| pubmed-article:15666084 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15666084 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:15666084 | lifeskim:mentions | umls-concept:C0033634 | lld:lifeskim |
| pubmed-article:15666084 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:15666084 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:15666084 | pubmed:dateCreated | 2005-1-24 | lld:pubmed |
| pubmed-article:15666084 | pubmed:abstractText | Pharmacological studies with drugs that activate or inhibit several protein kinase C (PKC) isozymes have identified the PKC family of serine-threonine kinases as important in the regulation of gamma-aminobutyric acid type A (GABA(A)) receptor function. PKC modulates GABA(A) receptor surface density, chloride conductance and receptor sensitivity to positive allosteric modulators such as neurosteroids, ethanol, benzodiazepines and barbiturates. Recent studies using PKC isozyme-selective reagents and gene-targeted mice have begun to identify critical roles for three isozymes, PKCbetaII, PKCvarepsilon and PKCgamma, in various aspects of GABA(A) receptor regulation. Progress in this field touches upon therapeutic areas that are of great clinical importance such as anxiety and addiction. Increased understanding of how PKC regulates GABA(A) receptors and which PKC isozymes are involved holds promise for development of new treatments for diverse neuropsychiatric disorders. | lld:pubmed |
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| pubmed-article:15666084 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15666084 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15666084 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15666084 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15666084 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:15666084 | pubmed:issn | 1420-682X | lld:pubmed |
| pubmed-article:15666084 | pubmed:author | pubmed-author:SongMM | lld:pubmed |
| pubmed-article:15666084 | pubmed:author | pubmed-author:MessingR ORO | lld:pubmed |
| pubmed-article:15666084 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15666084 | pubmed:volume | 62 | lld:pubmed |
| pubmed-article:15666084 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15666084 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15666084 | pubmed:pagination | 119-27 | lld:pubmed |
| pubmed-article:15666084 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
| pubmed-article:15666084 | pubmed:meshHeading | pubmed-meshheading:15666084... | lld:pubmed |
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| pubmed-article:15666084 | pubmed:meshHeading | pubmed-meshheading:15666084... | lld:pubmed |
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| pubmed-article:15666084 | pubmed:meshHeading | pubmed-meshheading:15666084... | lld:pubmed |
| pubmed-article:15666084 | pubmed:meshHeading | pubmed-meshheading:15666084... | lld:pubmed |
| pubmed-article:15666084 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15666084 | pubmed:articleTitle | Protein kinase C regulation of GABAA receptors. | lld:pubmed |
| pubmed-article:15666084 | pubmed:affiliation | Ernest Gallo Clinic and Research Center, Department of Neurology, Graduate Program in Neuroscience, University of California, San Francisco, 5858 Horton Street, Suite 200, Emeryville, California, 94608, USA. | lld:pubmed |
| pubmed-article:15666084 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15666084 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15666084 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:15666084 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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