The ATM protein is of a type called a kinase, a protein which plays a role in triggering or blocking the activity of other proteins in cellular processes. [10] ATM belongs to the superfamily of phosphatidylinositol 3-kinase-related kinases (PIKKs). [19][20] The phenotypic manifestation of AT is due to the broad range of substrates for the ATM kinase, involving DNA repair, apoptosis, G1/S, intra-S checkpoint and G2/M checkpoints, gene regulation, translation initiation, and telomere maintenance. The cellular distribution of this DNA binding protein features the nucleoplasm, chromosomes, a telomeric region, a nuclear telomere cap complex, the cytoplasm, the spindle, the nucleus and a nucleolus and a nuclear chromosome. [14], The protein kinase ATM may also be involved in mitochondrial homeostasis, as a regulator of mitochondrial autophagy (mitophagy) whereby old, dysfunctional mitochondria are removed. In the central nervous system the cerebellum has a paucity of Purkinje and granule cells. Phosphorylation of CDC25C by CHK1/CHK2 inactivates its phosphatase activity either directly or indirectly through the creation of a 14-3-3 binding site. 6.2). Proteins. ATM belongs to the superfamily of phosphatidylinositol 3-kinase-related kinases (PIKKs). In contrast, in astrocytes inhibition of ATM blocks the formation of new foci and disassembly of the existing radiation-induced foci (Adams etal., 2010a). The secondary structure of ATM protein was predicted by the software SOPMA (Self Optimized Prediction Method with MATERIALS AND METHODS Alignment). ATM protein is best known for its role in the DNA damage response. As a result the particular protein for which the gene contains instructions, also called ATM, is not produced. This inactivation apparently serves to prevent unnecessary activation of cellular functions in the absence of genotoxic stress. DNA damage and responds by phosphorylating down- Mutations in ATM are responsible for the recessive stream effectors involved in cell cycle arrest and DNA inherited disorder known as ataxia-telangiectasia (A-T). Orders of protein structure: primary, secondary, tertiary, and quaternary. The ATM protein is of a type called a kinase, a protein which plays a role in triggering or blocking the activity of other proteins in cellular processes. Ataxia telangiectasia mutated (ATM) is a serine protein kinase that is recruited and activated by DNA double-strand breaks. November 3, 2020 Uncategorized No Comments. Explore the latest full-text research PDFs, articles, conference papers, preprints and more on ATM. [11], People who carry a heterozygous ATM mutation have increased risk of mainly pancreas cancer, prostate cancer, stomach cancer and invasive ductal carcinoma of the breast. Cutaneous and ocular telangiectasias may not appear until 46 years of age. In addition, various options on sizes, excellent technical support, and recombinant ATM proteins N.A. Ataxia-telangiectasia. 1b). All AT patients contain mutations in the ATM gene. Inactive ATM is present in the cells without DSBs as dimers or multimers. The KD domain resumes kinase activity, while the PRD and the FATC domain regulate it. These newly tagged proteins then stop cells dividing until the DNA has been repaired. [9] High purity, Low endotoxin, Multiple Tags, Animal-free, Wide applications (Cell assay, Protein-protein interaction, Drug-related studies, Enzymatic activity in vitro, Protein structure analysis, etc.) The protein structure contains a C-terminal Myb motif, a dimerization domain (TERF homology) near its N-terminus and an acidic N-terminus.. Subcellular distribution.