{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T11:38:54Z","timestamp":1790163534716,"version":"4.1.0"},"reference-count":45,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,6,25]],"date-time":"2013-06-25T00:00:00Z","timestamp":1372118400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Br J Haematol"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>\n                    We have previously reported that\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\n                    <\/jats:italic>\n                    is silenced by promoter hypermethylation in germinal centre\u2010derived B\u2010cell lymphomas, but beyond these data the regulation and function of lipopolysaccharide\u2010induced tumour necrosis factor (\n                    <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\n                    ) factor (\n                    <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\n                    ) in B cells are unknown. Gene expression and immunohistochemical studies revealed that\n                    <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">BCL<\/jats:styled-content>\n                    6 show opposite expression in tonsil B\u2010cell subpopulations and B\u2010cell lymphomas, suggesting that\n                    <jats:styled-content style=\"fixed-case\">BCL<\/jats:styled-content>\n                    6 may regulate\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\n                    <\/jats:italic>\n                    expression. Accordingly,\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">BCL<\/jats:styled-content>\n                      6\n                    <\/jats:italic>\n                    silencing increased\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\n                    <\/jats:italic>\n                    expression, and chromatin immunoprecipitation and luciferase reporter assays demonstrated a direct transcriptional repression of\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\n                    <\/jats:italic>\n                    by\n                    <jats:styled-content style=\"fixed-case\">BCL<\/jats:styled-content>\n                    6. Gain\u2010 and loss\u2010of\u2010function experiments in different B\u2010cell lymphoma cell lines revealed that, in contrast to its function in monocytes,\n                    <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\n                    does not induce lipopolysaccharide\u2010mediated\n                    <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\n                    secretion in B cells. However, gene expression microarrays defined a\n                    <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\n                    \u2010related transcriptional signature containing genes regulating autophagy, including\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">MAP<\/jats:styled-content>\n                      1\n                      <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>\n                      3B\n                    <\/jats:italic>\n                    (\n                    <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>\n                    3B). In addition, immunofluorescence analysis co\u2010localized\n                    <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\n                    with autophagosomes, further suggesting a possible role in autophagy modulation. Accordingly, ectopic\n                    <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\n                    expression in B\u2010cell lymphoma cells enhanced autophagy responses to starvation, which were impaired upon\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\n                    <\/jats:italic>\n                    silencing. Our results indicate that the\n                    <jats:styled-content style=\"fixed-case\">BCL<\/jats:styled-content>\n                    6\u2010mediated transcriptional repression of\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">LITAF<\/jats:styled-content>\n                    <\/jats:italic>\n                    may inhibit autophagy in B cells during the germinal centre reaction, and suggest that the constitutive repression of autophagy responses in\n                    <jats:styled-content style=\"fixed-case\">BCL<\/jats:styled-content>\n                    6\u2010driven lymphomas may contribute to lymphomagenesis.\n                  <\/jats:p>","DOI":"10.1111\/bjh.12440","type":"journal-article","created":{"date-parts":[[2013,6,25]],"date-time":"2013-06-25T02:17:11Z","timestamp":1372126631000},"page":"621-630","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":45,"title":["<i>\n                      <scp>LITAF<\/scp>\n                    <\/i>\n                    , a\n                    <scp>BCL<\/scp>\n                    6 target gene, regulates autophagy in mature B\u2010cell lymphomas"],"prefix":"10.1111","volume":"162","author":[{"given":"Cristina","family":"Bertolo","sequence":"first","affiliation":[{"name":"Division of Oncology Center for Applied Medical Research (CIMA) University of Navarra Pamplona Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sergio","family":"Roa","sequence":"additional","affiliation":[{"name":"Division of Oncology Center for Applied Medical Research (CIMA) University of Navarra Pamplona 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