{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T23:26:02Z","timestamp":1790378762239,"version":"4.1.0"},"reference-count":14,"publisher":"National Academy of Sciences","issue":"24","license":[{"start":{"date-parts":[[2025,6,9]],"date-time":"2025-06-09T00:00:00Z","timestamp":1749427200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003407","name":"Ministero dell'Istruzione, dell'Universit\u00e0 e della Ricerca","doi-asserted-by":"publisher","award":["F53D23012270001"],"award-info":[{"award-number":["F53D23012270001"]}],"id":[{"id":"10.13039\/501100003407","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003407","name":"Ministero dell'Istruzione, dell'Universit\u00e0 e della Ricerca","doi-asserted-by":"publisher","award":["F53D23012270001"],"award-info":[{"award-number":["F53D23012270001"]}],"id":[{"id":"10.13039\/501100003407","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2025,6,17]]},"abstract":"<jats:p>\n                    The Mitochondrial Antiviral Signaling Protein (MAVS) is a key adaptor in antiviral immunity, mediating type I interferon responses downstream of RIG1 and TLR3. While MAVS regulation is essential for antiviral defense, its modulation in keratinocytes is poorly understood. Here, we examine the role of the CARD14\u2013BCL10\u2013MALT1 (CBM) complex, a skin-specific signaling module, in controlling MAVS-dependent antiviral responses. We identify CARD14\n                    <jats:italic toggle=\"yes\">short<\/jats:italic>\n                    as a dual regulator that activates NF-\u03baB while inhibiting IRF3 signaling. Psoriasis-associated CARD14 mutations are less efficient in restricting IRF3 activation and cytokine production upon Poly (I:C) stimulation, highlighting a potential mechanism in psoriasis pathogenesis. BCL10 is essential for MAVS-induced IRF3 activation, while MALT1 limits IRF3 signaling by promoting MAVS cleavage, K48-linked ubiquitination, and proteasomal degradation. Genetic and chemical inhibition of MALT1 enhances IRF3 activation and type I IFN expression. These findings reveal a MAVS-CBM regulatory network linking innate immunity to epithelial homeostasis.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2500711122","type":"journal-article","created":{"date-parts":[[2025,6,9]],"date-time":"2025-06-09T15:00:42Z","timestamp":1749481242000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":4,"title":["The CARD14\n                    <i>sh<\/i>\n                    \u2013BCL10\u2013MALT1 complex regulates MAVS-mediated antiviral response in keratinocytes"],"prefix":"10.1073","volume":"122","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5935-7077","authenticated-orcid":false,"given":"Lucrezia","family":"Zerillo","sequence":"first","affiliation":[{"name":"Genus Biotech, Unit of Molecular Biology and Genetics","place":["Benevento, Italy"]},{"name":"Department of Sciences and Technologies, University of Sannio","place":["Benevento, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4753-116X","authenticated-orcid":false,"given":"Tiziana","family":"Zotti","sequence":"additional","affiliation":[{"name":"Department of Sciences and Technologies, University of Sannio","place":["Benevento, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angelapia","family":"Tutela","sequence":"additional","affiliation":[{"name":"Department of Sciences and Technologies, University of Sannio","place":["Benevento, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessica Raffaella","family":"Madera","sequence":"additional","affiliation":[{"name":"Department of Sciences and Technologies, University of Sannio","place":["Benevento, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriella","family":"Grasso","sequence":"additional","affiliation":[{"name":"Department of Sciences and Technologies, University of Sannio","place":["Benevento, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pasquale","family":"Vito","sequence":"additional","affiliation":[{"name":"Genus Biotech, Unit of Molecular Biology and Genetics","place":["Benevento, Italy"]},{"name":"Department of Sciences and Technologies, University of Sannio","place":["Benevento, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Romania","family":"Stilo","sequence":"additional","affiliation":[{"name":"Department of Sciences and Technologies, University of Sannio","place":["Benevento, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2025,6,9]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-019-12253-y"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2018.05.012"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.29161"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1126\/sciimmunol.abi4425"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajhg.2012.03.013"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1824"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2016.02.031"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1007\/s11427-022-2169-x"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.02029-17"},{"key":"e_1_3_3_10_2","first-page":"1","article-title":"Type1 interferons potential initiating factors linking skin wounds with psoriasis pathogenesis","volume":"10","author":"Zhang L. J.","year":"2019","unstructured":"L. J. Zhang, Type1 interferons potential initiating factors linking skin wounds with psoriasis pathogenesis. Front. Immunol. 10, 1\u20138 (2019).","journal-title":"Front. Immunol."},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccr.2012.11.002"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaci.2024.05.031"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jhep.2022.09.013"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jmb.2012.02.018"}],"container-title":["Proceedings of the National Academy of Sciences"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/pnas.org\/doi\/pdf\/10.1073\/pnas.2500711122","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,6,9]],"date-time":"2025-06-09T15:00:48Z","timestamp":1749481248000},"score":1,"resource":{"primary":{"URL":"https:\/\/pnas.org\/doi\/10.1073\/pnas.2500711122"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2025,6,9]]},"references-count":14,"journal-issue":{"issue":"24","published-print":{"date-parts":[[2025,6,17]]}},"alternative-id":["10.1073\/pnas.2500711122"],"URL":"https:\/\/doi.org\/10.1073\/pnas.2500711122","relation":{},"ISSN":["0027-8424","1091-6490"],"issn-type":[{"value":"0027-8424","type":"print"},{"value":"1091-6490","type":"electronic"}],"subject":[],"published":{"date-parts":[[2025,6,9]]},"assertion":[{"value":"2025-01-13","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-04-29","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2025-06-09","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}],"article-number":"e2500711122"}}