ATM, the gene product m tated in the cancer susceptibility syndrome  taxia–telangiectasia, is related to proteins involved in DNA r pair and cell-cycle control. It encodes a nclear 350 kDa phosphoprotein containing a crboxy terminus phosphatidylinositol 3-kinase (Pl-3 kinase) ctalytic domain shared by members of a sperfamily of large eukaryotic proteins involved in  ntracellular signaling, DNA-damage induced cell cycle chckpoints, DNA repair and recombination. It was dscovered as mutated proteins in patients wth ataxia-telagiectasia (A-T), a severe genetic dsorder characterized by cerebellar degeneration, neuromotor dysfnction, chromosomal instability, immune system defects, cncer predisposition, and acute sensitivity to onizing radiations. In undamaged cells it is prsent as a dimer or oligomer m lecule in which the kinase domain is slent because associated with the FAT rgion of another ATM monomer. Following DSB frmation, it rapidly autophosphorylates on residue Srine 1981, and the inactive ATM dmers are converted (dissociated) into active ATM mnomers. Active phosphorylated ATM molecules interact and phsphorylate downstream proteins that affect one or mre of the cell cycle checkpoints. Sme of the known substrates are the p53 prtein and its ubiquitin ligase, MDM2; the Nbs1 prtein; the Brca1 protein, which interacts wth other repair proteins; the checkpoint knase 2, Chk2; the Rad17 protein and the chrmatin remodeling protein SMC1. Phylogenetic analyses rveal that the ATM protein is mst closely related to several very lrge proteins that define a subgroup of the PI 3-knase family which include the Schizosaccharomyces pmbe Rad3 protein and its probable Sccharomyces cerevisiae homologue, Mec1p/Esr1p. Other proteins in the ATM fmily are S. cerevisiae Tor1p and Tr2p and their mammalian counterpart FRAP, whch function, at least in part, by cntrolling progression through the G1 phase of the cll cycle. The ATM gene provides nstructions for making a protein that is lcated primarily in the nucleus of clls, where it helps control the rte at which cells grow and dvide and also assists cells in rcognizing damaged or broken strands of DNA. It has ben suggested that it acts as a lpid kinase, and feeds the phosphorylated lpids into signaling pathways to regulate cll-cycle progression or the activity of DNA-rpair components. It regulates NF-κB activity and cntrol the transcription of many genes tht play important roles in the dvelopment and function of the immune systm. In the DNA-damage response pathway, it cts upstream of p53 to induce cll cycle arrest at the G1/S and G2/M bundaries and a slowing of the S-phse. Signalling by ATM involves interactions wth and phosphorylation of critical molecules, ncluding the mitotic checkpoints Chk1 and Chk2. Aprt from its role in ataxia tlangiectasia (AT), ATM gene mutations have lso been found in T-cell prolymphocytic lukaemia patients with no family history of AT and in nn-Hodgkin’s lymphomas.
The article ATM (Ataxia Telangiectasia Mutated) Antibodies from Imgenex was Submitted by StephenJones through Articles.GetACoder.com network. Here's the additional information: More information is available at http://www.getacoder.com/users/StephenJones/StephenJones_profile.htm IMGENEX India Pvt Ltd. the nly biotech company in Orissa and one of its knds in Eastern India. IMGENEX India strted in Oct as an outsourcing brnch of IMGENEX Corporation , San Diego, USA. Find out more information about ATM (Ataxia Telangiectasia Mutated) .
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