Long-distance retinoid signaling in the zebra finch brain.
Berlin, Germany. In Plos One, 2013
To address this gap, we have determined the expression patterns of two obligatory RAR co-receptors, the retinoid X receptors (RXR) α and γ, and of the three ATRA-degrading cytochromes CYP26A1, CYP26B1, and CYP26C1.
Focal facial dermal dysplasia, type IV, is caused by mutations in CYP26C1.
San Francisco, United States. In Hum Mol Genet, 2013
Assuming autosomal recessive inheritance, two novel sequence variants were identified in both siblings in CYP26C1-a duplication of seven base pairs, which was maternally inherited, c.844_851dupCCATGCA, predicting p.Glu284fsX128 and a missense mutation, c.1433G>A, predicting p.Arg478His, that was paternally inherited.
The negative side of retinoic acid receptors.
Durham, United States. In Neurotoxicol Teratol, 2011
Dehydrogenases and a subset of cytochrome p450 genes (cyp26a1, cyp26b1, and cyp26c1) play the major role in providing the retinoic acid and limiting its access.
Positive association between ALDH1A2 and schizophrenia in the Chinese population.
Shanghai, China. In Prog Neuropsychopharmacol Biol Psychiatry, 2009
In the present study we chose to investigate 7 genes involved in the synthesis, degradation and transportation of RA, ALDH1A1, ALDH1A2, ALDH1A3, CYP26A1, CYP26B1, CYP26C1 and Transthyretin (TTR), for their roles in the development of schizophrenia.
Retinoids, eye development, and maturation of visual function.
Waltham, United States. In J Neurobiol, 2006
Throughout development CYP26A1 degrades RA in a horizontal region that extends across the retina, but during later embryonic and postnatal retina maturation this function is reinforced by another enzyme, CYP26C1.