Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Expression of G(alpha)(s) proteins and TSH receptor signalling in hyperfunctioning thyroid nodules with TSH receptor mutations.

European journal of endocrinology - 1 Jul 2002

Holzapfel Hans-Peter, Bergner Beate, Wonerow Peter, Paschke Ralf

Abstract excerpt

OBJECTIVE: Constitutively activating mutations of the thyrotrophin receptor (TSHR) are the main molecular cause of hyperfunctioning thyroid nodules (HTNs). The G protein coupling is an important and critical step in the TSHR signalling which mainly includes G(alpha)(s), G(alpha)(i) and G(alpha)(q)/11 proteins. DESIGN: We investigated the in vitro consequences of overexpressing G(alpha) proteins on signalling of...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to COS Cells
Share to Cyclic AMP
Share to GTP-Binding Protein alpha Subunits, Gs

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Hyperthyroidism

Share to In Vitro Techniques

Share to Inositol Phosphates

Share to Receptors, Thyrotropin

Share to Thyroid Nodule

Source

Identifiers

PMID: 12088927
DOI: 10.1530/eje.0.1470109

Genes

TSHR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Expression of G(alpha)(s) proteins and TSH receptor signalling in hyperfunctioning thyroid nodules with TSH receptor mutations.PMID 12088927Read ↗

Autonomously functioning thyroid nodules in a former iodine-deficient area commonly harbor gain-of-function mutations in the thyrotropin signaling pathway.Semantic proximity Read ↗

Novel insights on thyroid-stimulating hormone receptor signal transduction.Semantic proximity Read ↗

Constitutive activities in the thyrotropin receptor: regulation and significance.Semantic proximity Read ↗

Hyperfunctioning thyroid adenoma and activating mutations in the TSH receptor gene.Semantic proximity Read ↗

Identification and functional characterization of two novel activating thyrotropin receptor mutants in toxic thyroid follicular adenomas.Semantic proximity Read ↗

Mutations in the mouse TSH receptor equivalent to human constitutively activating TSH receptor mutations also cause constitutive activity.Semantic proximity Read ↗

Somatic mutations in the thyrotropin receptor gene and not in the Gs alpha protein gene in 31 toxic thyroid nodules.Semantic proximity Read ↗

Thyrotropin receptor-associated diseases: from adenomata to Graves disease.Semantic proximity Read ↗

Constitutive TSH receptor activation as a hallmark of thyroid autonomy.Semantic proximity Read ↗

Controversial constitutive TSHR activity: patients, physiology, and in vitro characterization.Semantic proximity Read ↗

Increased expression of G-protein-coupled receptor kinases 3 and 4 in hyperfunctioning thyroid nodules.Semantic proximity Read ↗

Comparative proteomic analysis to dissect differences in signal transduction in activating TSH receptor mutations in the thyroid.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.