| pubmed-article:1455507 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1455507 | lifeskim:mentions | umls-concept:C0014136 | lld:lifeskim |
| pubmed-article:1455507 | lifeskim:mentions | umls-concept:C0030274 | lld:lifeskim |
| pubmed-article:1455507 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:1455507 | lifeskim:mentions | umls-concept:C0017725 | lld:lifeskim |
| pubmed-article:1455507 | lifeskim:mentions | umls-concept:C0178566 | lld:lifeskim |
| pubmed-article:1455507 | lifeskim:mentions | umls-concept:C0086035 | lld:lifeskim |
| pubmed-article:1455507 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:1455507 | pubmed:dateCreated | 1993-1-6 | lld:pubmed |
| pubmed-article:1455507 | pubmed:abstractText | Crosstalk between intracellular signalling systems is recognized as the principal means by which a cell orchestrates coordinate responses to stimulation by neurotransmitters, hormones or growth factors. The functional consequences of crosstalk are evident at multiple levels within a given signalling cascade, including the regulation of receptor-ligand interactions, guanine nucleotide-binding proteins, enzyme activities, ion channel function and gene expression. Here we focus on the pancreatic beta-cells of the islets of Langerhans to illustrate the important role crosstalk plays in the regulation of glucose-induced insulin secretion. Recent studies indicating a synergistic interaction in beta-cells between the glucose-regulated ATP-dependent signalling system and the hormonally regulated cAMP-dependent signalling system are emphasized. This interaction gives beta-cells the ability to match the ambient concentration of glucose to an appropriate insulin secretory response, a process we refer to as the induction of glucose competence. The glucose competence concept may provide new insights into the etiology and treatment of non-insulin-dependent diabetes mellitus (Type II diabetes). | lld:pubmed |
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| pubmed-article:1455507 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1455507 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1455507 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1455507 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1455507 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:1455507 | pubmed:issn | 0968-0004 | lld:pubmed |
| pubmed-article:1455507 | pubmed:author | pubmed-author:HabenerJ FJF | lld:pubmed |
| pubmed-article:1455507 | pubmed:author | pubmed-author:HungJ SJS | lld:pubmed |
| pubmed-article:1455507 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1455507 | pubmed:volume | 17 | lld:pubmed |
| pubmed-article:1455507 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1455507 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1455507 | pubmed:pagination | 388-93 | lld:pubmed |
| pubmed-article:1455507 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:1455507 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1455507 | pubmed:articleTitle | Signal transduction crosstalk in the endocrine system: pancreatic beta-cells and the glucose competence concept. | lld:pubmed |
| pubmed-article:1455507 | pubmed:affiliation | Laboratory of Molecular Endocrinology, Massachusetts General Hospital, Boston. | lld:pubmed |
| pubmed-article:1455507 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1455507 | pubmed:publicationType | Review | lld:pubmed |
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