| pubmed-article:9188092 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9188092 | lifeskim:mentions | umls-concept:C0699040 | lld:lifeskim |
| pubmed-article:9188092 | lifeskim:mentions | umls-concept:C0205145 | lld:lifeskim |
| pubmed-article:9188092 | lifeskim:mentions | umls-concept:C0033634 | lld:lifeskim |
| pubmed-article:9188092 | lifeskim:mentions | umls-concept:C0205146 | lld:lifeskim |
| pubmed-article:9188092 | lifeskim:mentions | umls-concept:C0547047 | lld:lifeskim |
| pubmed-article:9188092 | lifeskim:mentions | umls-concept:C0070750 | lld:lifeskim |
| pubmed-article:9188092 | lifeskim:mentions | umls-concept:C0332291 | lld:lifeskim |
| pubmed-article:9188092 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:9188092 | pubmed:dateCreated | 1997-8-7 | lld:pubmed |
| pubmed-article:9188092 | pubmed:abstractText | The effect of protein kinase C (PKC) stimulation on the pump current (Ip) generated by the Na,K-ATPase was measured in A6 epithelia apically permeabilized with amphotericin B. Phorbol 12-myristate 13-acetate (PMA) produced a decrease in Ip carried by sodium pumps containing the endogenous Xenopus laevis or transfected Bufo marinus alpha 1 subunits (approximately 30% reduction within 25 min, maximum after 40 min) independent of the PKC phosphorylation site (T15A/S16A). In addition to this major effect of PMA, which was independent of the intracellular sodium concentration and was prevented by the PKC inhibitor bisindolylmaleimide GF 109203X (BIM), another BIM-resistant, PKC site-independent decrease was observed when the Ip was measured at low sodium concentrations (total reduction approximately 50% at 5 mM sodium). Using ouabain binding and cell surface biotinylation, stimulation of PKC was shown to reduce surface Na,K-ATPase by 14 to 20% within 25 min. The same treatment stimulated fluid phase endocytosis sevenfold and decreased by 16.5% the basolateral cell surface area measured by transepithelial capacitance measurements. In conclusion, PKC stimulation produces a decrease in sodium pump function which can be attributed, to a large extent, to a withdrawal of sodium pumps from the basolateral cell surface independent of their PKC site. This reduction of the number of sodium pumps is parallel to a decrease in basolateral membrane area. | lld:pubmed |
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| pubmed-article:9188092 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9188092 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9188092 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9188092 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9188092 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:9188092 | pubmed:issn | 1059-1524 | lld:pubmed |
| pubmed-article:9188092 | pubmed:author | pubmed-author:GeeringKK | lld:pubmed |
| pubmed-article:9188092 | pubmed:author | pubmed-author:BeguinPP | lld:pubmed |
| pubmed-article:9188092 | pubmed:author | pubmed-author:VerreyFF | lld:pubmed |
| pubmed-article:9188092 | pubmed:author | pubmed-author:ForsterII | lld:pubmed |
| pubmed-article:9188092 | pubmed:author | pubmed-author:BeronJJ | lld:pubmed |
| pubmed-article:9188092 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9188092 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:9188092 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9188092 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9188092 | pubmed:pagination | 387-98 | lld:pubmed |
| pubmed-article:9188092 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:9188092 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9188092 | pubmed:articleTitle | Phorbol 12-myristate 13-acetate down-regulates Na,K-ATPase independent of its protein kinase C site: decrease in basolateral cell surface area. | lld:pubmed |
| pubmed-article:9188092 | pubmed:affiliation | Institute of Physiology, University of Zurich, Switzerland. | lld:pubmed |
| pubmed-article:9188092 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9188092 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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