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Cited by 257

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

A potential novel mechanism for precocious puberty in juvenile hypothyroidism

Anasti, J. N.·1995·Journal of Clinical Endocrinology & Metabolism

Abstract

Some children with juvenile hypothyroidism exhibit unexplained precocious puberty. Interaction of TSH with the human FSH receptor (hFSH-R) is a possible pathophysiological mechanism for this syndrome that has not been explored due to the lack of hFSH-free TSH preparations and the scarcity of a suitable hFSH-R-based assay system. To devise an in vitro FSH bioassay suitable for exploring this mechanism, we expressed hFSH-R complementary DNA in COS-7 cells and stimulated them with recombinant hTSH (rec-hTSH). Rec-hTSH elicited a dose-dependent cAMP response in the in vitro hFSH-R bioassay; however, the concentration of rec-hTSH required for half-maximal stimulation was several logs greater than that of hFSH. Rec-hTSH acted as a competitive inhibitor of hFSH at the hFSH-R, indicating that hTSH and hFSH are acting through the same receptor, namely the hFSH-R. This provides a potential novel mechanism for the precocious puberty of juvenile hypothyroidism.

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Metadata

Authors
Anasti, J. N.
Venue
Journal of Clinical Endocrinology & Metabolism
Published
1995-01-01
Volume
80
Issue
1
Pages
276-279
ISSN
0021-972X (ISSN-L)
OpenAlex
W2170116261
Cited by
257
References
9
FWCI
3.32
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: A potential novel mechanism for precocious puberty in juvenile hypothyroidism. https://app.cochat.ai/papers/10.1210/jc.80.1.276
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Anasti, J. N. (1995). A potential novel mechanism for precocious puberty in juvenile hypothyroidism. Journal of Clinical Endocrinology & Metabolism. https://doi.org/10.1210/jc.80.1.276

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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