| pubmed-article:8622915 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C0040300 | lld:lifeskim |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C0001492 | lld:lifeskim |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C0086376 | lld:lifeskim |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C0599220 | lld:lifeskim |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C0205349 | lld:lifeskim |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C0449774 | lld:lifeskim |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:8622915 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:8622915 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:8622915 | pubmed:dateCreated | 1996-6-18 | lld:pubmed |
| pubmed-article:8622915 | pubmed:abstractText | The inhibition of alpha i2-/- mouse cardiac isoproterenol-stimulated adenylyl cyclase (AC; EC 4.6.1.1) activity by carbachol and that of alpha i2-/- adipocyte AC by phenylisopropyladenosine (PIA), prostaglandin E2, and nicotinic acid were partially, but not completely, inhibited. While the inhibition of cardiac AC was affected in all alpha i2-/- animals tested, only 50% of the alpha i2-/- animals showed an impaired inhibition of adipocyte AC, indicative of a partial penetrance of this phenotype. In agreement with previous results, the data show that Gi2 mediates hormonal inhibition of AC and that Gi3 and/or Gi1 is capable of doing the same but with a lower efficacy. Disruption of the alpha i2 gene affected about equally the actions of all the receptors studied, indicating that none of them exhibits a striking specificity for one type of Gi over another and that receptors are likely to he selective rather than specific in their interaction with functionally homologous G proteins (e.g., Gi1, Gi2, Gi3). Western analysis of G protein subunit levels in simian virus 40-transformed primary embryonic fibroblasts from alpha i2+/+ and alpha i2-/- animals showed that alpha i2 accounts for about 50% of the immunopositive G protein alpha subunits and that loss of the alpha i2 is accompanied by a parallel reduction in G beta 35 and G beta 36 subunits and by a 30-50% increase in alpha i3. This suggests that G beta-gamma levels may be regulated passively through differential rates of turnover in their free vs. trimeric states. The existence of compensatory increase(s) in alpha i subunit expression raises the possibility that the lack of effect of a missing alpha i2 on AC inhibition in adipocytes of some alpha i2-/- animals may be the reflection of a more pronounced compensatory expression of alpha i3 and/or alpha i1. | lld:pubmed |
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| pubmed-article:8622915 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8622915 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8622915 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8622915 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:8622915 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:8622915 | pubmed:author | pubmed-author:BirnbaumerLL | lld:pubmed |
| pubmed-article:8622915 | pubmed:author | pubmed-author:RudolphUU | lld:pubmed |
| pubmed-article:8622915 | pubmed:author | pubmed-author:SpicherKK | lld:pubmed |
| pubmed-article:8622915 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8622915 | pubmed:day | 16 | lld:pubmed |
| pubmed-article:8622915 | pubmed:volume | 93 | lld:pubmed |
| pubmed-article:8622915 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8622915 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8622915 | pubmed:pagination | 3209-14 | lld:pubmed |
| pubmed-article:8622915 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8622915 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8622915 | pubmed:articleTitle | Adenylyl cyclase inhibition and altered G protein subunit expression and ADP-ribosylation patterns in tissues and cells from Gi2 alpha-/-mice. | lld:pubmed |
| pubmed-article:8622915 | pubmed:affiliation | Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030, USA. | lld:pubmed |
| pubmed-article:8622915 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8622915 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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