{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T10:08:02Z","timestamp":1785146882508,"version":"3.55.0"},"reference-count":58,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T00:00:00Z","timestamp":1782950400000},"content-version":"vor","delay-in-days":1,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000890","name":"National Multiple Sclerosis Society","doi-asserted-by":"publisher","award":["RG\u20101901\u201033219"],"award-info":[{"award-number":["RG\u20101901\u201033219"]}],"id":[{"id":"10.13039\/100000890","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008501","name":"East Carolina University","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008501","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R03NS131908"],"award-info":[{"award-number":["R03NS131908"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["nyaspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Ann NY Acad Sci"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Recent evidence from genome\u2010wide association studies has linked the ataxin\u20101 gene (\n                    <jats:italic>ATXN1<\/jats:italic>\n                    ) to an increased risk of developing the autoimmune demyelinating disorder multiple sclerosis. From a mechanistic standpoint, our previous work explained this genetic association by defining an immunomodulatory function for ataxin\u20101 in controlling specific genetic programs underlying B cell proliferation, activation, immunoglobulin production, and antigen presentation. Here, we employed a high\u2010resolution multiomics analytical pipeline to further dissect the role of ataxin\u20101 in distinct B cell subsets upon encephalitogenic stress. By combining single\u2010nuclei RNA\u2010seq and ATAC\u2010seq, along with mass\u2010spectrometry proteomics, we documented that ataxin\u20101 is significantly enriched in B1 cells, marginal zone B cells, memory B cells, and precursor B cells. Pathway analysis highlighted that ataxin\u20101 is implicated in RNA splicing and translation processes. Conversely, no major effects were implicated for ataxin\u20101 in chromatin remodeling in the B cell population. Our findings expand the current knowledge of the cellular functions controlled by ataxin\u20101 outside of the central nervous system, and further describe a key regulator of B cell biology in health and disease.\n                  <\/jats:p>","DOI":"10.1111\/nyas.70329","type":"journal-article","created":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T12:48:00Z","timestamp":1782996480000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Multiomics Profiling During Autoimmune Demyelination Highlights a Complex Regulatory Role for Ataxin\u20101 in B Cells"],"prefix":"10.1111","volume":"1561","author":[{"given":"Jonathan J.","family":"Carver","sequence":"first","affiliation":[{"name":"Department of Anatomy and Cell Biology, Brody School of Medicine East Carolina University  Greenville North Carolina USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rachael 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