Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Apr 26;12:587518. doi: 10.3389/fendo.2021.587518

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2021 Fröhlich and Wahl

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Transporters and mechanisms of genomic and non-genomic actions of thyroid hormones. TH enters cells by diffusion or via transporters like monocarboxylate transporter MCT8 and MCT10, organic anion transporting polypeptide (OATP)1C1, L-amino acid transporter (LAT) 1 and 2, and Na+/taurocholate cotransporting polypeptide (NCTP). Hormones inside the cell can bind to thyroid hormone transporter (TR) α and β1 and induce genomic changes via transcription. Nuclear receptor co-repressor protein (NCoR) and Adenovirus early region 1A binding protein p300 (p300) are involved in this process. Non-genomic regulation occurs by binding to integrin αvβ3 with activation of phospholipase C (PLC), protein kinase C (PKC), phosphorylated mitogen-activated protein kinase (pMAPK), and extracellular signal-regulated kinase (ERK) to induce trafficking of the phosphorylated TRβ1 and estrogen receptor (ER) into the nucleus. Cross-talk of αvβ3 integrin with growth factor receptors (GFR) is particularly important for cancer cells. T4 and rT3 can also act via TRΔα1 on actin, and T3 through pMAPK/ERK1/2 on Na⁺/H⁺ antiporter and via phosphatidyl-inositol 3 kinase (PI3K) and Akt/protein kinase B (PKB) on Na⁺/K⁺-ATPase.