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Loss of JBTS-26 allows kinesin-II to invade the distal cilium and slows down IFT. Conversely, JBTS-26 overexpression accelerates IFT by prematurely releasing kinesin-II. Our findings reveal a mechanism for compartmentalized motor regulation and link defective motor handover to ciliopathy pathogenesis.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2504374122","type":"journal-article","created":{"date-parts":[[2025,11,20]],"date-time":"2025-11-20T16:21:33Z","timestamp":1763655693000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":1,"title":["Joubert syndrome 26 protein enforces compartmentalized motility of a ciliary kinesin"],"prefix":"10.1073","volume":"122","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-1841-6901","authenticated-orcid":false,"given":"Shimin","family":"Wang","sequence":"first","affiliation":[{"name":"Tsinghua-Peking Center for Life Sciences, Tsinghua University","place":["Beijing, China"]},{"name":"Beijing Frontier Research Center for Biological Structure, Tsinghua University","place":["Beijing, China"]},{"name":"McGovern Institute for Brain Research, Tsinghua 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