The rat thyroid hormone receptor (TR) Deltabeta3 displays cell-, TR isoform-, and thyroid hormone response element-specific actions.

The THRB gene encodes the well-described thyroid hormone (T3) receptor (TR) isoforms TRbeta1 and TRbeta2 and two additional variants, TRbeta3 and TRDeltabeta3, of unknown physiological significance. TRbeta1, TRbeta2, and TRbeta3 are bona fide T3 receptors that bind DNA and T3 and regulate expression of T3-responsive target genes. TRDeltabeta3 retains T3 binding activity but lacks a DNA binding domain and does not activate target gene transcription.

Multiple messenger ribonucleic acid variants regulate cell-specific expression of human thyroid hormone receptor beta1.

Thyroid hormones are essential for development, growth, and metabolism and act via T3 receptors (TR) alpha and beta. The THRA and THRB genes have discrete physiological roles but their mRNAs are expressed widely in overlapping patterns. There is poor correlation between TR mRNA and protein, indicating that expression may be regulated by posttranscriptional mechanisms.

Mechanisms of thyroid hormone receptor-specific nuclear and extra nuclear actions.

Triiodothyronine (T3) classically regulates gene expression by binding to high-affinity thyroid hormone receptors (TR) that recognize specific response elements in the promoters of T3-target genes and activate or repress transcription in response to hormone. However, a number of thyroid hormone effects occur rapidly and are unaffected by inhibitors of transcription and translation, suggesting that thyroid hormones may also mediate non-genomic actions. Such actions have been described in many tissues and cell types, including brown adipose tissue, the heart and pituitary.

Thyroid hormone activates fibroblast growth factor receptor-1 in bone.

Thyroid hormone (T3) and the T3 receptor (TR) alpha gene are essential for bone development whereas adult hyperthyroidism increases the risk of osteoporotic fracture. We isolated fibroblast growth factor receptor-1 (FGFR1) as a T3-target gene in osteoblasts by subtraction hybridization. FGFR1 mRNA was induced 2- to 3-fold in osteoblasts treated with T3 for 6-48 h, and FGFR1 protein was stimulated 2- to 4-fold.

A thyrotoxic skeletal phenotype of advanced bone formation in mice with resistance to thyroid hormone.

Thyroid hormone (T3) regulates bone turnover and mineralization in adults and is essential for skeletal development during childhood. Hyperthyroidism is an established risk factor for osteoporosis. Nevertheless, T3 actions in bone remain poorly understood.

Mechanism of thyroid hormone action.

Thyroid hormone (triiodothyronine [T3]) regulates gene expression by binding to high-affinity nuclear receptors. Thyroid hormone receptors (TRs) recognize specific response element sequences in the promoters of T3-target genes and activate or repress transcription in response to hormone. In this paper, we review the TR proteins and thyroid hormone response elements (TREs) to which they bind, the mechanisms of action of TRs bound to the TRE in basal and liganded conformations, and the interacting proteins implicated in these complexes.