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Expression of G(alpha)(s) proteins and TSH receptor signalling in hyperfunctioning thyroid nodules with TSH receptor mutations
Author(s) -
HP Holzapfel,
Benjamin Bergner,
Peter Wonerow,
Ralf Paschke
Publication year - 2002
Publication title -
european journal of endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.897
H-Index - 148
eISSN - 1479-683X
pISSN - 0804-4643
DOI - 10.1530/eje.0.1470109
Subject(s) - endocrinology , medicine , receptor , alpha (finance) , g protein , biology , basal (medicine) , thyrotropin receptor , alpha 2 adrenergic receptor , signal transduction , thyroid , microbiology and biotechnology , graves' disease , construct validity , nursing , insulin , patient satisfaction
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.

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