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<h2>ATM (Ataxia Telangiectasia Mutated) Antibodies from Imgenex</h2>by Stephen Jones 
 
ATM, the gene product mutated in 
the cancer susceptibility syndrome ataxia�telangiectasia, is related to 
proteins involved in DNA repair and cell-cycle control. It encodes a nuclear 
350 kDa phosphoprotein containing a carboxy terminus phosphatidylinositol 
3-kinase (Pl-3 kinase) catalytic domain shared by members of a superfamily of 
large eukaryotic proteins involved in intracellular signaling, DNA-damage 
induced cell cycle checkpoints, DNA repair and recombination. It was discovered 
as mutated proteins in patients with ataxia-telagiectasia (A-T), a severe 
genetic disorder characterized by cerebellar degeneration, neuromotor 
dysfunction, chromosomal instability, immune system defects, cancer 
predisposition, and acute sensitivity to ionizing radiations. In undamaged 
cells it is present as a dimer or oligomer molecule in which the kinase domain 
is silent because associated with the FAT region of another ATM monomer. 
Following DSB formation, it rapidly autophosphorylates on residue Serine 1981, 
and the inactive ATM dimers are converted (dissociated) into active ATM 
monomers. Active phosphorylated ATM molecules interact and phosphorylate 
downstream proteins that affect one or more of the cell cycle checkpoints. Some 
of the known substrates are the p53 protein and its ubiquitin ligase, MDM2; the 
Nbs1 protein; the Brca1 protein, which interacts with other repair proteins; 
the checkpoint kinase 2, Chk2; the Rad17 protein and the chromatin remodeling 
protein SMC1. Phylogenetic analyses reveal that the ATM protein is most closely 
related to several very large proteins that define a subgroup of the PI 
3-kinase family which include the Schizosaccharomyces 
pombe Rad3 protein and its probable Saccharomyces 
cerevisiae homologue, Mec1p/Esr1p. Other proteins in the ATM family are S. cerevisiae Tor1p and Tor2p and their 
mammalian counterpart FRAP, which function, at least in part, by controlling 
progression through the G1 phase of the cell cycle. The ATM gene provides 
instructions for making a protein that is located primarily in the nucleus of 
cells, where it helps control the rate at which cells grow and divide and also 
assists cells in recognizing damaged or broken strands of DNA. It has been 
suggested that it acts as a lipid kinase, and feeds the phosphorylated lipids 
into signaling pathways to regulate cell-cycle progression or the activity of 
DNA-repair components. It regulates NF-κB activity and control the 
transcription of many genes that play important roles in the development and 
function of the immune system. In the DNA-damage response pathway, it acts 
upstream of p53 to induce cell cycle arrest at the G1/S and G2/M boundaries and 
a slowing of the S-phase. Signalling by ATM involves interactions with and 
phosphorylation of critical molecules, including the mitotic checkpoints Chk1 
and Chk2. Apart from its role in ataxia telangiectasia (AT), ATM gene mutations 
have also been found in T-cell prolymphocytic leukaemia patients with no family 
history of AT and in non-Hodgkin�s lymphomas. 
 
 
<h3>About the Author</h3>

IMGENEX India Pvt Ltd. the only
biotech company in Orissa and one of its kinds in <st1:place w:st="on">Eastern
 India</st1:place>. IMGENEX India started in Oct as an outsourcing branch of <a href="http://www.imgenex.com">IMGENEX Corporation</a> ,
<st1:place w:st="on"><st1:city w:st="on">San Diego</st1:city>, <st1:country-region w:st="on">USA</st1:country-region></st1:place>.  Find out more information about  <a href="http://www.imgenex.com/antibody_details.php?catalog=IMG-80237">ATM</a>
(Ataxia Telangiectasia Mutated) .<o:p />

<o:p> </o:p>

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