Biochemical and Biophysical Research Communications
Regular ArticleMarkedly Increased Constitutive CYP1A1 mRNA Levels in the Fertilized Ovum of the Mouse
References (36)
Biochem. Pharmacol.
(1994)- et al.
Dev. Biol.
(1985) - et al.
Anal. Biochem.
(1987) - et al.
J. Biol. Chem.
(1984) - et al.
Cell
(1992) - et al.
J. Biol. Chem.
(1995) - et al.
Biochem. Biophys. Res. Commun.
(1995) - et al.
Trends Biochem. Sci.
(1997) - et al.
Toxicol. Appl. Pharmacol.
(1995) - et al.
Mech. Dev.
(1998)
Biochem. Biophys. Res. Commun.
Arch. Biochem. Biophys.
Pharmacogenetics
Ann. N.Y. Acad. Sci.
Proc. Natl. Acad. Sci. USA
Proc. Natl. Acad. Sci. USA
Cited by (39)
Does the aryl hydrocarbon receptor regulate pluripotency?
2017, Current Opinion in ToxicologyCitation Excerpt :Appropriate control of AHR expression appears to be essential to maintain pluripotency, an objective that the blastomeres attain by maintaining the AHR in a state of positive repression mediated by the pluripotency factors themselves in combination with Polycomb Group repressors [18,21]. AHR repression may provide the ICM cells with the opportunity to reprogram gene expression, implementing epigenetic mechanisms that bring about global changes in DNA methylation [22–27]. In addition, the AHR might also play a significant role in the determination of cell fate decisions, as suggested by the correlation between AHR expression and lineage specification after implantation [9,28].
Pluripotency factors and Polycomb Group proteins repress aryl hydrocarbon receptor expression in murine embryonic stem cells
2014, Stem Cell ResearchCitation Excerpt :Several studies have shown a complex pattern of Ahr expression during early mouse embryogenesis. Fertilized eggs at the 1-cell stage show detectable levels of Ahr mRNA (Dey and Nebert, 1998; Wu et al., 2002) and high levels of AHR activity, as determined by an elevated constitutive mRNA level of the AHR target gene Cyp1a1 (Dey and Nebert, 1998). Thereafter, Ahr mRNA expression is completely silenced between the 2- and 8-cell stages and afterwards increases to a detectable level by late pre-implantation blastocysts (Peters and Wiley, 1995; Dey and Nebert, 1998; Wu et al., 2002).
The aryl hydrocarbon receptor agonist 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) alters early embryonic development in a rat IVF exposure model
2011, Reproductive ToxicologyCitation Excerpt :Both AHR and Cyp1a1 mRNA are strongly expressed in mouse pre-implantation embryos. Interestingly, it was shown that immediately following fertilization, there is an increase in constitutive CYP1a1 mRNA levels in mouse embryos [9]. AHR ligands (such as dioxins and polychlorinated biphenyls) induce a spectrum of maldevelopmental and toxic responses [10].
Endogenous functions of the aryl hydrocarbon receptor (AHR): Intersection of cytochrome P450 1 (CYP1)-metabolized eicosanoids and AHR biology
2008, Journal of Biological ChemistryCitation Excerpt :It should now be possible to identify CYP1-mediated AHR ligands by comparing metabolite profiles from an assortment of tissues of the wild-type mouse with those of various combinations of the Cyp1 knock-out lines that are now available. Other Evidence of Endogenous Functions of AHR—In untreated mice, the highest AHR level in any cell type is seen in the oocyte (19), and incredibly high levels of CYP1A1 mRNA are found in the oocyte after fertilization (20). Interestingly, retinoic acid-induced differentiation in cultured cells and hepatic regeneration in the intact mouse are both associated with up-regulation of CYP1A1 in the absence of an exogenous inducer (21).
- 1
Present address: Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.
- 2
Corresponding author. Fax: 513-558-0925. E-mail:[email protected].