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Article

Immunochemical analysis of the alpha-subunit of the stimulatory G-protein of adenylyl cyclase in patients with Albright's hereditary osteodystrophy.

The Journal of clinical endocrinology and metabolism - 1 Nov 1990

Patten J L, Levine M A

Abstract excerpt

Albright's hereditary osteodystrophy (AHO) is an autosomal dominant disorder characterized by an unusual phenotypic appearance and reduced biological activity of the alpha-subunit of the stimulatory G-protein of adenylyl cyclase (Gs alpha). In most AHO patients deficient Gs alpha activity is asso...

Topics

Adenylyl Cyclases
Cell Membrane
Electrophoresis, Polyacrylamide Gel
Erythrocytes
Fibroblasts
GTP-Binding Proteins
Gene Expression Regulation, Enzymologic
Humans
Immunoblotting
Membrane Proteins
Phenotype

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Pseudohypoparathyroidism

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Identifiers

PMID: 2121768
DOI: 10.1210/jcem-71-5-1208

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026. Prepared record publication-2121768-2026-08-30.1. Manifest publication-graph-cohort-2026-08-30.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 30 Aug 2026.

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Immunochemical analysis of the alpha-subunit of the stimulatory G-protein of adenylyl cyclase in patients with Albright's hereditary osteodystrophy.PMID 2121768Read ↗

A novel Gs alpha mutant in a patient with Albright hereditary osteodystrophy uncouples cell surface receptors from adenylyl cyclase.Semantic proximity Read ↗

Mutation in the gene encoding the stimulatory G protein of adenylate cyclase in Albright's hereditary osteodystrophy.Semantic proximity Read ↗

Analysis of the GNAS1 gene in Albright's hereditary osteodystrophy.Semantic proximity Read ↗

Heterogeneous mutations in the gene encoding the alpha-subunit of the stimulatory G protein of adenylyl cyclase in Albright hereditary osteodystrophy.Semantic proximity Read ↗

The stimulatory G protein alpha-subunit Gs alpha is imprinted in human thyroid glands: implications for thyroid function in pseudohypoparathyroidism types 1A and 1B.Semantic proximity Read ↗

Functional characterization of GNAS mutations found in patients with pseudohypoparathyroidism type Ic defines a new subgroup of pseudohypoparathyroidism affecting selectively Gsα-receptor interaction.Semantic proximity Read ↗

Pseudohypoparathyroidism type Ia. Albright hereditary osteodystrophy: a model for research on G protein-coupled receptors and genomic imprinting.Semantic proximity Read ↗

Determination of Gs alpha protein activity in Albright's hereditary osteodystrophy.Semantic proximity Read ↗

Deficiency of the alpha-subunit of the stimulatory G protein and severe extraskeletal ossification.Semantic proximity Read ↗

Selective resistance to parathyroid hormone caused by a novel uncoupling mutation in the carboxyl terminus of G alpha(s). A cause of pseudohypoparathyroidism type Ib.Semantic proximity Read ↗

An inherited mutation associated with functional deficiency of the alpha-subunit of the guanine nucleotide-binding protein Gs in pseudo- and pseudopseudohypoparathyroidism.Semantic proximity Read ↗

A disruptive mutation in exon 3 of the GNAS gene with albright hereditary osteodystrophy, normocalcemic pseudohypoparathyroidism, and selective long transcript variant Gsalpha-L deficiency.Semantic proximity Read ↗

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