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- W2025363595 abstract "We have previously shown that oral treatment of pregnant mice with all-trans retinoic acid (RA) at doses which cause 100% fetal dysmorphogenesis results in a rapid elevation in the mRNA of one specific isoform of the RA receptor-β, RAR-β2, in susceptible embryonic regions. To further investigate the involvement of RAR-β2 mRNA in teratogenesis, we have examined its expression in mouse embryos exposed to marginal/nonteratogenic and teratogenic dosing regimens of both 13-cis RA and all-trans RA. We have found that the mere elevation in embryonic RAR-β2 mRNA levels and free retinoid levels is not sufficient to result in dysmorphogenesis. Rather, retinoid-induced dysmorphogenesis of embryos appears to occur only when RAR-β2 mRNA and unbound retinoid levels remain elevated for at least 6–9 h following retinoid treatment resulting in a significant and prolonged elevation in RAR-β protein levels." @default.
- W2025363595 created "2016-06-24" @default.
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- W2025363595 date "1994-03-01" @default.
- W2025363595 modified "2023-10-16" @default.
- W2025363595 title "A sustained elevation in retinoic acid receptor-β2 mRNA and protein occurs during retinoic acid-induced fetal dysmorphogenesis" @default.
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- W2025363595 doi "https://doi.org/10.1016/0925-4773(94)90011-6" @default.
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