Monocarboxylate transporter 8

[1]. Stefan Groeneweg, et al. In Vitro Characterization of Human, Mouse, and Zebrafish MCT8 Orthologues. Thyroid. 2019 Oct;29(10):1499-1510. [Content Brief]

[2]. W Edward Visser, et al. Novel pathogenic mechanism suggested by ex vivo analysis of MCT8 (SLC16A2) mutations. Hum Mutat. 2009 Jan;30(1):29-38. [Content Brief]

[3]. Edith C H Friesema, et al. Effective cellular uptake and efflux of thyroid hormone by human monocarboxylate transporter 10. Mol Endocrinol. 2008 Jun;22(6):1357-69. [Content Brief]

[4]. Simone Kersseboom, et al. Mutations in MCT8 in patients with Allan-Herndon-Dudley-syndrome affecting its cellular distribution. Mol Endocrinol. 2013 May;27(5):801-13. [Content Brief]

[5]. Francesca Novara, et al. Clinical and Molecular Characteristics of SLC16A2 (MCT8) Mutations in Three Families with the Allan-Herndon-Dudley Syndrome. Hum Mutat. 2017 Mar;38(3):260-264. [Content Brief]

[6]. Christine M Armour, et al. Further Insights into the Allan-Herndon-Dudley Syndrome: Clinical and Functional Characterization of a Novel MCT8 Mutation. PLoS One. 2015 Oct 1;10(10):e0139343. [Content Brief]

[7]. Edith C H Friesema, et al. Thyroid hormone transport by the human monocarboxylate transporter 8 and its rate-limiting role in intracellular metabolism. Mol Endocrinol. 2006 Nov;20(11):2761-72. [Content Brief]

[8]. Anita Kinne, et al. Essential molecular determinants for thyroid hormone transport and first structural implications for monocarboxylate transporter 8. J Biol Chem. 2010 Sep 3;285(36):28054-63. [Content Brief]

[9]. Gad D Vatine, et al. Modeling Psychomotor Retardation using iPSCs from MCT8-Deficient Patients Indicates a Prominent Role for the Blood-Brain Barrier. Cell Stem Cell. 2017 Jun 1;20(6):831-843.e5. [Content Brief]