{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T07:45:51Z","timestamp":1776411951961,"version":"3.51.2"},"reference-count":86,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T00:00:00Z","timestamp":1776211200000},"content-version":"vor","delay-in-days":14,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T00:00:00Z","timestamp":1775001600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biology International"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Alternative splicing is a finely regulated process which defines the final maturation of pre\u2010mRNAs. Modulation of trans\u2010acting spliceosome proteins changes specific patterns of splicing and contributes to the development of diseases. During Amyotrophic Lateral Sclerosis (ALS) disease progression, loss of nuclear trans\u2010acting splicing protein TDP43 leads to accumulation of cryptic exons in mRNAs, which inhibits expression of proteins and aggravates the disease. One of the affected genes is\n                    <jats:italic>DNAJC5<\/jats:italic>\n                    , which codes for a protein responsible for clearance of misfolded proteins in the cytoplasm. We first observed that TDP43 knockdown regulates DNAJC5 transcript splicing. A similar phenotype was observed upon hnRNP K knockdown. We hypothesized canonical splicing of DNAJC5 is dependent on the activity of both TDP43 and hnRNP K. Our results confirmed TDP43 and hnRNP K interaction is dependent on RNA. We also confirmed that DNAJC5 canonical splicing is dependent on its internal TDP43 and hnRNP K binding sites. Taken together, our work enrolls both TDP43 and hnRNP K on splicing regulation of DNAJC5 transcript, affecting activity of the protein encoded by\n                    <jats:italic>DNAJC5<\/jats:italic>\n                    on endosomal traffic. As a result, activity of both TDP43 and hnRNP K and their association are important for ALS progression.\n                  <\/jats:p>","DOI":"10.1002\/cbin.70158","type":"journal-article","created":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T11:30:50Z","timestamp":1776252650000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["TDP43 and hnRNP K Regulate Alternative Splicing of DNAJC5"],"prefix":"10.1002","volume":"50","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7897-3556","authenticated-orcid":false,"given":"Helder Y.","family":"Nagasse","sequence":"first","affiliation":[{"name":"Department of Cell and Developmental Biology, Institute of Biomedical Sciences University of S\u00e3o Paulo S\u00e3o Paulo S\u00e3o Paulo Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-7704-2125","authenticated-orcid":false,"given":"Ellen 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