Transcriptional regulation by the nuclear receptor superfamily.
In the past year, additional experimental data have expanded our understanding of the molecular mechanisms that underlie nuclear receptor control of regulatory programs. It is increasingly clear that steroid members (e.g. glucocorticoid and estrogen) and non-steroid members (e.g. retinoic acid, thyroid hormone, and vitamin D) of the nuclear receptor superfamily may utilize distinct strategies in achieving their complex control of gene regulation.
Howard Hughes Medical Institute, School of Medicine, University of California, San Diego, La Jolla 92093-0648.
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D000818:Animals; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism*; D002467:Cell Nucleus / Q000378:metabolism*; D002884:Chromosomes, Human, Pair 15; D002886:Chromosomes, Human, Pair 17; D005786:Gene Expression Regulation; D006801:Humans; D015473:Leukemia, Promyelocytic, Acute; D005810:Multigene Family; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism*; D018168:Receptors, Retinoic Acid; D047488:Retinoid X Receptors; D012176:Retinoids / Q000378:metabolism; D014157:Transcription Factors; D014158:Transcription, Genetic; D014178:Translocation, Genetic; D014212:Tretinoin / Q000378:metabolism
D002352:Carrier Proteins; D011956:Receptors, Cell Surface; D018168:Receptors, Retinoic Acid; D047488:Retinoid X Receptors; D012176:Retinoids; D014157:Transcription Factors; D014212:Tretinoin