Stanniocalcin 1 induction by thyroid hormone depends on thyroid hormone receptor β and phosphatidylinositol 3-kinase activation

• Published in: Experimental and clinical endocrinology & diabetes Vol. 119; no. 2; p. 81
• Main Authors: Moeller, L C, Haselhorst, N E, Dumitrescu, A M, Cao, X, Seo, H, Refetoff, S, Mann, K, Janssen, O E
• Format: Journal Article
• Language: English
• Published: Germany 01.02.2011
• Subjects: Cells, Cultured; Dose-Response Relationship, Drug; Enzyme Activation - drug effects; Fibroblasts - metabolism; Fibroblasts - pathology; Fibroblasts - physiology; Gene Expression Regulation - drug effects; Glycoproteins - genetics; Glycoproteins - metabolism; Humans; Mutant Proteins - metabolism; Mutant Proteins - physiology; Phosphatidylinositol 3-Kinase - metabolism; Protein Biosynthesis - drug effects; Protein Biosynthesis - genetics; Thyroid Hormone Receptors beta - agonists; Thyroid Hormone Receptors beta - genetics; Thyroid Hormone Receptors beta - metabolism; Thyroid Hormone Receptors beta - physiology; Thyroid Hormone Resistance Syndrome - genetics; Thyroid Hormone Resistance Syndrome - metabolism; Thyroid Hormone Resistance Syndrome - pathology; Transcriptional Activation - drug effects; Triiodothyronine - pharmacology

Thyroid hormone (TH) mediated changes in gene expression were thought to be primarily initiated by the nuclear TH receptor (TR) binding to a thyroid hormone response element in the promoter of target genes. A recently described extranuclear mechanism of TH action consists of the association of TH-li...