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| pubmed-article:8382496 | lifeskim:mentions | umls-concept:C0034650 | lld:lifeskim |
| pubmed-article:8382496 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:8382496 | lifeskim:mentions | umls-concept:C0033634 | lld:lifeskim |
| pubmed-article:8382496 | lifeskim:mentions | umls-concept:C0288263 | lld:lifeskim |
| pubmed-article:8382496 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:8382496 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
| pubmed-article:8382496 | lifeskim:mentions | umls-concept:C1627358 | lld:lifeskim |
| pubmed-article:8382496 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:8382496 | pubmed:dateCreated | 1993-3-26 | lld:pubmed |
| pubmed-article:8382496 | pubmed:abstractText | The effect of protein kinase C (PKC) stimulation on Ca2+ channels was studied in frog sympathetic neurons. 12,13-Phorbol dibutyrate (PDBu) consistently augmented Ca2+ channel currents in whole-cell recordings. This enhancement was blocked by staurosporine and PKC(19-31), but not produced by 4 alpha-phorbol 12,13-didecanoate, indicating that PDBu acts via PKC. Both N- and L-type currents, as isolated pharmacologically, were increased. PKC enhancement was independent of the extent of G protein activation, indicating that it was not caused by removal of tonic G protein inhibition. In unitary recordings PDBu produced dramatic increases in single N- and L-type channel activity by sharply decreasing closed time intervals between adjacent openings, but did not alter the unitary current size or mean open time. This up-modulation by PKC may constitute a positive feedback mechanism in the regulation of neuronal Ca2+ channel activity. | lld:pubmed |
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| pubmed-article:8382496 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8382496 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8382496 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8382496 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:8382496 | pubmed:issn | 0896-6273 | lld:pubmed |
| pubmed-article:8382496 | pubmed:author | pubmed-author:TsienR WRW | lld:pubmed |
| pubmed-article:8382496 | pubmed:author | pubmed-author:YangJJ | lld:pubmed |
| pubmed-article:8382496 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8382496 | pubmed:volume | 10 | lld:pubmed |
| pubmed-article:8382496 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8382496 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8382496 | pubmed:pagination | 127-36 | lld:pubmed |
| pubmed-article:8382496 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:8382496 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8382496 | pubmed:articleTitle | Enhancement of N- and L-type calcium channel currents by protein kinase C in frog sympathetic neurons. | lld:pubmed |
| pubmed-article:8382496 | pubmed:affiliation | Department of Molecular and Cellular Physiology, Stanford University, California 94305. | lld:pubmed |
| pubmed-article:8382496 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8382496 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8382496 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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