ArticleMolecular pharmacology2011
Thyrotropin receptor stimulates internalization-independent persistent phosphoinositide signaling.
Article in Molecular pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Genotype Combinations and Genetic Risk Score Analyses ofCurrent issues in molecular biology · 2025Article
- Amelioration of Glutamate-induced Toxicity by a New Thyrotropin-releasing Hormone (TRH) Analogue PYR-l-(2,5-Dibromo)-His-l-ProNHAnnals of neurosciences · 2025Article
- The Role of Inositol in Thyroid Physiology and in Subclinical Hypothyroidism Management.Frontiers in endocrinology · 2021Review
- Structural-Functional Features of the Thyrotropin Receptor: A Class A G-Protein-Coupled Receptor at Work.Frontiers in endocrinology · 2017Review
- Multiple Transduction Pathways Mediate Thyrotropin Receptor Signaling in Preosteoblast-Like Cells.Endocrinology · 2016Article
- Kinin-stimulated B1 receptor signaling depends on receptor endocytosis whereas B2 receptor signaling does not.Neurochemical research · 2014Article
- GPCR signaling along the endocytic pathway.Current opinion in cell biology · 2014Review
- Persistent cAMP signaling by TSH receptors revealed by phosphodiesterase inhibition.Thyroid : official journal of the American Thyroid Association · 2013Article
- A small molecule antagonist inhibits thyrotropin receptor antibody-induced orbital fibroblast functions involved in the pathogenesis of Graves ophthalmopathy.The Journal of clinical endocrinology and metabolism · 2013Article
- Update in TSH receptor agonists and antagonists.The Journal of clinical endocrinology and metabolism · 2012Review
- Persistent signaling by thyrotropin-releasing hormone receptors correlates with G-protein and receptor levels.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The thyrotropin [thyroid-stimulating hormone (TSH)] receptor (TSHR) is known to acutely and persistently stimulate cAMP signaling and at higher TSH concentrations to acutely stimulate phosphoinositide signaling. We measured persistent signaling by stimulating TSHR-expressing human embryonic kidney-EM293 cells with TSH and measuring cAMP or inositol monophosphate (IP1) production, a measure of phosphoinositide signaling, 60 min or longer after TSH removal. In contrast to persistent cAMP production, persistent IP1 production increased progressively when TSH exposure was increased from 1 to 30 min, whereas the rates of decay of persistent signaling were similar. A small-molecule agonist and a thyroid-stimulating antibody also caused persistent IP1 and cAMP signaling. A small-molecule inverse agonist and a neutral antagonist inhibited TSH-stimulated persistent IP1 production, whereas the inverse agonist but not the neutral antagonist inhibited persistent cAMP production. As with persistent cAMP production, persistent IP1 production was not affected when TSHR internalization was inhibited or enhanced. Moreover, Alexa546-TSH-activated TSHR internalization was not accompanied by Gα(q) coupling protein internalization. Thus, transient exposure to high concentrations of TSH causes persistent phosphoinositide and cAMP signaling that is not dependent on internalization. To our knowledge, this is the first demonstration of persistent activation by any G protein-coupled receptor (GPCR) via the Gα(q) pathway and of two G protein-mediated pathways by any GPCR.
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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.