scholarly journals Neuronal Activity Controls the Antagonistic Balance Between Peroxisome Proliferator-Activated Receptor-γ Coactivator-1α and Silencing Mediator of Retinoic Acid and Thyroid Hormone Receptors in Regulating Antioxidant Defenses

2011 ◽  
Vol 14 (8) ◽  
pp. 1425-1436 ◽  
Author(s):  
Francesc X. Soriano ◽  
Frédéric Léveillé ◽  
Sofia Papadia ◽  
Karen F.S. Bell ◽  
Clare Puddifoot ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Neuronal Activity ◽  
Hormone Receptors ◽  
Antioxidant Defenses ◽  
Thyroid Hormone Receptors ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

Dual regulatory role for thyroid-hormone receptors allows control of retinoic-acid receptor activity

Nature ◽  
1989 ◽  
Vol 340 (6235) ◽  
pp. 653-656 ◽  
Author(s):  
Gerhart Graupner ◽  
Ken N. Wills ◽  
Maty Tzukerman ◽  
Xiao-kun Zhang ◽  
Magnus Pfahl
Keyword(s):  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Hormone Receptors ◽  
Retinoic Acid Receptor ◽  
Receptor Activity ◽  
Regulatory Role ◽  
Thyroid Hormone Receptors ◽  
Acid Receptor

Post-transcriptional induction of β1-adrenergic receptor by retinoic acid, but not triiodothyronine, in C6 glioma cells expressing thyroid hormone receptors

1996 ◽  
Vol 135 (6) ◽  
pp. 709-715 ◽  
Author(s):  
Mònica López-Barahona ◽  
Teresa Iglesias ◽  
Irene García-Higuera ◽  
Federico Mayor ◽  
Angel Zaballos ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Adrenergic Receptor ◽  
Hormone Receptors ◽  
Glioma Cells ◽  
C6 Glioma ◽  
High Expression ◽  
Thyroid Hormone Receptors ◽  
C6 Glioma Cells ◽  
C6 Cells

López-Barahona M, Iglesias T, García-Higuera I, Mayor Jr F, Zaballos A, Bernal J, Muñoz A. Posttranscriptional induction of β1 -adrenergic receptor by retinoic acid, but not triiodothyronine, in C6 glioma cells expressing thyroid hormone receptors. Eur J Endocrinol 1996:135:709–15. ISSN 0804–4643 Thyroid hormone (triiodothyronine; T3) has been shown to control the expression of β1 -adrenergic receptors (β1-AR) in cardiac myocytes, but not in C6 glioma cells. This cell specificity has been attributed to low expression of T3 receptors and high expression of the c-erbAα2 splice variant that interferes with the action of T3. To check this hypothesis we have expressed the c-erbA/thyroid hormone receptor (TR) α1 gene in C6 glioma cells and investigated their response to thyroid hormone. Cells expressing TRα1, but not wild-type cells, were responsive to T3 as shown by increased expression of mitochrondrial hydroxymethylglutaryl CoA synthase after T3 exposure. However, T3 had no effect on β1-AR gene expression in either set of cells. The β1-AR mRNA concentrations were, however, altered by retinoic acid (RA) treatment. Retinoic acid caused a rapid up-regulation of β1-AR mRNA levels that was blocked by cycloheximide. Retinoic acid did not increase the β1-AR gene transcription rate in run-on experiments. These results indicate an indirect post-transcriptional effect of RA. Control of β1-AR expression in C6 cells is also exerted at the translational level, because there was no correlation between mRNA and protein induction, as determined by radioligand binding studies. We conclude that lack of responsiveness of the β1-AR gene in C6 cells to T3 is not due to high expression of c-erbAα2 but to undefined cell-specific factors. Alberto Muñoz, Instituto Investigaciones Biomedicas, Arturo Duperier 4, 28029 Madrid, Spain

scholarly journals The Book of Opposites: The Role of the Nuclear Receptor Co-regulators in the Suppression of Epidermal Genes by Retinoic Acid and Thyroid Hormone Receptors

2005 ◽  
Vol 124 (5) ◽  
pp. 1034-1043 ◽  
Author(s):  
Sang H. Jho ◽  
Constantinos Vouthounis ◽  
Brian Lee ◽  
Olivera Stojadinovic ◽  
Mark J. Im ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Nuclear Receptor ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptors
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