{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T01:24:23Z","timestamp":1780449863086,"version":"3.54.1"},"reference-count":39,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2024,12,8]],"date-time":"2024-12-08T00:00:00Z","timestamp":1733616000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100017868","name":"Human Islet Research Network","doi-asserted-by":"publisher","award":["U24 DK104162"],"award-info":[{"award-number":["U24 DK104162"]}],"id":[{"id":"10.13039\/100017868","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01 DK138335"],"award-info":[{"award-number":["R01 DK138335"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["U01 DK127505"],"award-info":[{"award-number":["U01 DK127505"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01 DK125360"],"award-info":[{"award-number":["R01 DK125360"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["U01 DK127786"],"award-info":[{"award-number":["U01 DK127786"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01 DK060581"],"award-info":[{"award-number":["R01 DK060581"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Proteomics"],"published-print":{"date-parts":[[2025,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Type 1 diabetes (T1D) results from the autoimmune destruction of the insulin\u2010producing \u03b2 cells of the pancreas. Omega\u20103 fatty acids protect \u03b2 cells and reduce the incidence of T1D, but the mechanism is poorly understood. We have shown that omega\u20103 fatty acids reduce pro\u2010inflammatory cytokine\u2010mediated \u03b2\u2010cell apoptosis by upregulating the expression of the ADP\u2010ribosylhydrolase ARH3. Here, we further investigate the \u03b2\u2010cell protection mechanism of ARH3 by performing siRNA analysis of its gene\n                    <jats:italic>Adprhl2<\/jats:italic>\n                    in MIN6 insulin\u2010producing cells, subsequent treatment with a cocktail of the pro\u2010inflammatory cytokines IL\u20101\u03b2\u00a0+\u00a0IFN\u2010\u03b3\u00a0+\u00a0TNF\u2010\u03b1, followed by proteomics analysis. ARH3 regulated proteins from several pathways related to the nucleus (splicing, RNA surveillance, and nucleocytoplasmic transport), mitochondria (metabolic pathways), and endoplasmic reticulum (protein folding). ARH3 also regulated the levels of proteins related to antigen processing and presentation, and the chemokine\u2010signaling pathway. We further studied the role of ARH3 in regulating the chemokine CXCL9. We found that ARH3 reduces the cytokine\u2010induced expression of CXCL9, which is dependent on omega\u20103 fatty acids. In conclusion, we demonstrate that omega\u20103 fatty acids regulate CXCL9 expression via ARH3, which may have a role in protecting \u03b2 cells from immune attack thereby preventing T1D development.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Significance of the Study<\/jats:italic>\n                    : Omega\u20103 fatty acids have a variety of health benefits. In type 1 diabetes, omega\u20103 fatty acids reduce the islet autoimmune response and the disease development. Here, we studied the pathways regulated by the adenosine diphosphate (ADP)\u2010ribosylhydrolase ARH3, a protein whose expression is regulated by omega\u20103 fatty acids. We showed that ARH3 reduces the expression of chemokines in response to omega\u20103 fatty acids. This represents an anti\u2010inflammatory mechanism of omega\u20103 fatty acids that might be involved with protection against type 1 diabetes development.\n                  <\/jats:p>","DOI":"10.1002\/pmic.202400053","type":"journal-article","created":{"date-parts":[[2024,12,9]],"date-time":"2024-12-09T01:21:12Z","timestamp":1733707272000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Reduction of Chemokine CXCL9 Expression by Omega\u20103 Fatty Acids via ADP\u2010Ribosylhydrolase ARH3 in MIN6 Insulin\u2010Producing Cells"],"prefix":"10.1002","volume":"25","author":[{"given":"Youngki","family":"You","sequence":"first","affiliation":[{"name":"Biological Sciences Division Pacific Northwest National Laboratory  Richland Washington USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soumyadeep","family":"Sarkar","sequence":"additional","affiliation":[{"name":"Biological Sciences Division Pacific 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