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Gene Review

Cyp26a1  -  cytochrome P450, family 26, subfamily a,...

Mus musculus

Synonyms: Cyp26, Cytochrome P450 26A1, Cytochrome P450RAI, P450RA, P450RAI, ...
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Disease relevance of Cyp26a1


High impact information on Cyp26a1


Chemical compound and disease context of Cyp26a1

  • We have previously reported that the retinoic acid (RA) catabolizing enzyme CYP26A1 plays an important role in protecting tail bud tissues from inappropriate exposure to RA generated in the adjacent trunk tissues by RALDH2, and that Cyp26a1-null animals exhibit spina bifida and caudal agenesis [6].

Biological context of Cyp26a1


Anatomical context of Cyp26a1

  • We demonstrate in mouse embryos that an RA signal initially travels from the paraxial mesoderm to r3, forming a boundary next to the r2 expression domain of Cyp26a1 (which encodes an RA-degrading enzyme) [10].
  • Like its human and zibrafish counterparts, the mouse P450RAI cDNA catalyzes metabolism of retinoic acid into 4-OH-retinoic acid, 4-oxo-retinoic acid, 18-OH-retinoic acid, and unidentified water-soluble metabolites when transfected into COS-1 cells [11].
  • Initially, both RALDH2 and RARE-LacZ activity were restricted to the sinus venosa in unlooped hearts, but were high in the dorsal mesocardium, while P450RA expression was restricted to the endocardium [12].

Associations of Cyp26a1 with chemical compounds

  • We now show that, in the absence of Cyp26a1, retinoic acid receptor gamma (RARgamma) mediates ectopic RA-signaling in the tail bud [6].
  • Regulation of CYP26 (cytochrome P450RAI) mRNA expression and retinoic acid metabolism by retinoids and dietary vitamin A in liver of mice and rats [13].
  • Activation of a lacZ transgene controlled by an RA response element (RARE) was compared to the localization of the retinaldehyde-oxidizing dehydrogenase RALDH2, the earliest RA synthetic enzyme in the mouse embryo, and to the expression of a gene encoding an RA-degrading enzyme (P450RA) [12].

Regulatory relationships of Cyp26a1

  • Similarly, we found that Cyp26a1 transcription is epigenetically regulated by RARbeta2 [7].

Other interactions of Cyp26a1

  • Developing with lethal RA levels: genetic ablation of Rarg can restore the viability of mice lacking Cyp26a1 [6].
  • Our findings suggest that Raldh2 and Cyp26 generate shifting boundaries of RA activity, such that r3-r4 receives a short pulse of RA and r5-r8 receives a long pulse of RA [10].
  • Apparently, RARalpha, RARbeta2 and Cyp26a1 are components of a RA-regulated gene network [7].
  • While RA applications increased retinal Cyp26a1 expression, they slightly reduced Cyp26c1 [14].

Analytical, diagnostic and therapeutic context of Cyp26a1


  1. Genetic evidence that oxidative derivatives of retinoic acid are not involved in retinoid signaling during mouse development. Niederreither, K., Abu-Abed, S., Schuhbaur, B., Petkovich, M., Chambon, P., Dollé, P. Nat. Genet. (2002) [Pubmed]
  2. Cyp26 genes a1, b1 and c1 are down-regulated in Tbx1 null mice and inhibition of Cyp26 enzyme function produces a phenocopy of DiGeorge Syndrome in the chick. Roberts, C., Ivins, S., Cook, A.C., Baldini, A., Scambler, P.J. Hum. Mol. Genet. (2006) [Pubmed]
  3. Mouse liver CYP2C39 is a novel retinoic acid 4-hydroxylase. Its down-regulation offers a molecular basis for liver retinoid accumulation and fibrosis in aryl hydrocarbon receptor-null mice. Andreola, F., Hayhurst, G.P., Luo, G., Ferguson, S.S., Gonzalez, F.J., Goldstein, J.A., De Luca, L.M. J. Biol. Chem. (2004) [Pubmed]
  4. Metabolic inactivation of retinoic acid by a novel P450 differentially expressed in developing mouse embryos. Fujii, H., Sato, T., Kaneko, S., Gotoh, O., Fujii-Kuriyama, Y., Osawa, K., Kato, S., Hamada, H. EMBO J. (1997) [Pubmed]
  5. Positively charged retinoids are potent and selective inhibitors of the trans-cis isomerization in the retinoid (visual) cycle. Golczak, M., Kuksa, V., Maeda, T., Moise, A.R., Palczewski, K. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  6. Developing with lethal RA levels: genetic ablation of Rarg can restore the viability of mice lacking Cyp26a1. Abu-Abed, S., Dollé, P., Metzger, D., Wood, C., MacLean, G., Chambon, P., Petkovich, M. Development (2003) [Pubmed]
  7. RAR-mediated epigenetic control of the cytochrome P450 Cyp26a1 in embryocarcinoma cells. Pozzi, S., Rossetti, S., Bistulfi, G., Sacchi, N. Oncogene (2006) [Pubmed]
  8. Regulation of retinoic acid signaling during lung morphogenesis. Malpel, S., Mendelsohn, C., Cardoso, W.V. Development (2000) [Pubmed]
  9. Cytochrome P450RAI(CYP26) promoter: a distinct composite retinoic acid response element underlies the complex regulation of retinoic acid metabolism. Loudig, O., Babichuk, C., White, J., Abu-Abed, S., Mueller, C., Petkovich, M. Mol. Endocrinol. (2000) [Pubmed]
  10. Shifting boundaries of retinoic acid activity control hindbrain segmental gene expression. Sirbu, I.O., Gresh, L., Barra, J., Duester, G. Development (2005) [Pubmed]
  11. Mouse P450RAI (CYP26) expression and retinoic acid-inducible retinoic acid metabolism in F9 cells are regulated by retinoic acid receptor gamma and retinoid X receptor alpha. Abu-Abed, S.S., Beckett, B.R., Chiba, H., Chithalen, J.V., Jones, G., Metzger, D., Chambon, P., Petkovich, M. J. Biol. Chem. (1998) [Pubmed]
  12. Dynamic patterns of retinoic acid synthesis and response in the developing mammalian heart. Moss, J.B., Xavier-Neto, J., Shapiro, M.D., Nayeem, S.M., McCaffery, P., Dräger, U.C., Rosenthal, N. Dev. Biol. (1998) [Pubmed]
  13. Regulation of CYP26 (cytochrome P450RAI) mRNA expression and retinoic acid metabolism by retinoids and dietary vitamin A in liver of mice and rats. Yamamoto, Y., Zolfaghari, R., Ross, A.C. FASEB J. (2000) [Pubmed]
  14. CYP26A1 and CYP26C1 cooperate in degrading retinoic acid within the equatorial retina during later eye development. Sakai, Y., Luo, T., McCaffery, P., Hamada, H., Dräger, U.C. Dev. Biol. (2004) [Pubmed]
  15. Dynamic expression of retinoic acid-synthesizing and -metabolizing enzymes in the developing mouse inner ear. Romand, R., Kondo, T., Fraulob, V., Petkovich, M., Dollé, P., Hashino, E. J. Comp. Neurol. (2006) [Pubmed]
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