Cellular and molecular basis of deiodinase-regulated thyroid hormone signaling.

By B. Gereben, A. Zavacki, S. Ribich, Brian W Kim, Stephen A. Huang, W. Simonides, Anikó Zeöld, A. Bianco. Endocrine reviews, 2008

832 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism

View Paper: https://www.semanticscholar.org/paper/0e4cb289ef4bebebbe49ec613287f6d5cbc39653

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In Endocrinology, Diabetes and Metabolism

1. M. Holmes
2. J. Seckl
3. G. Brent

Citations in the corpus

• Thyroid hormone regulation of metabolism. (2014, background): “Sirtuin expression Selenium required for D2 activity (90) Fat intake Crosstalk with PPAR , , (157, 158) Fat intake”
• 11β-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action. (2013, background): “Analogous biology had been described for thyroid hormone receptors with mono-deiodinase isozymes inactivating or activating thyroid hormones in a cell-specific manner (228).”
• Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014, neutral): “A fundamental characteristic of D2 is that its enzymatic activity is tightly coupled to plasma T4 levels by the ubiquitinproteasomal system (358).”
• Selenoproteins: molecular pathways and physiological roles. (2014, background): “However, DI2 and DI3 have been implicated in fine-tuning local intracellular T3 concentrations in a tissue-specific manner, without changing overall serum levels of T3 (114).”