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               <dc:title>Cholesterol depletion in adipocytes causes caveolae collapse concomitant with proteosomal degradation of cavin-2 in a switch-like fashion</dc:title>
               <dc:creator>Breen, Michael P., 1940-</dc:creator>
               <dc:creator>Camps Camprubí, Marta</dc:creator>
               <dc:creator>Carvalho-Simoes, Francisco</dc:creator>
               <dc:creator>Zorzano Olarte, Antonio</dc:creator>
               <dc:creator>Pilch, Paul F.</dc:creator>
               <dc:subject>Colesterol</dc:subject>
               <dc:subject>Proteïnes de membrana</dc:subject>
               <dc:subject>Cèl·lules animals</dc:subject>
               <dc:subject>Cholesterol</dc:subject>
               <dc:subject>Membrane proteins</dc:subject>
               <dc:subject>Animal cells</dc:subject>
               <dc:description>Caveolae, little caves of cell surfaces, are enriched in cholesterol, a certain level of which is required for their structural integrity. Here we show in adipocytes that cavin-2, a peripheral membrane protein and one of 3 cavin isoforms present in caveolae from non-muscle tissue, is degraded upon cholesterol depletion in a rapid fashion resulting in collapse of caveolae. We exposed 3T3-L1 adipocytes to the cholesterol depleting agent methyl-β-cyclodextrin, which results in a sudden and extensive degradation of cavin-2 by the proteasome and a concomitant movement of cavin-1 from the plasma membrane to the cytosol along with loss of caveolae. The recovery of cavin-2 at the plasma membrane is cholesterol-dependent and is required for the return of cavin-1 from the cytosol to the cell surface and caveolae restoration. Expression of shRNA directed against cavin-2 also results in a cytosolic distribution of cavin-1 and loss of caveolae. Taken together, these data demonstrate that cavin-2 functions as a cholesterol responsive component of caveolae that is required for cavin-1 localization to the plasma membrane, and caveolae structural integrity.</dc:description>
               <dc:date>2018-09-17T13:11:26Z</dc:date>
               <dc:date>2018-09-17T13:11:26Z</dc:date>
               <dc:date>2012-04-06</dc:date>
               <dc:date>2018-09-17T13:11:26Z</dc:date>
               <dc:type>info:eu-repo/semantics/article</dc:type>
               <dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
               <dc:relation>Reproducció del document publicat a: https://doi.org/10.1371/journal.pone.0034516</dc:relation>
               <dc:relation>PLoS One, 2012, vol. 7, num. 4, p. 1-8</dc:relation>
               <dc:relation>https://doi.org/10.1371/journal.pone.0034516</dc:relation>
               <dc:rights>cc-by (c) Breen, Michael P., 1940- et al., 2012</dc:rights>
               <dc:rights>http://creativecommons.org/licenses/by/3.0/es</dc:rights>
               <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
               <dc:publisher>Public Library of Science (PLoS)</dc:publisher>
               <dc:source>Articles publicats en revistes (Bioquímica i Biomedicina Molecular)</dc:source>
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