ArticleEndocrine1996
Effect of colchicine and taxol on thyrotropin-releasing hormone receptor coupling to G protein in GH(3) cells.
Article in Endocrine, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of membrane-associated tubulin in TRH receptor-G protein coupling was investigated with the use of compounds that influence tubulin function. TRH-stimulated G protein GTPase activity in GH(3) cell membranes was used to determine receptor-G protein coupling. TRH-stimulated GTPase activity was abolished by G(qα) antibody, suggesting that TRH receptor coupling to G(q) results in the activation of G(qα) and the subsequent hydrolysis of GTP. TRH (1 μM) stimulated the enzymatic activity by up to 69 pmol/min/mg protein, and in the presence of 1 μM colchicine the hormone-stimulated activity was only 26 pmol/min/mg protein. Similar inhibition of TRH receptor-G protein coupling was observed with tubulin antibodies and purified tubulin, suggesting that perturbation of membrane-associated tubulin and/or tubulin-G protein interaction by these compounds disrupts receptor-G protein interaction. Next, the events occurring at the initial stages of TRH-mediated signal transduction were correlated to prolactin (PRL) secretion in GH(3) cells. Colchicine (1 μM) and taxol (1 μM) inhibited the basal PRL secretion by 38 and 44%, respectively. In addition, colchicine (1 μM) and taxol (1 μM) significantly inhibited TRH-stimulated PRL secretion. TRH-stimulated PRL secretion in control, colchicine-, and taxol-treated cells was 13.9, 9.1, and 6 ng/mL, respectively. Furthermore, polymerized tubulin levels were decreased by colchicine and increased by taxol. These results suggest that perturbation of the steady state of tubulin-G(q) interaction may disrupt the initial events in TRH-mediated signal transduction.
Identifiers
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Registered trials
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