| pubmed-article:1646818 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1646818 | lifeskim:mentions | umls-concept:C0330390 | lld:lifeskim |
| pubmed-article:1646818 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:1646818 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:1646818 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:1646818 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:1646818 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:1646818 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:1646818 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:1646818 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:1646818 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:1646818 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:1646818 | pubmed:dateCreated | 1991-7-24 | lld:pubmed |
| pubmed-article:1646818 | pubmed:abstractText | Cross-regulation from the stimulatory (Gs alpha)-mediated) to the inhibitory (Gi alpha-mediated) pathways controlling adenylylcyclase has been described (Hadcock, J. R., Ros, M., Watkins, D. C., and Malbon, C. C. (1990) J. Biol. Chem. 265, 14784-14790). The extent to which cross-regulation occurs from inhibitory to stimulatory pathways for adenylylcyclase was explored. Persistent activation of the inhibitory pathway of adenylylcyclase by the A1-adenosine receptor agonist (-)-N6 (R-phenylisopropyl) adenosine (PIA) in hamster smooth muscle DDT1 MF-2 cells enhanced the stimulatory pathway of adenylylcyclase and its activation by the beta 2-adrenergic receptor agonist isoproterenol. PIA treatment (48 h) of cells increased isoproterenol-stimulated adenylylcyclase by 2-fold. In addition, the ED50 for stimulation of adenylylcyclase by isoproterenol decreased 50-fold to approximately 1 nM. Persistent activation of cells with PIA increased beta 2-adrenergic receptor number in a time- and dose-dependent manner. The steady-state levels of beta 2-adrenergic receptors (radioligand binding and immunoblotting) and receptor mRNA levels increased by more than 70%, while the half-life of the receptor (24 h) was unaltered. Both A1-adenosine receptor binding and Gi alpha 2 levels declined by half in cells persistently activated with PIA. Although Gi alpha 2 mRNA levels and the relative rate of synthesis of Gi alpha 2 protein upon persistent activation of the inhibitory pathway were found to increase, a decrease in the half-life of Gi alpha 2 from approximately 75 h in naive cells to approximately 40 in cells provides the basis for the decline in Gi alpha 2 levels. The steady-state level of mRNA and half-life of Gs alpha protein were unaltered in persistently activated cells. Thus, activation of the inhibitory pathway of adenylylcyclase cross-regulates the stimulatory, hormone-sensitive adenylylcyclase system by: (i) up-regulating beta 2-adrenergic receptors and enhancing the activation of the stimulatory adenylylcyclase pathway and (ii) down-regulating elements of the inhibitory adenylylcyclase pathway (Gi alpha 2 and A1-adenosine receptor binding). | lld:pubmed |
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| pubmed-article:1646818 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1646818 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1646818 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1646818 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:1646818 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:1646818 | pubmed:author | pubmed-author:MalbonC CCC | lld:pubmed |
| pubmed-article:1646818 | pubmed:author | pubmed-author:PortJ DJD | lld:pubmed |
| pubmed-article:1646818 | pubmed:author | pubmed-author:HadcockJ RJR | lld:pubmed |
| pubmed-article:1646818 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1646818 | pubmed:day | 25 | lld:pubmed |
| pubmed-article:1646818 | pubmed:volume | 266 | lld:pubmed |
| pubmed-article:1646818 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1646818 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1646818 | pubmed:pagination | 11915-22 | lld:pubmed |
| pubmed-article:1646818 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:1646818 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1646818 | pubmed:articleTitle | Cross-regulation between G-protein-mediated pathways. Activation of the inhibitory pathway of adenylylcylclase increases the expression of beta 2-adrenergic receptors. | lld:pubmed |
| pubmed-article:1646818 | pubmed:affiliation | Department of Pharmacology, Diabetes and Metabolic Diseases Research Program, School of Medicine, State University of New York, Stony Brook 11794-8651. | lld:pubmed |
| pubmed-article:1646818 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1646818 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1646818 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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