Retinoic acid receptors are important in the regulation of growth and differentiation of epithelial tissues, embryonic and central nervous system development and hematopoiesis. Retinoids mediate their effect by two classes of nuclear receptor proteins, the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs), that each consist of three isotypes ( α, β, and γ) encoded in separate genes. Upon dimerization with RXR, RARs can bind to specific enhancer sequences in the DNA, so-called retinoic acid response elements (RAREs), resulting in transcriptional activation of target genes in the presence of ligand. Retinoids, the natural and synthetic vitamin A derivatives, are known to inhibit the proliferation of lung cancer and breast cancer cells and the growth of carcinogen-induced bronchogenic squamous cell carcinoma and mammary tumors, and have been used as chemoprevention agents against both types of cancer. A growing body of evidence supports the hypotheses that the RAR beta gene is a tumor suppressor gene and the chemopreventive effects of retinoids are due to induction of RAR beta. RAR beta expression is reduced in many malignant tumors including breast carcinoma.
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Clear and colorless frozen liquid solution
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Trends in biochemical sciences, 17(10), 427-433 (1992-10-01)
Complexity in the retinoid signalling system arises from a combination of several forms of retinoic acid, multiple cytoplasmic binding proteins and nuclear receptors, and the existence of polymorphic retinoic acid response elements. Additional diversity appears to be generated by heterodimeric
Nonsteroid nuclear receptors: what are genetic studies telling us about their role in real life?
P Kastner et al.
Cell, 83(6), 859-869 (1995-12-15)
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