Involved in the metabolism of retinoic acid (RA), rendering this classical morphogen inactive through oxidation (PubMed:10823918, PubMed:22020119). Involved in the specific inactivation of all-trans-retinoic acid (all-trans-RA), with a preference for the following substrates: all-trans-RA > 9-cis-RA > 13-cis-RA (PubMed:10823918, PubMed:22020119). Generates several hydroxylated forms of RA, including 4-OH-RA, 4-oxo-RA, and 18-OH-RA (PubMed:10823918). Catalyzes the hydroxylation of carbon hydrogen bonds of atRA primarily at C-4 (PubMed:10823918, PubMed:22020119). Essential for postnatal survival (By similarity). Plays a central role in germ cell development: acts by degrading RA in the developing testis, preventing STRA8 expression, thereby leading to delay of meiosis (By similarity). Required for the maintenance of the undifferentiated state of male germ cells during embryonic development in Sertoli cells, inducing arrest in G0 phase of the cell cycle and preventing meiotic entry (By similarity). Plays a role in skeletal development, both at the level of patterning and in the ossification of bone and the establishment of some synovial joints (PubMed:22019272). Has also a significant activity in oxidation of tazarotenic acid and may therefore metabolize that xenobiotic in vivo. all-trans-retinoate + O2 + reduced [NADPH--hemoprotein reductase] = all-trans-4-hydroxyretinoate + H(+) + H2O + oxidized [NADPH--hemoprotein reductase] Highly expressed in brain, particularly in the cerebellum and pons. By retinoic acid. The disease is caused by variants affecting the gene represented in this entry. Belongs to the cytochrome P450 family. Truncated N-terminus.