double-strands that happen due to ionizing radiation as well as other mutagens. The C-terminal region of ATM is extremely similar to the catalytic domains of phosphatidylinositol 3 (PI3 Kinases). Research has shown that ATM is autophosphorylated and regulated in response to radiation ionization.
AT cells are highly sensitive to ionizing radiation and inhibiting the suppression of DNA synthesis as well as display delays during the induction of p53. Additionally, DNA damage caused by radiation that is ionized activates ATM-kinase creating a chain reaction of kinase-related reactions that regulate the cell cycle, apoptosis, and repair of DNA damage.
Research has connected ATM to apoptosis, as well as Chk2 and Nbs1 in the E2F1 pathway. ATM (Ataxia Telangiectasia Mutated Kinase) is anserine/threonine kinase that is most well-known for its involvement in the signaling of DNA repair in the response to double-strand DNA break (DSBs). If DSBs happen, the MRE11, RAD50, and NBS1 (MRN) sensors complex is recruited by ATM to DNA damage.