Gonadotrophin-releasing hormone receptor agonist-mediated down-regulation of Gq alpha/G11 alpha (pertussis toxin-insensitive) G proteins in alpha T3-1 gonadotroph cells reflects increased G protein turnover but not alterations in mRNA levels.
basic_science · Level V
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- Record sourced from PubMed, PMID 7892195.
- Also identified by PMC identifier 42387.
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Abstract
Prolonged exposure of alpha T3-1 pituitary gonadotrophs to a gonadotrophin-releasing hormone receptor agonist results in marked down-regulation of the pertussis toxin-insensitive G proteins Gq alpha and G11 alpha. The turnover of Gq alpha/G11 alpha was substantially accelerated in the presence of agonist. By contrast, the rate of degradation of the G protein Gi2 alpha was unaffected by agonist treatment. Analysis of Gq alpha/G11 alpha mRNA levels by reverse transcription-PCR demonstrated no detectable differences between control and agonist-treated cells. These studies indicate that gonadotrophin-releasing hormone receptor agonist-mediated down-regulation of Gq alpha/G11 alpha is a reflection of enhanced proteolysis of the activated G proteins.
Medical subject headings
- GTP-Binding Proteins
- Gene Expression Regulation
- Gonadotropin-Releasing Hormone
- Pertussis Toxin
- Receptors, LH
- Virulence Factors, Bordetella