{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T17:26:10Z","timestamp":1790961970252,"version":"4.1.0"},"reference-count":35,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2010,12,28]],"date-time":"2010-12-28T00:00:00Z","timestamp":1293494400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2011,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Redistribution of acid\u2010base transporters is a crucial regulatory mechanism for many types of cells to cope with extracellular pH changes. In epithelial cells, however, translocation of acid\u2010base transporters ultimately leads to changes in vectorial transport of H<jats:sup>+<\/jats:sup> and HCO<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/tex2gif-stack-1.gif\" xlink:title=\"urn:x-wiley:00219541:media:JCP22388:tex2gif-stack-1\"\/>. We have previously shown that the bicarbonate\u2010secreting epithelium of salivary ducts responds to changes of systemic acid\u2010base balance by adaptive redistribution of H<jats:sup>+<\/jats:sup> and HCO<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/tex2gif-stack-2.gif\" xlink:title=\"urn:x-wiley:00219541:media:JCP22388:tex2gif-stack-2\"\/> transporters, thereby influencing the ionic composition and buffering capacity of saliva. However, the specific proteins involved in regulated vesicular traffic of acid\u2010base transporters are largely unknown. In the present study we have investigated the impact of Rab11 family members on the acidosis\u2010induced trafficking of the vacuolar\u2010type H<jats:sup>+<\/jats:sup>\u2010ATPase (V\u2010ATPase) in salivary duct cells in vitro using the human submandibular cell line of ductal origin HSG as an experimental model. The results show that Rab11b is expressed in salivary ducts and exhibits a significantly higher co\u2010localization with V\u2010ATPase than Rab11a and Rab25. We also show that Rab11 but not Rab25 interacts with the \u03b5 subunit of V\u2010ATPase. Extracellular acidosis up\u2010regulates Rab11b expression and protein abundance in HSG cells and causes translocation of the V\u2010ATPase from intracellular pools toward the plasma membrane. Loss\u2010of\u2010function experiments using specific siRNA either against Rab11b or against its effector Rip11 prevent acidosis\u2010induced V\u2010ATPase translocation. These data introduce Rab11b as a crucial regulator and Rip11 as mediator of acidosis\u2010induced V\u2010ATPase traffic in duct cells of submandibular gland. J. Cell. Physiol. 226: 638\u2013651, 2011. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.22388","type":"journal-article","created":{"date-parts":[[2010,8,17]],"date-time":"2010-08-17T12:36:00Z","timestamp":1282048560000},"page":"638-651","source":"Crossref","is-referenced-by-count":32,"title":["Rab11b and its effector Rip11 regulate the acidosis\u2010induced traffic of V\u2010ATPase in salivary ducts"],"prefix":"10.1002","volume":"226","author":[{"given":"Oliver","family":"Oehlke","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henno 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