Editorial: Thyrotropin receptor polymorphisms and thyroid diseases

Journal of Clinical Endocrinology and Metabolism

Volumn 85, Issue 8, 2000, Pages 2637-2639

  Tonacchera, Massimo ^a   Pinchera, Aldo ^a  

^a UNIVERSITY OF PISA   (Italy)

Author keywords

[No Author keywords available]

Indexed keywords

THYROTROPIN RECEPTOR;

CELL DIFFERENTIATION; DISEASE TRANSMISSION; EDITORIAL; GENE DELETION; GENETIC POLYMORPHISM; POINT MUTATION; PRIORITY JOURNAL; THYROID DISEASE; GENETICS; HUMAN; NOTE;

HUMANS; POINT MUTATION; POLYMORPHISM, GENETIC; RECEPTORS, THYROTROPIN; THYROID DISEASES;

EID: 85047683478     PISSN: 0021972X     EISSN: None     Source Type: Journal    
DOI: 10.1210/jcem.85.8.6801     Document Type: Editorial

References (12)

1. TSH receptor mutations and thyroid disease
2. Lack of association of nonautoimmune hyperfunctioning thyroid disorders and a germ line polymorphism of codon 727 of the human thyrotropin receptor in a European Caucasian population
3. Thyrotropin receptor mutations in hyperfunctioning thyroid adenomas from Brazil
4. Germline polymorphism of codon 727 of human thyroid-stimulating hormone receptor is associated with toxic multinodular goiter
5. Constitutive activation of the Gsα protein-adenylate cyclase pathway may not be sufficient to generate toxic thyroid adenomas
6. Hyperfunctioning thyroid nodules in toxic multinodular goiter share activating somatic thyrotropin receptor mutations with solitary toxic adenoma
7. Identification of constitutively activating somatic thyrotropin receptor mutations in a subset of toxic multinodular goiter
8. Activating thyrotropin receptor mutations in histologically heterogeneous hyperfunctioning nodules of multinodular goiter
9. Activating TSH receptor mutations are present in nonadenomatous hyperfunctioning nodules of toxic or autonomous multinodular goiter
10. Functional analysis of a variant of the thyrotropin receptor gene in a family with Graves' disease
11. Enhanced cAMP accumulation by the human thyrotropin receptor variant with the Pro52Thr substitution in the extracellular domain
12. Normal function in vivo of a homozygotic polymorphism in the human thyrotropin receptor