Editing Vitamin A (section)

===Gene regulation===
RA regulates gene transcription by binding to nuclear receptors known as retinoic acid receptors (RARs; RARα, RARβ, RARγ) which are bound to [[DNA]] as heterodimers with retinoid "X" receptors (RXRs; RXRα, RXRβ, RXRγ). RARs and RXRs must dimerize before they can bind to the DNA. Expression of more than 500 genes is responsive to retinoic acid.<ref name=PKIN2020VitA/> RAR-RXR heterodimers recognize retinoic acid response elements on DNA.<ref>{{cite journal | vauthors = Duester G | title = Retinoic acid synthesis and signaling during early organogenesis | journal = Cell | volume = 134 | issue = 6 | pages = 921–931 | date = September 2008 | pmid = 18805086 | pmc = 2632951 | doi = 10.1016/j.cell.2008.09.002 }}</ref> Upon binding retinoic acid, the receptors undergo a conformational change that causes co-repressors to dissociate from the receptors. Coactivators can then bind to the receptor complex, which may help to loosen the chromatin structure from the histones or may interact with the transcriptional machinery.<ref>{{cite book |title=Biochemical, Physiological and Molecular Aspects of Human Nutrition | vauthors = Stipanuk MH |year=2006 |edition=2nd |publisher=Saunders |location=Philadelphia |isbn=9781416002093}}</ref> This response upregulates or downregulates the expression of target genes, including the genes that encode for the receptors themselves.<ref name="Combs2008" /> To deactivate retinoic acid receptor signaling, three cytochromes (Cyp26A1, Cyp26B1 Cyp26C1) catalyze the oxidation of RA. The genes for these proteins are induced by high concentrations of RA, thus providing a regulatory feedback mechanism.<ref name=PKIN2020VitA/>