ArticleEndocrinology2019
Arrestin-β-1 Physically Scaffolds TSH and IGF1 Receptors to Enable Crosstalk.
Article in Endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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
36 citing papers in PubMed, 50 citations in OpenAlex.
- Thyroid hormone signaling in ocular development and diseases.Biological research · 2025Review
- Thyroid-related orbitopathy: clinical overview, novel medical treatments and the role of orbital surgery.International ophthalmology · 2025Review
- Linsitinib Decreases Thyrotropin-Induced Thyroid Hormone Synthesis by Inhibiting Crosstalk Between Thyroid-Stimulating Hormone and Insulin-Like Growth Factor 1 Receptors in Human ThyrocytesThyroid : official journal of the American Thyroid Association · 2025Article
- Mechanisms in Thyroid Eye Disease: The TSH Receptor Interacts Directly With the IGF-1 Receptor.Endocrinology · 2025Article
- Unexpected Crosslinking Effects of a Human Thyroid Stimulating Monoclonal Autoantibody, M22, with IGF1 on Adipogenesis in 3T3L-1 Cells.International journal of molecular sciences · 2023Article
- Linsitinib, an IGF-1R inhibitor, attenuates disease development and progression in a model of 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
- Opposing Effects of EGF Receptor Signaling on Proliferation and Differentiation Initiated by EGF or TSH/EGF Receptor Transactivation.Endocrinology · 2022Article
- The risk factors for Graves' ophthalmopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022Review
- 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
- 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
- 2021 update on thyroid-associated ophthalmopathy.Journal of endocrinological investigation · 2022Review
- TSH stimulation of human thyroglobulin and thyroid peroxidase gene transcription is partially dependent on internalization.Cellular signalling · 2022Article
- Is Estrogen a Missing Culprit in Thyroid Eye Disease? Sex Steroid Hormone Homeostasis Is Key to Other Fibrogenic Autoimmune Diseases - Why Not This One?Frontiers in immunology · 2022Article
- Proximity ligation assay to study TSH receptor homodimerization and crosstalk with IGF-1 receptors in human thyroid cells.Frontiers in endocrinology · 2022Article
- Research progress on the pathogenesis of Graves' ophthalmopathy: Based on immunity, noncoding RNA and exosomes.Frontiers in immunology · 2022Review
- Cytokines in Thyroid-Associated Ophthalmopathy.Journal of immunology research · 2022Review
- New Therapeutic Horizon of Graves' Hyperthyroidism: Treatment Regimens Based on Immunology and Ingredients From Traditional Chinese Medicine.Frontiers in pharmacology · 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
- Pharmacokinetics and Exposure-Response Relationship of Teprotumumab, an Insulin-Like Growth Factor-1 Receptor-Blocking Antibody, in Thyroid Eye Disease.Clinical pharmacokinetics · 2021Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Endogenously expressed TSH receptors (TSHRs) on orbital fibroblasts of patients with Graves ophthalmopathy (GO) use crosstalk with IGF1 receptors (IGF1R) to synergistically stimulate secretion of hyaluronan (HA), a major component of GO pathology. We previously showed crosstalk occurred upstream of mitogen-activated protein kinase (ERK) phosphorylation. Because other G protein-coupled receptors engage arrestin-β-1 (ARRB1) and ERK, we tested whether ARRB1 was a necessary component of TSHR/IGF1R crosstalk. HA secretion was stimulated by the TSHR-stimulating monoclonal antibodies M22 and KSAb1, or immunoglobulins from patients with GO (GO-Igs). Treatment with M22, as previously shown, resulted in biphasic dose-response stimulation of HA secretion. The high-potency phase was IGF1R dependent, and the low-potency phase was partly IGF1R independent. KSAb1 produced a monophasic dose-response stimulation of HA secretion, whose potency was lowered >20-fold after IGF1R knockdown. ARRB1 knockdown abolished M22's high-potency phase and lowered KSAb1's potency and efficacy. ARRB1 knockdown inhibited GO-Ig stimulation of HA secretion and of ERK phosphorylation. Last, ARRB1 was shown to be necessary for TSHR/IGF1R proximity. In contrast, ARRB2 knockdowns did not show these effects. Thus, TSHR must neighbor IGF1R for crosstalk in GO fibroblasts to occur, and this depends on ARRB1 acting as a scaffold. Similar scaffolding of TSHR and IGF1R by ARRB1 was found in human osteoblast-like cells and human thyrocytes. These findings support a model of TSHR/IGF1R crosstalk that may be a general mechanism for G-protein-coupled receptor/receptor tyrosine kinase crosstalk dependent on ARRB1.
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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.