ESPEYB21 3. Thyroid Defects in Thyroid Hormone Transport, Metabolism and Action (2 abstracts)
3.11. Identification of human TRIAC transmembrane transporters
Paul Carlos Becker , Mandy Güth-Steffens , Katina Lazarow , Niklas Sonntag , Doreen Braun , Islam Masfaka , Kostja Renko , Lutz Schomburg , Josef Köhrle , Jens Peter von Kries , Ulrich Schweizer , Gerd Krause & Jonas Protze
Thyroid. 2024 Jul;34(7):920-930. doi: 10.1089/thy.2023.0592. PMID: 38801167
Brief Summary: This basic science study examined how 3,5,3’-triiodothyroacetic acid (TRIAC) - a thyroid hormone (TH) receptor agonist used in patients with resistance to TH, and in patients with Allan-Herndon-Dudley syndrome (AHDS), caused by mutations in monocarboxylate transporter 8 (MCT8) - is transported into cells independent of MCT8. Through a genome-wide RNAi screening in HepG2 cells, two key transporters, SLC22A9 (OAT7) and SLC29A2 (ENT2), were identified that facilitate the uptake of TRIAC into cells. These transporters are expressed in tissues like brain, liver, and pituitary, suggesting their role in enabling TRIAC to cross cellular membranes and exert its effects in these tissues. Furthermore, ABCD1, an ATP-dependent peroxisomal pump, was identified as a TRIAC exporter, which may limit the efficacy of TRIAC therapy in certain tissues.
These findings have clear clinical relevance, particularly in conditions such as AHDS, where TRIAC treatment has variable results. Better understanding of the expression patterns and function of these transporters may improve the therapeutic use of TRIAC in pediatric patients with TH transport disorders. The study also highlights the importance of screening for transporter expression in other tissues to optimize treatment outcomes.
Volume 21
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ESPE Yearbook of Paediatric Endocrinology
ISSN 1662-4009 (Online)
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