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Fig. 4 | Clinical Diabetes and Endocrinology

Fig. 4

From: A clinician’s guide to understanding resistance to thyroid hormone due to receptor mutations in the TRα and TRβ isoforms

Fig. 4

Model for resistance to thyroid hormone in RTHβ patients. a In both normal and RTH patients, wild-type TRβ and TRα isoforms derived from normal THRB and THRA alleles bind as TR/RXR heterodimers to the TRE and are able to activate transcription. b The mutant TRβ encoded by the abnormal THRB allele in RTH patients bind to the TRE constitutively in both the presence and absence of T3. Since it has decreased ligand-binding affinity, its ability to recruit co-activators and activate transcription is impaired. The unliganded mutant TR/RXR heterodimer thus competes with T3-bound wild type TR/RXR heterodimer for binding to the TRE

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