{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T13:43:25Z","timestamp":1791380605305,"version":"4.3.3"},"reference-count":31,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"6003","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[2010,10,22]]},"abstract":"<jats:title>Stress, DNA Damage, and ATM<\/jats:title>\n                  <jats:p>\n                    The protein kinase ATM (ataxia-telangiectasia mutated) is a key component of the signaling pathway through which cells are protected from DNA damage. ATM becomes activated within a protein complex at sites of double-stranded breaks in DNA. ATM is also activated in response to increased production of reactive oxygen species (ROS). Such activation was thought to reflect DNA damage caused by ROS, but\n                    <jats:bold>\n                      Guo\n                      <jats:italic>et al.<\/jats:italic>\n                    <\/jats:bold>\n                    (p.\n                    <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" page=\"517\" related-article-type=\"in-this-issue\" vol=\"330\" xlink:href=\"10.1126\/science.1192912\">517<\/jats:related-article>\n                    ) showed that ATM was in fact directly activated by ROS. A cysteine residue in ATM contributes to the formation of disulfide-linked dimers of activated ATM on exposure to ROS in vitro. Experiments using mutated forms of the enzyme suggested that two distinct mechanisms regulated ATM activity.\n                  <\/jats:p>","DOI":"10.1126\/science.1192912","type":"journal-article","created":{"date-parts":[[2010,10,21]],"date-time":"2010-10-21T14:25:42Z","timestamp":1287671142000},"page":"517-521","source":"Crossref","is-referenced-by-count":1022,"title":["ATM Activation by Oxidative Stress"],"prefix":"10.1126","volume":"330","author":[{"given":"Zhi","family":"Guo","sequence":"first","affiliation":[{"name":"Howard Hughes Medical Institute, Department of Molecular Genetics and Microbiology, and Institute for Cellular and Molecular Biology (ICMB), University of Texas at Austin, Austin, TX 78712, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sergei","family":"Kozlov","sequence":"additional","affiliation":[{"name":"Radiation Biology and Oncology Laboratory, Queensland Institute of Medical Research, and School of Medicine, University of Queensland, Brisbane Q4006, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin F.","family":"Lavin","sequence":"additional","affiliation":[{"name":"Radiation Biology and Oncology Laboratory, Queensland Institute of Medical Research, and School of Medicine, University of Queensland, Brisbane Q4006, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria D.","family":"Person","sequence":"additional","affiliation":[{"name":"ICMB Analytical Instrumentation Facility Core, College of Pharmacy, University of Texas at Austin, Austin, TX 78712, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tanya T.","family":"Paull","sequence":"additional","affiliation":[{"name":"Howard Hughes Medical Institute, Department of Molecular Genetics and Microbiology, and Institute for Cellular and Molecular Biology (ICMB), University of Texas at Austin, Austin, TX 78712, 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