Modeling the Biochemical Phenotype of MCT8 Mutations In Vitro: Resolving a Troubling Inconsistency
Author:
Affiliation:
1. Institut für Biochemie und Molekularbiologie, Rheinische Friedrich-Wilhelms-Universität Bonn, 53115 Bonn, Germany
Funder
Rheinische Friedrich-Wilhelms-Universität Bonn
Sherman Family Foundation
Publisher
The Endocrine Society
Subject
Endocrinology
Link
http://academic.oup.com/endo/advance-article-pdf/doi/10.1210/en.2019-00069/28521143/en.2019-00069.pdf
Reference27 articles.
1. Identification of monocarboxylate transporter 8 as a specific thyroid hormone transporter;Friesema;J Biol Chem,2003
2. Essential molecular determinants for thyroid hormone transport and first structural implications for monocarboxylate transporter 8;Kinne;J Biol Chem,2010
3. A novel syndrome combining thyroid and neurological abnormalities is associated with mutations in a monocarboxylate transporter gene;Dumitrescu;Am J Hum Genet,2004
4. Association between mutations in a thyroid hormone transporter and severe X-linked psychomotor retardation;Friesema;Lancet,2004
5. Surface translocation and tri-iodothyronine uptake of mutant MCT8 proteins are cell type-dependent;Kinne;J Mol Endocrinol,2009
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1. Phenylbutyrate Treatment in a Boy With MCT8 Deficiency: Improvement of Thyroid Function Tests and Possible Hepatotoxicity;The Journal of Clinical Endocrinology & Metabolism;2024-05-24
2. Sodium Phenylbutyrate Rescues Thyroid Hormone Transport in Brain Endothelial-Like Cells;Thyroid;2022-07-01
3. The Protein Translocation Defect of MCT8L291R Is Rescued by Sodium Phenylbutyrate;European Thyroid Journal;2020
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