AI Article Synopsis
- Thyroid hormone and p44/42 MAPK inactivation play key roles in intestinal differentiation, particularly in the regulation of the GLUT5 gene.
- Treatment with the p44/42 MAPK inhibitor U0126 in Caco-2 cells decreased phosphorylation of TRalpha-1, while T(3) and U0126 together significantly promoted GLUT5 gene expression.
- Experimental methods showed that the combination of T(3) and U0126 enhances TRalpha-1's ability to bind to the GLUT5 transcriptional response element, suggesting that de-phosphorylation of TRalpha-1 boosts its activity in regulating GLUT5 expression.
Article Abstract
Thyroid hormone and p44/42 MAPK inactivation are important in intestinal differentiation. We demonstrated not only that treatment with p44/42 MAPK inhibitor U0126 in intestinal cell line Caco-2 cells reduced the phosphorylation of serine and threonine residues of TRalpha-1, but also that T(3) and U0126 synergistically induced GLUT5 gene expression. EMSA demonstrated that the binding activity of TRalpha-1-RXR heterodimer on GLUT5-TRE in nuclear proteins of Caco-2 cells was synergistically enhanced by co-incubation in vitro with T(3) and CIAP, which strongly de-phosphorylates proteins. ChIP and transfection assays revealed that co-treatment of T(3) and U0126 induces TRalpha-1-RXR binding to GLUT5-TRE on the human GLUT5 enhancer region, and recruitment of the transcriptional complex in cells. These results suggest that inactivation of p44/42 MAPK enhances T(3)-induced GLUT5 gene expression in Caco-2 cells through increasing TRalpha-1 transactivity and binding activity to the GLUT5-TRE, probably due to de-phosphorylation of TRalpha-1.
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| http://dx.doi.org/10.1016/j.bbrc.2007.06.012 | DOI Listing |
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