{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T11:55:30Z","timestamp":1791201330477,"version":"4.2.0"},"reference-count":79,"publisher":"National Academy of Sciences","issue":"1","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2010,1,5]]},"abstract":"<jats:p>\n                    Chromosome translocations between Ig (\n                    <jats:italic>Ig<\/jats:italic>\n                    ) and non-\n                    <jats:italic>Ig<\/jats:italic>\n                    genes are frequently associated with B-cell lymphomas in humans and mice. The best characterized of these is\n                    <jats:italic>c-myc\/IgH<\/jats:italic>\n                    translocation, which is associated with Burkitt\u2019s lymphoma. These translocations are caused by activation-induced cytidine deaminase (AID), which produces double-strand DNA breaks in both genes.\n                    <jats:italic>c-myc\/IgH<\/jats:italic>\n                    translocations are rare events, in part because ATM, p53, and p19 actively suppress them. To further define the mechanism of protection against the accumulation of cells that bear\n                    <jats:italic>c-myc\/IgH<\/jats:italic>\n                    translocation, we assayed B cells from mice that carry mutations in cell-cycle and apoptosis regulator proteins that act downstream of p53. We find that PUMA, Bim, and PKC\u03b4 are required for protection against\n                    <jats:italic>c-myc\/IgH<\/jats:italic>\n                    translocation, whereas Bcl-XL and BAFF enhance\n                    <jats:italic>c-myc\/IgH<\/jats:italic>\n                    translocation. Whether these effects are general or specific to\n                    <jats:italic>c-myc\/IgH<\/jats:italic>\n                    translocation and whether AID produces dsDNA breaks in genes other than\n                    <jats:italic>c-myc<\/jats:italic>\n                    and\n                    <jats:italic>Ig<\/jats:italic>\n                    is not known. To examine these questions, we developed an assay for translocation between\n                    <jats:italic>IgH<\/jats:italic>\n                    and\n                    <jats:italic>Ig<\/jats:italic>\n                    \u03b2, both of which are somatically mutated by AID.\n                    <jats:italic>Ig<\/jats:italic>\n                    \u03b2\n                    <jats:italic>\/IgH<\/jats:italic>\n                    , like\n                    <jats:italic>c-myc\/IgH<\/jats:italic>\n                    translocations, are AID-dependent, and AID is responsible for lesions on\n                    <jats:italic>IgH<\/jats:italic>\n                    and the non-\n                    <jats:italic>IgH<\/jats:italic>\n                    translocation partners. However, ATM, p53, and p19 do not protect against\n                    <jats:italic>Ig\u03b2\/IgH<\/jats:italic>\n                    translocations. Instead, B cells are protected against\n                    <jats:italic>Ig<\/jats:italic>\n                    \u03b2\n                    <jats:italic>\/IgH<\/jats:italic>\n                    translocations by a BAFF- and PKC\u03b4-dependent pathway. We conclude that AID-induced double-strand breaks in non-\n                    <jats:italic>Ig<\/jats:italic>\n                    genes other than\n                    <jats:italic>c-myc<\/jats:italic>\n                    lead to their translocation, and that at least two nonoverlapping pathways protect against translocations in primary B cells.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0908946107","type":"journal-article","created":{"date-parts":[[2009,12,6]],"date-time":"2009-12-06T15:26:48Z","timestamp":1260113208000},"page":"187-192","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":31,"title":["Role of the translocation partner in protection against AID-dependent chromosomal translocations"],"prefix":"10.1073","volume":"107","author":[{"given":"Mila","family":"Jankovic","sequence":"first","affiliation":[{"name":"Laboratory of Molecular Immunology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Davide F.","family":"Robbiani","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Immunology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yair","family":"Dorsett","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Immunology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Eisenreich","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Immunology and"},{"name":"Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Xu","sequence":"additional","affiliation":[{"name":"Division of Biological Sciences, University of California, San Diego, CA 92093;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander","family":"Tarakhovsky","sequence":"additional","affiliation":[{"name":"Laboratory of Lymphocyte Signaling, The Rockefeller University, New York, NY 10065; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andre","family":"Nussenzweig","sequence":"additional","affiliation":[{"name":"Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michel C.","family":"Nussenzweig","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Immunology and"},{"name":"Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2009,12,29]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1204640"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.6356357"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/372143a0"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(89)90760-5"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.2360047"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00675-X"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1385\/IR:32:1-3:253"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.26.021607.090248"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)00078-7"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.26.18470"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)00079-9"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature01574"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20030481"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature00862"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni920"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature01760"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(02)01215-0"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.biochem.76.061705.090740"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1038\/88732"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.280.5370.1750"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.20.11816"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0735266100"},{"key":"e_1_3_3_23_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.192.12.1833"},{"key":"e_1_3_3_24_2","doi-asserted-by":"publisher","DOI":"10.1038\/35085588"},{"key":"e_1_3_3_25_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature06547"},{"key":"e_1_3_3_26_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2008.09.062"},{"key":"e_1_3_3_27_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20070882"},{"key":"e_1_3_3_28_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature04495"},{"key":"e_1_3_3_29_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2004.08.006"},{"key":"e_1_3_3_30_2","doi-asserted-by":"publisher","DOI":"10.1038\/onc.2008.312"},{"key":"e_1_3_3_31_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.281.5383.1677"},{"key":"e_1_3_3_32_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.281.5383.1674"},{"key":"e_1_3_3_33_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.19.4.2828"},{"key":"e_1_3_3_34_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.dnarep.2004.03.033"},{"key":"e_1_3_3_35_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.22.18.6521-6532.2002"},{"key":"e_1_3_3_36_2","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/cdf506"},{"key":"e_1_3_3_37_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4401182"},{"key":"e_1_3_3_38_2","first-page":"2615","article-title":"Ser18 and 23 phosphorylation is required for p53-dependent apoptosis and tumor suppression","volume":"25","author":"Chao C","year":"2006","unstructured":"C Chao, D Herr, J Chun, Y Xu, Ser18 and 23 phosphorylation is required for p53-dependent apoptosis and tumor suppression. 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