| pubmed-article:6325502 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:6325502 | lifeskim:mentions | umls-concept:C1180347 | lld:lifeskim |
| pubmed-article:6325502 | lifeskim:mentions | umls-concept:C0033806 | lld:lifeskim |
| pubmed-article:6325502 | lifeskim:mentions | umls-concept:C0221099 | lld:lifeskim |
| pubmed-article:6325502 | lifeskim:mentions | umls-concept:C0815047 | lld:lifeskim |
| pubmed-article:6325502 | lifeskim:mentions | umls-concept:C1522492 | lld:lifeskim |
| pubmed-article:6325502 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:6325502 | pubmed:dateCreated | 1984-6-5 | lld:pubmed |
| pubmed-article:6325502 | pubmed:abstractText | Decreased activity of the guanine nucleotide regulatory protein (N) of the adenylate cyclase system is present in cell membranes of some patients with pseudohypoparathyrodism (PHP-Ia) whereas others have normal activity of N (PHP-Ib). Low N activity in PHP-Ia results in a decrease in hormone (H)-stimulatable adenylate cyclase in various tissues, which might be due to decreased ability to form an agonist-specific high affinity complex composed of H, receptor (R), and N. To test this hypothesis, we compared beta-adrenergic agonist-specific binding properties in erythrocyte membranes from five patients with PHP-Ia (N = 45% of control), five patients with PHP-Ib (N = 97%), and five control subjects. Competition curves that were generated by increasing concentrations of the beta-agonist isoproterenol competing with [125I]pindolol were shallow (slope factors less than 1) and were computer fit to a two-state model with corresponding high and low affinity for the agonist. The agonist competition curves from the PHP-Ia patients were shifted significantly (P less than 0.02) to the right as a result of a significant (P less than 0.01) decrease in the percent of beta-adrenergic receptors in the high affinity state from 64 +/- 22% in PHP-Ib and 56 +/- 5% in controls to 10 +/- 8% in PHP-Ia. The agonist competition curves were computer fit to a "ternary complex" model for the two-step reaction: H + R + N in equilibrium HR + N in equilibrium HRN. The modeling was consistent with a 60% decrease in the functional concentration of N, and was in good agreement with the biochemically determined decrease in erythrocyte N protein activity. These in vitro findings in erythrocytes taken together with the recent observations that in vivo isoproterenol-stimulated adenylate cyclase activity is decreased in patients with PHP (Carlson, H. E., and A. S. Brickman, 1983, J. Clin. Endocrinol. Metab. 56:1323-1326) are consistent with the notion that N is a bifunctional protein interacting with both R and the adenylate cyclase. It may be that in patients with PHP-Ia a single molecular and genetic defect accounts for both decreased HRN formation and decreased adenylate cyclase activity, whereas in PHP-Ib the biochemical lesion(s) appear not to affect HRN complex formation. | lld:pubmed |
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| pubmed-article:6325502 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:6325502 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:6325502 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:6325502 | pubmed:month | May | lld:pubmed |
| pubmed-article:6325502 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:6325502 | pubmed:author | pubmed-author:LefkowitzR... | lld:pubmed |
| pubmed-article:6325502 | pubmed:author | pubmed-author:CaronM GMG | lld:pubmed |
| pubmed-article:6325502 | pubmed:author | pubmed-author:De LeanAA | lld:pubmed |
| pubmed-article:6325502 | pubmed:author | pubmed-author:SpiegelA MAM | lld:pubmed |
| pubmed-article:6325502 | pubmed:author | pubmed-author:DreznerM KMK | lld:pubmed |
| pubmed-article:6325502 | pubmed:author | pubmed-author:LevineM AMA | lld:pubmed |
| pubmed-article:6325502 | pubmed:author | pubmed-author:WreggettK AKA | lld:pubmed |
| pubmed-article:6325502 | pubmed:author | pubmed-author:DownsR WRW | lld:pubmed |
| pubmed-article:6325502 | pubmed:author | pubmed-author:DaviesA OAO | lld:pubmed |
| pubmed-article:6325502 | pubmed:author | pubmed-author:HeinsimerJ... | lld:pubmed |
| pubmed-article:6325502 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:6325502 | pubmed:volume | 73 | lld:pubmed |
| pubmed-article:6325502 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:6325502 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:6325502 | pubmed:pagination | 1335-43 | lld:pubmed |
| pubmed-article:6325502 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:6325502 | pubmed:year | 1984 | lld:pubmed |
| pubmed-article:6325502 | pubmed:articleTitle | Impaired formation of beta-adrenergic receptor-nucleotide regulatory protein complexes in pseudohypoparathyroidism. | lld:pubmed |
| pubmed-article:6325502 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:6325502 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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