Correction: Lin, K.-H., et al. Molecular Functions of Thyroid Hormone Signaling in Regulation of Cancer Progression and Anti-Apoptosis. Int. J. Mol. Sci., 2019, 20, 4986

The authors wish to make the following corrections to this paper [1]:

There were labeling mistakes in the column TRα2 displaying the T3 binding ability in the original version of Figure 1 (page 3). Circulating THs interact with thyroid hormone receptors to promote downstream signaling pathways and activate transcription factors. The four major TR isoforms, TRα1, TRα2, TRβ1, and TRβ2, are produced by c-erbAα and c-erbAβ genes. Their human homologs are designated THRA and THRB. The c-erbAα gene located on chromosome 17 encodes two different TRα isoforms. One is functional TH-binding TRα1 and the other is a dominant-negative splice variant, TR𝛼2, lacking TH binding activity [2]. T3 interacts with thyroid hormone receptors via C-terminal activation function-2 (AF-2) in the ligand-binding domain (LBD), however, only TRα2 has a distinct C-terminal extension and absent activation function-2 (AF-2) region, which suggested that TRα2 does not bind T3 [3]. TR𝛼2 is unique in regard to its lack of binding to THs while interacting with DNA, and its precise function is unclear at present. We have made a correction to show that the TRα2 did not bind T3 and marked presence or lack of presence of the AF-2 domain in Figure 1 as follows:

The authors would like to apologize for any inconvenience caused to the readers by these changes.