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- W139798664 abstract "Retinoic acid (RA), an active metabolite of dietary vitamin A (1,2), is essential to maintain normal growth and differentiation of epithelial cells (3,4). RA and certain of its analogs have also been used in experimental animals to prevent and treat cancers of a variety of epithelial tissues (4-9). The mode of action of RA remains speculative. Accumulating evidence indicate that RA mediates its effects through specific nuclear receptors (10-16). RA nuclear receptors belong to a super-family of steroid, thyroid and vitamin D receptors, the ligand-inducible transcriptional factors (10-12). Two major families of RA nuclear receptors (RAR and RXR) have been identified. The RAR (α,β, γ) are activated by both all trans-RA and 9-cis-RA while RXR (α, β, γ) are activated by 9-cis-RA only (16,17). Thus, RAR and RXR are distinct retinoid receptor subfamilies (16,17). RAR require co-regulators to bind effectively to RA responsive element (RARE) in a target gene. RXR functions as auxiliary receptor for RAR and related receptors (18). RXRI3 forms heterodimers with RAR to increase its DNA binding and transcriptional activity (16,19). Other transcriptional factors such as COUP-TF can also modulate RAR activities (20). We determined the role that RAR plays in the signal transduction pathway leading to the expression of tissue transglutaminase (TG) by RA (21,22). Data indicating that vitamin A nutritional status in rats influences the expression of both RAR and tissue TG in certain tissues will be presented. The results that imply that the levels of RAR determine the magnitude of tissue TG induction by retinoic acid will also be summarized." @default.
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- W139798664 date "1995-01-01" @default.
- W139798664 modified "2023-09-28" @default.
- W139798664 title "Involvement of Retinoic Acid Nuclear Receptors in Transcriptional Regulation of Tissue Transglutaminase, the Gene Involved in Apoptosis" @default.
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- W139798664 doi "https://doi.org/10.1007/978-1-4612-0237-0_9" @default.
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