ArticleEndocrinology2009
Characterization of thyrotropin receptor antibody-induced signaling cascades.
Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 163 citations in OpenAlex.
- TSH suppression therapy from an individualized perspective: from mechanism to clinical decision-making.Frontiers in endocrinology · 2026Review
- Molecular and Functional Insights into Thyrostimulin and Its Subunits-GPA2/GPB5.International journal of molecular sciences · 2025Review
- Monoclonal Antibodies to Thyrotropin Receptor With Thyroid-Stimulating Activity Activate the NF-κB Pathway to Induce Chemokine Expression.Journal of cellular and molecular medicine · 2025Article
- Molecular pathway and mechanism responsible for the progress of thyroid-associated orbitopathy.International ophthalmology · 2025Review
- Proangiogenic effect of thyrotropin receptor stimulating antibody in human umbilical vein endothelial cells.Endocrine · 2025Article
- Transcriptomic analysis reveals a critical role for activating GScientific reports · 2024Article
- Graves disease: latest understanding of pathogenesis and treatment options.Nature reviews. Endocrinology · 2024Review
- The TSH Receptor Antibody Reactome Contributes to Retro-Orbital Inflammation.Journal of the Endocrine Society · 2024Article
- Cytokine Storm-Induced Thyroid Dysfunction in COVID-19: Insights into Pathogenesis and Therapeutic Approaches.Drug design, development and therapy · 2024Review
- Article
- TSH enhances neurite outgrowth.Frontiers in endocrinology · 2024Article
- Prevalence of Papillary Thyroid Carcinoma is Significantly Higher in Graves Disease with Synchronous Thyroid Nodules.Turk patoloji dergisi · 2024Article
- Allosteric Regulation of G-Protein-Coupled Receptors: From Diversity of Molecular Mechanisms to Multiple Allosteric Sites and Their Ligands.International journal of molecular sciences · 2023Review
- The Clinical Implications of Anti-thyroid Peroxidase Antibodies in Graves' Disease in Basrah.Cureus · 2023Article
- Poly (lactic-co-glycolic acid)-encapsulated iodine-131 nanoparticles fabricated with rhTSH induce apoptosis and immobilization of thyroid cancer cells.Frontiers in oncology · 2023Article
- Article
- Mechanisms in Graves Eye Disease: Apoptosis as the End Point of Insulin-Like Growth Factor 1 Receptor Inhibition.Thyroid : official journal of the American Thyroid Association · 2022Article
- Rescue of thyroid cells from antibody induced cell death via induction of autophagy.Journal of autoimmunity · 2022Article
- Insulin-Like Growth Factor Pathway and the Thyroid.Frontiers in endocrinology · 2021Review
- Epstein-Barr Virus Reactivation-Induced Immunoglobulin Production: Significance on Autoimmunity.Microorganisms · 2020Review
9 more citing papers are in PubMed but not listed here.
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
Abstract
The TSH receptor (TSHR) is constitutively active and is further enhanced by TSH ligand binding or by stimulating TSHR antibodies (TSHR-Abs) as seen in Graves' disease. TSH is known to activate the thyroid epithelial cell via both Galphas-cAMP/protein kinase A/ERK and Galphaq-Akt/protein kinase C coupled signaling networks. The recent development of monoclonal antibodies to the TSHR has enabled us to investigate the hypothesis that different TSHR-Abs may have unique signaling imprints that differ from TSH ligand itself. We have, therefore, performed sequential studies, using rat thyrocytes (FRTL-5, passages 5-20) as targets, to examine the signaling pathways activated by a series of monoclonal TSHR-Abs in comparison with TSH itself. Activation of key signaling molecules was estimated by specific immunoblots and/or enzyme immunoassays. Continuing constitutive TSHR activity in thyroid cells, deprived of TSH and serum for 48 h, was demonstrated by pathway-specific chemical inhibition. Under our experimental conditions, TSH ligand and TSHR-stimulating antibodies activated both Galphas and Galphaq effectors. Importantly, some TSHR-blocking and TSHR-neutral antibodies were also able to generate signals, influencing primarily the Galphaq effectors and induced cell proliferation. Most strikingly, antibodies that used the Galphaq cascades used c-Raf-ERK-p90RSK as a unique signaling cascade not activated by TSH. Our study demonstrated that individual TSHR-Abs had unique molecular signatures which resulted in sequential preferences. Because downstream thyroid cell signaling by the TSHR is both ligand dependent and independent, this may explain why TSHR-Abs are able to have variable influences on thyroid cell biology.
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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.