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Article

TSH compensates thyroid-specific IGF-I receptor knockout and causes papillary thyroid hyperplasia.

Molecular endocrinology (Baltimore, Md.) - 1 Nov 2011

Müller Kathrin, Führer Dagmar, Mittag Jens, Klöting Nora, Blüher Matthias, Weiss Roy E, Many Marie-Christine, Schmid Kurt Werner, Krohn Knut

Abstract excerpt

Although TSH stimulates all aspects of thyroid physiology IGF-I signaling through a tyrosine kinase-containing transmembrane receptor exhibits a permissive impact on TSH action. To better understand the importance of the IGF-I receptor in the thyroid in vivo, we inactivated the Igf1r with a Tg promoter-driven Cre-lox system in mice. We studied male and female mice with thyroidal wild-type, Igf1r(+/-), and...

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Identifiers

PMID: 21980075
DOI: 10.1210/me.2011-0065
PMCID: PMC5417177

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