ATM Research Reagents

Serine-protein kinase ATM is a protein in humans that is encoded by ATM gene. Serine/threonine protein kinase which activates checkpoint signaling upon double strand breaks (DSBs), apoptosis and genotoxic stresses such as ionizing ultraviolet A light (UVA), thereby acting as a DNA damage sensor. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates 'Ser-139' of histone variant H2AX/H2AFX at double strand breaks (DSBs), thereby regulating DNA damage response mechanism. Also plays a role in pre-B cell allelic exclusion, a process leading to expression of a single immunoglobulin heavy chain allele to enforce clonality and monospecific recognition by the B-cell antigen receptor (BCR) expressed on individual B-lymphocytes.

The following ATM reagents supplied by CUSABIO are manufactured under a strict quality control system. Multiple applications have been validated and solid technical support is offered.

ATM Antibodies

ATM Antibodies for Homo sapiens (Human)

ATM Antibodies for Arabidopsis thaliana (Mouse-ear cress)

ATM Proteins

ATM Proteins for Homo sapiens (Human)

ATM Proteins for Mus musculus (Mouse)

ATM Proteins for Sus scrofa (Pig)

ATM Proteins for Arabidopsis thaliana (Mouse-ear cress)

ATM Background

ATM (ataxia-telangiectasia mutated) gene, responsible for the autosomal recessive disorder ataxia-telangiectasia (AT), was identified by positional cloning on chromosome 11q22-23 [2]. AT is characterized by cerebellar degeneration, immunodeficiency, chromosomal instability, cancer predisposition, radiation sensitivity, and cell cycle abnormalities [1]. The coding product of the gene is a crucial tumor suppressor ATM, which is activated by DNA double-strand breaks (DSBs) through its autophosphorylation [3]. Activated ATM further phosphorylates various downstream target molecules such as histone H2AX (H2AX), nibrin (Nbs1), BRCA1, cell-cycle checkpoint kinases Chk1 and Chk2, and p53 that play important roles in DNA-damage functions including regulation of cell-cycle checkpoints, induction of damaged DNA repair, or apoptosis via p53 [4][5]. Rami Khosravi et al. suggested that ATM is responsive to DNA strand breaks, probably by promoting p53 activity and stability through the mediation of simultaneous phosphorylation of both partners of the p53-MDM2 autoregulatory feedback loop [6]. Hdm2 (human Mdm2)-mediated ubiquitylation and degradation through the proteasome pathway causes low expression of p53. DSBs- activated ATM also phosphorylates p53 at Serine-15 [7], which is key for p53-mediated apoptosis after DNA damage. Thus, the modulation of ATM-p53 interaction is fairly important in DNA damage-induced apoptosis. Besides, ATM exerts important roles during meiotic prophase [8]. Many findings show that ATM-mediated homologous recombinational repair is a crucial function of meiosis [9]. ATM deficiency makes humans and mice infertile. And the frequent epigenetic deficiency of ATM in various cancers possibly promote the progression of those cancers.

[1] Rothblum-Oviatt, C., Wright, J., et al. Ataxia telangiectasia: a review [J]. Orphanet J Rare Dis 2016, 11, 159.
[2] K Savitsky, A Bar-Shira, et al. A single ataxia telangiectasia gene with a product similar to PI-3 kinase [J]. Science. 1995 Jun 23;268(5218):1749-53.
[3] Shiloh, Y. ATM and related protein kinases: safeguarding genome integrity [J]. Nat. Rev. Cancer 3, 2003, 155-68.
[4] Kastan, M. B. & Bartek, J. Cell-cycle checkpoints and cancer [J]. Nature 2004, 432, 316-23.
[5] Bartek, J. & Lukas, J. Chk1 and Chk2 kinases in checkpoint control and cancer [J]. Cancer Cell 2003, 3, 421-29.
[6] Rami Khosravi, Ruth Maya, et al. Rapid ATM-dependent phosphorylation of MDM2 precedes p53 accumulation in response to DNA damage [J]. PNAS December 21, 1999 96 (26) 14973-14977.
[7] Banin, S. et al. Enhanced phosphorylation of p53 by ATM in response to DNA damage. Science 1998, 281, 1674-677.
[8] Hamer G, Kal HB, et al. Ataxia telangiectasia mutated expression and activation in the testis [J]. Biol. Reprod. 2004, 70 (4): 1206-2.
[9] Titus S, Li F, et al. Impairment of BRCA1-related DNA double-strand break repair leads to ovarian aging in mice and humans [J]. Sci Transl Med. 2013, 5 (172): 172ra21.

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