ArticleEndocrinology2017
TSH/IGF-1 Receptor Cross-Talk Rapidly Activates Extracellular Signal-Regulated Kinases in Multiple Cell Types.
Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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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
34 citing papers in PubMed, 48 citations in OpenAlex.
- The IGF signaling axis in thyroid cancer: biological complexity and therapeutic challenges.Endocrine connections · 2026Review
- Exploring the Therapeutic Mechanism of Xiehuo Pingtu San in Treating Thyroid Eye Disease Based on Network Pharmacology, Molecular Docking, and Molecular Dynamics Simulation.International journal of endocrinology · 2026Article
- Thyroid hormone signaling in ocular development and diseases.Biological research · 2025Review
- Article
- Effects of linsitinib on M22 and IGF:1-treated 3D spheroids of human orbital fibroblasts.Scientific reports · 2025Article
- Review
- Defining theThyroid : official journal of the American Thyroid Association · 2024Article
- Linsitinib inhibits proliferation and induces apoptosis of both IGF-1R and TSH-R expressing cells.Frontiers in immunology · 2024Article
- Article
- Potential involvement of the bone marrow in experimental Graves' disease and thyroid eye disease.Frontiers in endocrinology · 2023Article
- A review of TSHR- and IGF-1R-related pathogenesis and treatment of Graves' orbitopathy.Frontiers in immunology · 2023Review
- Linsitinib, an IGF-1R inhibitor, attenuates disease development and progression in a model of thyroid eye disease.Frontiers in endocrinology · 2023Article
- Research progress in Th17 cells and the relevant cytokines in GravesZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- Inhibition of TSH/IGF-1 Receptor Crosstalk by Teprotumumab as a Treatment Modality of Thyroid Eye Disease.The Journal of clinical endocrinology and metabolism · 2022Article
- Research progress on the pathogenesis of Graves' ophthalmopathy: Based on immunity, noncoding RNA and exosomes.Frontiers in immunology · 2022Review
- Graves' Autoantibodies Exhibit Different Stimulating Activities in Cultures of Thyrocytes and Orbital Fibroblasts Not Reflected by Clinical Assays.Thyroid : official journal of the American Thyroid Association · 2022Article
- New Therapeutic Horizon of Graves' Hyperthyroidism: Treatment Regimens Based on Immunology and Ingredients From Traditional Chinese Medicine.Frontiers in pharmacology · 2022Review
- Human leucocyte antigen alleles confer susceptibility and progression to Graves' ophthalmopathy in a Southern Chinese population.The British journal of ophthalmology · 2021Article
- COVID-19 and the Endocrine System: A Comprehensive Review on the Theme.Journal of clinical medicine · 2021Review
- Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
We previously showed that thyrotropin (TSH)/insulinlike growth factor (IGF)-1 receptor cross-talk appears to be involved in Graves' orbitopathy (GO) pathogenesis and upregulation of thyroid-specific genes in human thyrocytes. In orbital fibroblasts from GO patients, coadministration of TSH and IGF-1 induces synergistic increases in hyaluronan secretion. In human thyrocytes, TSH plus IGF-1 synergistically increased expression of the sodium-iodide symporter that appeared to involve ERK1/2 activation. However, the details of ERK1/2 activation were not known, nor was whether ERK1/2 was involved in this synergism in other cell types. Using primary cultures of GO fibroblasts (GOFs) and human thyrocytes, as well as human embryonic kidney (HEK) 293 cells overexpressing TSH receptors (HEK-TSHRs), we show that simultaneous activation of TSHRs and IGF-1 receptors (IGF-1Rs) causes rapid, synergistic phosphorylation/activation of ERK1 and ERK2 in all three cell types. This effect is partially inhibited by pertussis toxin, an inhibitor of TSHR coupling to Gi/Go proteins. In support of a role for Gi/Go proteins in ERK1/2 phosphorylation, we found that knockdown of Gi(1-3) and Go in HEK-TSHRs inhibited ERK1/2 phosphorylation stimulated by TSH and TSH plus IGF-1. These data demonstrate that the synergistic effects of TSH plus IGF-1 occur early in the TSHR signaling cascade and further support the idea that TSHR/IGF-1R cross-talk is an important mechanism for regulation of human GOFs and thyrocytes.
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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.