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

Lack of mutations in the TSHr and Gsalpha genes in TSHr antibody negative Graves' disease.

Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association - 1 Oct 2005

Elgadi A, Frisk T, Larsson C, Wallin G, Höög A, Zedenius J, Norgren S

Abstract excerpt

The aim of this study was to investigate whether TSHr antibody negative Graves' disease is associated with somatic mutations in the TSHr or Gsalpha genes and whether histopathologically defined thyroid lesions, i.e., hyperfunctioning adenoma, non-functioning follicular adenomas, or nodules in toxic and non-toxic multinodular goiters are associated with such mutations. No mutations but three germ-line...

Read the complete abstract on PubMed

Topics

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

Share to Adenoma
Share to Autoantibodies

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

Share to Goiter, Nodular

Share to Graves Disease

Share to GTP-Binding Protein alpha Subunits, Gs

Share to Receptors, Thyrotropin

Share to Thyroid Neoplasms

Source

Identifiers

PMID: 16235153
DOI: 10.1055/s-2005-872887

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.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Lack of mutations in the TSHr and Gsalpha genes in TSHr antibody negative Graves' disease.PMID 16235153Read ↗

Non-hyperfunctioning nodules from multinodular goiters: a minor role in pathogenesis for somatic activating mutations in the TSH-receptor and Gsalpha subunit genes.Semantic proximity Read ↗

Structural studies of the thyrotropin receptor and Gs alpha in human thyroid cancers: low prevalence of mutations predicts infrequent involvement in malignant transformation.Semantic proximity Read ↗

Identification of constitutively activating somatic thyrotropin receptor mutations in a subset of toxic multinodular goiters.Semantic proximity Read ↗

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

Toxic thyroid adenoma: absence of DNA mutations of the TSH receptor and Gs alpha.Semantic proximity Read ↗

Thyroid-stimulating hormone receptor and its role in Graves' disease.Semantic proximity Read ↗

A new phenotype of nongoitrous and nonautoimmune hyperthyroidism caused by a heterozygous thyrotropin receptor mutation in transmembrane helix 6.Semantic proximity Read ↗

Thyroid hyperfunctioning adenomas with and without Gsp/TSH receptor mutations show similar clinical features.Semantic proximity Read ↗

Pathology of the TSH receptor.Semantic proximity Read ↗

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

Diversity and prevalence of somatic mutations in the thyrotropin receptor and Gs alpha genes as a cause of toxic thyroid adenomas.Semantic proximity Read ↗

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