Akr1c12 is a member of the aldo-keto reductase (AKR) superfamily. It functions as a dehydrogenase for endogenous hydroxysteroids and geranylgeraniol in mouse stomach and myeloid cells [2]. It may also be involved in the detoxification of xenobiotics in the stomach [1]. Akr1c12 is part of the hydroxysteroid dehydrogenase sub-family, which is related to processes like steroid metabolism [3]. Mouse models are valuable for studying its function.

Although no knockout (KO) or conditional knockout (CKO) mouse model-specific findings for Akr1c12 were directly presented in the provided abstracts, its expression has been observed in various tissues such as stomach, liver, ileum, and also in the context of diabetic nephropathy in BTBR mice where it was up-regulated in both male and female mice with the disease [1,4]. Additionally, electromagnetic pulse irradiation was shown to up-regulate Akr1c12 expression in mouse small intestines [5].

In conclusion, Akr1c12 has functions related to steroid-associated metabolism and potential xenobiotic detoxification. While KO/CKO mouse model-specific data is lacking from the given references, its expression changes in disease-related (diabetic nephropathy) and stress-related (electromagnetic pulse irradiation) contexts suggest its importance in these biological scenarios, potentially providing insights into disease mechanisms and responses to external stimuli.