{"title":"Endosomal chloride-proton exchange rather than chloride conductance is crucial for renal endocytosis","citation":{"chicago":"Novarino, Gaia, Stefanie Weinert, Gesa Rickheit, and Thomas Jentsch. “Endosomal Chloride-Proton Exchange Rather than Chloride Conductance Is Crucial for Renal Endocytosis.” <i>Science</i>. American Association for the Advancement of Science, 2010. <a href=\"https://doi.org/10.1126/science.1188070\">https://doi.org/10.1126/science.1188070</a>.","mla":"Novarino, Gaia, et al. “Endosomal Chloride-Proton Exchange Rather than Chloride Conductance Is Crucial for Renal Endocytosis.” <i>Science</i>, vol. 328, no. 5984, American Association for the Advancement of Science, 2010, pp. 1398–401, doi:<a href=\"https://doi.org/10.1126/science.1188070\">10.1126/science.1188070</a>.","ieee":"G. Novarino, S. Weinert, G. Rickheit, and T. Jentsch, “Endosomal chloride-proton exchange rather than chloride conductance is crucial for renal endocytosis,” <i>Science</i>, vol. 328, no. 5984. American Association for the Advancement of Science, pp. 1398–1401, 2010.","apa":"Novarino, G., Weinert, S., Rickheit, G., &#38; Jentsch, T. (2010). Endosomal chloride-proton exchange rather than chloride conductance is crucial for renal endocytosis. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.1188070\">https://doi.org/10.1126/science.1188070</a>","short":"G. Novarino, S. Weinert, G. Rickheit, T. Jentsch, Science 328 (2010) 1398–1401.","ista":"Novarino G, Weinert S, Rickheit G, Jentsch T. 2010. Endosomal chloride-proton exchange rather than chloride conductance is crucial for renal endocytosis. Science. 328(5984), 1398–1401.","ama":"Novarino G, Weinert S, Rickheit G, Jentsch T. Endosomal chloride-proton exchange rather than chloride conductance is crucial for renal endocytosis. <i>Science</i>. 2010;328(5984):1398-1401. doi:<a href=\"https://doi.org/10.1126/science.1188070\">10.1126/science.1188070</a>"},"quality_controlled":0,"intvolume":"       328","publication":"Science","date_updated":"2021-01-12T06:56:42Z","_id":"2310","status":"public","type":"journal_article","year":"2010","author":[{"last_name":"Novarino","first_name":"Gaia","orcid":"0000-0002-7673-7178","id":"3E57A680-F248-11E8-B48F-1D18A9856A87","full_name":"Gaia Novarino"},{"full_name":"Weinert, Stefanie","first_name":"Stefanie","last_name":"Weinert"},{"full_name":"Rickheit, Gesa","last_name":"Rickheit","first_name":"Gesa"},{"last_name":"Jentsch","first_name":"Thomas","full_name":"Jentsch, Thomas J"}],"publist_id":"4617","publisher":"American Association for the Advancement of Science","month":"06","volume":328,"page":"1398 - 1401","publication_status":"published","day":"11","date_published":"2010-06-11T00:00:00Z","doi":"10.1126/science.1188070","date_created":"2018-12-11T11:56:55Z","extern":1,"issue":"5984","abstract":[{"text":"Loss of the endosomal anion transport protein ClC-5 impairs renal endocytosis and underlies human Dent's disease. ClC-5 is thought to promote endocytosis by facilitating endosomal acidification through the neutralization of proton pump currents. However, ClC-5 is a 2 chloride (Cl-)/proton (H+) exchanger rather than a Cl- channel. We generated mice that carry the uncoupling E211A (unc) mutation that converts CLC-5 into a pure CL- conductor. Adenosine triphosphate (ATP)-dependent acidification of renal endosomes was reduced in mice in which ClC-5 was knocked out, but normal in Clcn5unc mice. However, their proximal tubular endocytosis was also impaired. Thus, endosomal chloride concentration, which is raised by CLC-5 in exchange for protons accumulated by the H+-ATPase, may play a role in endocytosis.","lang":"eng"}]}