ArticleThe Biochemical journal2004
Agonist-dependent up-regulation of thyrotrophin-releasing hormone receptor protein.
Article in The Biochemical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Developmental and tissue-specific expression of thyrotropin-releasing hormone signaling genes in zebrafish and its association with glycemic regulation.Biology open · 2026Article
- Genetic and Functional Analyses of Patients with Marked Hypo-High-Density Lipoprotein Cholesterolemia.Journal of atherosclerosis and thrombosis · 2024Article
- Biochemical and physiological insights into TRH receptor-mediated signaling.Frontiers in cell and developmental biology · 2022Review
- Glutamate differently modulates metabotropic glutamate receptors in neuronal and glial cells.Neurochemical research · 2010Article
- Subcellular trafficking of the TRH receptor: effect of phosphorylation.Molecular endocrinology (Baltimore, Md.) · 2009Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
To study the effect of agonist on the TRH (thyrotrophin-releasing hormone) receptor protein, an epitope-tagged receptor was stably expressed in HEK-293 cells (human embryonic kidney 293 cells) and receptor levels were measured by immunoblotting. TRH caused a 5-25-fold increase in receptor protein during 48 h, which was half-maximal at 1 nM and was slowly reversible after hormone withdrawal. Chlordiazepoxide, an inverse agonist, had no effect. TRH up-regulation was mimicked by phorbol ester and blocked by the protein kinase C inhibitor GF109203X in combination with thapsigargin, which prevents a calcium response. TRH and phorbol ester increased the density of immunoreactive receptors localized at the cell surface and [3H]MeTRH (where MeTRH stands for [N3-methyl-His]TRH) binding. TRH also increased the concentration of a truncated, internalization-defective receptor. Analysis of cell lines stably expressing TRH receptors fused to the green fluorescent protein on a fluorescence-activated cell sorter showed that TRH and phorbol ester caused 2.7- and 6.8-fold increases in fusion protein expression respectively. TRH receptor up-regulation was only partially accounted for by changes in receptor mRNA, which increased 1.7-fold. TRH caused a small increase in receptor concentration in the presence of cycloheximide, actinomycin D or MG132. In contrast with the results obtained with the TRH receptor, agonist decreased the concentration of stably expressed b2-adrenergic receptors. These results show that TRH increases receptor concentration by a complex mechanism that requires signal transduction but not receptor endocytosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.