Paul J. Davis

TL;DR: Genetically engineered knockin mouse models provide valuable tools to ascertain further the molecular actions of unliganded TRs in vivo that could underlie the pathogenesis of hypothyroidism.

TL;DR: Nongenomic actions expand the repertoire of cellular events controlled by thyroid hormone and can modulate TR-dependent nuclear events.

TL;DR: Tetrac is a T(4) analog that inhibits binding of iodothyronines to the integrin receptor and is a probe for the participation of this receptor in cellular actions of the hormone.

TL;DR: The physiologic significance at the cellular level of certain of thyroid hormone actions has been demonstrated, for example, in the cases of myocardiocyte Na+ current, red cell Ca2+ content, and the control by hormone-induced alterations in actin solubility of cell surface activity of iodothyronine 5'-monodeiodinase activity and the intracellular distribution of protein disulfide isomerase activity.

TL;DR: Results of studies involving tetraiodothyroacetic acid (tetrac) and Arg-Gly-Asp (RGD) peptide are consistent with the presence of two iodothyronine receptor domains on the integrin, and a model proposes that one site binds T(3) exclusively, activates PI3-kinase via Src kinase, and stimulates TRalpha trafficking and HIF-1alpha gene expression.