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| pubmed-article:10088994 | lifeskim:mentions | umls-concept:C0006772 | lld:lifeskim |
| pubmed-article:10088994 | lifeskim:mentions | umls-concept:C0033634 | lld:lifeskim |
| pubmed-article:10088994 | lifeskim:mentions | umls-concept:C0443193 | lld:lifeskim |
| pubmed-article:10088994 | lifeskim:mentions | umls-concept:C0220781 | lld:lifeskim |
| pubmed-article:10088994 | lifeskim:mentions | umls-concept:C1515032 | lld:lifeskim |
| pubmed-article:10088994 | lifeskim:mentions | umls-concept:C1883254 | lld:lifeskim |
| pubmed-article:10088994 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:10088994 | lifeskim:mentions | umls-concept:C1522138 | lld:lifeskim |
| pubmed-article:10088994 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:10088994 | pubmed:dateCreated | 1999-5-4 | lld:pubmed |
| pubmed-article:10088994 | pubmed:abstractText | Evidence is accumulating that suggests that Ca2+-calmodulin (Ca2+-CaM) and the protein kinase Cs (PKCs) obstruct each other's actions because of the embedding of PKC phosphorylation sites in CaM or Ca2+-CaM-binding domains of a growing number of crucial substrates in neurons (and other cells). These substrates include the CaM storage proteins (neurogranin, neuromodulin), the membrane-associated MARCKS (myristoylated alanine-rich C-kinase substrate) protein, the NMDA receptor RI subunit and the autoinhibitory domain of the plasma membrane Ca2+ pump. In this review, the emerging data are woven into a hypothetical picture of the conflicting, timing-dependent convergence of two major signalers on neuronal functions. | lld:pubmed |
| pubmed-article:10088994 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10088994 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10088994 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10088994 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10088994 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:10088994 | pubmed:issn | 0166-2236 | lld:pubmed |
| pubmed-article:10088994 | pubmed:author | pubmed-author:ChakravarthiR... | lld:pubmed |
| pubmed-article:10088994 | pubmed:author | pubmed-author:MorleyPP | lld:pubmed |
| pubmed-article:10088994 | pubmed:author | pubmed-author:WhitfieldJJ | lld:pubmed |
| pubmed-article:10088994 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10088994 | pubmed:volume | 22 | lld:pubmed |
| pubmed-article:10088994 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10088994 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10088994 | pubmed:pagination | 12-6 | lld:pubmed |
| pubmed-article:10088994 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:10088994 | pubmed:meshHeading | pubmed-meshheading:10088994... | lld:pubmed |
| pubmed-article:10088994 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10088994 | pubmed:articleTitle | Ca2+-calmodulin and protein kinase Cs: a hypothetical synthesis of their conflicting convergences on shared substrate domains. | lld:pubmed |
| pubmed-article:10088994 | pubmed:affiliation | Institute for Biological Sciences, National Research Council of Canada, Ottawa, Ontario. | lld:pubmed |
| pubmed-article:10088994 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10088994 | pubmed:publicationType | Review | lld:pubmed |
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