{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,28]],"date-time":"2026-03-28T06:41:34Z","timestamp":1774680094784,"version":"3.50.1"},"reference-count":78,"publisher":"The Company of Biologists","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,1,1]]},"abstract":"<jats:p>DNA damage can induce a tumor suppressive response termed cellular senescence. Damaged senescent cells permanently arrest growth, secrete inflammatory cytokines and other proteins and harbor persistent nuclear foci that contain DNA damage response (DDR) proteins. To understand how persistent damage foci differ from transient foci that mark repairable DNA lesions, we identify sequential events that differentiate transient foci from persistent foci, which we term \u2018DNA segments with chromatin alterations reinforcing senescence\u2019 (DNA-SCARS). Unlike transient foci, DNA-SCARS associate with PML nuclear bodies, lack the DNA repair proteins RPA and RAD51, lack single-stranded DNA and DNA synthesis and accumulate activated forms of the DDR mediators CHK2 and p53. DNA-SCARS form independently of p53, pRB and several other checkpoint and repair proteins but require p53 and pRb to trigger the senescence growth arrest. Importantly, depletion of the DNA-SCARS-stabilizing component histone H2AX did not deplete 53BP1 from DNA-SCARS but diminished the presence of MDC1 and activated CHK2. Furthermore, depletion of H2AX reduced both the p53-dependent senescence growth arrest and p53-independent cytokine secretion. DNA-SCARS were also observed following severe damage to multiple human cell types and mouse tissues, suggesting that they can be used in combination with other markers to identify senescent cells. Thus, DNA-SCARS are dynamically formed distinct structures that functionally regulate multiple aspects of the senescent phenotype.<\/jats:p>","DOI":"10.1242\/jcs.071340","type":"journal-article","created":{"date-parts":[[2010,12,1]],"date-time":"2010-12-01T03:17:17Z","timestamp":1291173437000},"page":"68-81","source":"Crossref","is-referenced-by-count":461,"title":["DNA-SCARS: distinct nuclear structures that sustain damage-induced senescence growth arrest and inflammatory cytokine secretion"],"prefix":"10.1242","volume":"124","author":[{"given":"Francis","family":"Rodier","sequence":"first","affiliation":[{"name":"Lawrence Berkeley National Laboratory, One Cyclotron Road, Berkeley, CA 94720, USA"},{"name":"The Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA"}]},{"given":"Denise P.","family":"Mu\u00f1oz","sequence":"additional","affiliation":[{"name":"Lawrence Berkeley National Laboratory, One Cyclotron Road, Berkeley, CA 94720, USA"},{"name":"The Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA"}]},{"given":"Robert","family":"Teachenor","sequence":"additional","affiliation":[{"name":"Lawrence Berkeley National Laboratory, One Cyclotron Road, Berkeley, CA 94720, USA"}]},{"given":"Victoria","family":"Chu","sequence":"additional","affiliation":[{"name":"Lawrence Berkeley National Laboratory, One Cyclotron Road, Berkeley, CA 94720, USA"}]},{"given":"Oanh","family":"Le","sequence":"additional","affiliation":[{"name":"CHU Ste-Justine, D\u00e9partement de Pharmacologie, Universit\u00e9 de Montr\u00e9al, 3175 Cote Ste-Catherine, Montreal, QC H3T 1C5, Canada"}]},{"given":"Dipa","family":"Bhaumik","sequence":"additional","affiliation":[{"name":"The Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA"}]},{"given":"Jean-Philippe","family":"Copp\u00e9","sequence":"additional","affiliation":[{"name":"Lawrence Berkeley National Laboratory, One Cyclotron Road, Berkeley, CA 94720, USA"},{"name":"The Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA"}]},{"given":"Eric","family":"Campeau","sequence":"additional","affiliation":[{"name":"Program in Gene Function and Expression, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA"}]},{"given":"Christian M.","family":"Beaus\u00e9jour","sequence":"additional","affiliation":[{"name":"CHU Ste-Justine, D\u00e9partement de Pharmacologie, Universit\u00e9 de Montr\u00e9al, 3175 Cote Ste-Catherine, Montreal, QC H3T 1C5, Canada"}]},{"given":"Sahn-Ho","family":"Kim","sequence":"additional","affiliation":[{"name":"Lawrence Berkeley National Laboratory, One Cyclotron Road, Berkeley, CA 94720, USA"}]},{"given":"Albert R.","family":"Davalos","sequence":"additional","affiliation":[{"name":"Lawrence Berkeley National Laboratory, One Cyclotron Road, Berkeley, CA 94720, USA"},{"name":"The Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA"}]},{"given":"Judith","family":"Campisi","sequence":"additional","affiliation":[{"name":"Lawrence Berkeley National Laboratory, One Cyclotron Road, Berkeley, CA 94720, USA"},{"name":"The Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA"}]}],"member":"237","reference":[{"key":"2021042521272102900_R1","doi-asserted-by":"crossref","first-page":"1006","DOI":"10.1016\/j.cell.2008.03.038","article-title":"Chemokine signaling via the CXCR2 receptor reinforces senescence","volume":"133","author":"Acosta","year":"2008","journal-title":"Cell"},{"key":"2021042521272102900_R2","doi-asserted-by":"crossref","first-page":"4599","DOI":"10.1128\/JVI.71.6.4599-4613.1997","article-title":"The major immediate-early proteins IE1 and IE2 of human cytomegalovirus colocalize with and disrupt PML-associated nuclear bodies at very early times in infected permissive cells","volume":"71","author":"Ahn","year":"1997","journal-title":"J. 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