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Trapping and Characterization of Novel Retinoid Response Elements

Department of Biology (M.A.G., Y.L., R.R., M.B.R.) and Institute for Biomolecular Science (M.B.R.), University of South Florida, Tampa, Florida 33620; Departments of Genetics, Cell Biology, and Biochemistry (K.H.K., M.-N.V.), Washington State University, Pullman, Washington 99164; and Department of Biochemistry and Molecular Biology (M.B.R.), UMDNJ-New Jersey Medical School, Newark, New Jersey 07103

Address all correspondence and requests for reprints to: Dr. Melissa Rogers, Biochemistry & Molecular Biology (MSB E627), UMDNJ-New Jersey Medical School, 185 South Orange Avenue, Newark, New Jersey 07103-2714. E-mail: rogersmb{at}umdnj.edu.

Retinoids, such as retinoic acid (RA), play a critical role in normal vertebrate development and physiology. However, embryonic exposure to excess retinoids also causes severe malformations. Retinoids bind RA receptors and retinoid X receptors, thus activating a plethora of genes. Separating the genes induced directly by retinoid-bound receptors from those induced subsequently by other transcription factors is difficult. The loose consensus defining known RA responsive elements (RAREs) further complicates this effort. We developed a yeast-based system to trap functional RAREs in the mouse genome. Several of the clones contain RAREs near RA-induced genes. Mammalian reporter gene analyses and EMSAs showed that these are bona fide RAREs. This functional genomics approach should identify RA-regulated genes that initiate critical signaling cascades in cells.

NURSA Molecule Pages Link:

Nuclear Receptors:   RARβ  |  RXRγ

Ligands:   all-trans-Retinoic acid  |  9-cis-Retinoic acid

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