Triiodothyroacetic acid has unique potential for therapy of resistance to thyroid hormone.

To evaluate whether T3 analogs would have a differential effect on TR beta 1 and TR beta 1 mutants and be a specific treatment for patients with resistance to thyroid hormone, we examined the induction of the transcriptional activation of wild-type TR alpha 1, TR beta 1, and mutant TR beta 1s by T3, Triiodothyroacetic acid, and triiodothyropropionic acid

T Takeda; S Suzuki; R T Liu; L J DeGroot

2014

Scholarcy highlights

  • 3,5,3,'-Triiodothyroacetic acid has been used in therapy of resistance to thyroid hormone on an empirical basis and appears beneficial in some studies
  • We observed that the T3 analogs, Triac and 3,5,3'-triiodothyropropionic acid, have a higher affinity for the thyroid hormone receptor-beta 1 than does T3, whereas the affinities of the three compounds for TR alpha 1 are the same
  • To evaluate whether T3 analogs would have a differential effect on TR beta 1 and TR beta 1 mutants and be a specific treatment for patients with resistance to thyroid hormone, we examined the induction of the transcriptional activation of wild-type TR alpha 1, TR beta 1, and mutant TR beta 1s by T3, Triac, and Triprop
  • The dose response of transcriptional activation by T3 analogs was measured by transient cotransfections with TRs and a rat malic enzyme-TRE fused to thymidine kinase-chloramphenicol acetyltransferase in COS-1 cells
  • For TR alpha 1 wt, induction of CAT activity by T3 and Triac occurred at the same concentration
  • Cotransfection studies were performed using a rat malic enzyme-TK-CAT reporter plasmid to analyze the effects of hormones at near-physiological concentrations of T3 and Triac
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