We showed that steroid receptor coactivator 1 deficient mice exhibit partial resistance to thyroid hormone at the level of the pituitary thyrotrophs
2014
Steroid Receptor Coactivator-1 Deficiency Causes Variable Alterations in the Modulation of T3-Regulated Transcription of Genesin Vivo
Key concepts
Scholarcy highlights
- For this study we examined the expression of two or three T3-responsive genes in each of three target organs: GH and TSH -subunit in pituitary; type 1 iodothyronine 5Ј-deiodinase, spot 14 and malic enzyme in liver; and sarcoplasmic reticulum calcium adenosine triphosphatase 2, myosin heavy chain ␣, and - in heart
- It is well known that the transcription of TSH␣ and - genes is markedly activated by thyroid hormone deficiency and suppressed by l-T3
- Hypothyroid SRC-1ϩ/ϩ mice showed an approximately 6-fold increase in S14 mRNA content from thyroid hormone deprivation to l-T3 treatment. These results suggest that down-regulation of S14 mRNA during thyroid hormone deprivation is completely abolished in the steroid receptor coactivator 1 knockout mouse
- The present study shows that the inactivation of the SRC-1 gene affects T3-mediated modulation of expression of some T3-responsive genes, but not all
- Expression of GH in the pituitary, of 5ЈDI and ME in liver, as well as any of three T3-responsive genes in heart was not affected by inactivation of the SRC-1 gene in either the thyroid hormone-deprived or rRNA are shown in arbitrary units
- Some differences in the SRC1-modulated effects may be TR isoform specific, such as the presence or absence of resistance to thyroid hormone on genes negatively regulated through TR2 or TR␣1, respectively
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