Commd3-KO Mouse

Commd3, short for copper metabolism MURR1 domain-containing 3, is involved in multiple biological processes. It forms a complex with Commd8, acting as a signaling adaptor for chemoattractant receptors, and is also associated with copper homeostasis regulation, endosomal trafficking, and angiogenesis-related pathways [1,2,3,4]. Its functions impact immune responses, cancer development, and other physiological processes, making it an important gene for in-vivo functional studies using gene knockout (KO) or conditional knockout (CKO) mouse models.

In mouse models, deficiency of the Commd3/8 complex recapitulates the effects of celastrol, a compound that dissociates the complex, in suppressing humoral immune responses, B cell migration, and antibody responses, indicating its role in autoimmune diseases [1]. In breast cancer, Commd3 loss promotes invasive growth, while in ovarian carcinoma, Commd3-mediated endosomal trafficking of HER2 inhibits cancer progression [2,3]. In hepatocellular carcinoma, low expression of Commd3 can inhibit angiogenesis through the HIF1α/VEGF/NF-κB pathway [4].

In conclusion, Commd3 is crucial in regulating immune responses, copper metabolism, endosomal trafficking, and angiogenesis. Studies using KO or CKO mouse models have revealed its significant roles in autoimmune diseases, breast, ovarian, and liver cancers, providing valuable insights into disease mechanisms and potential therapeutic targets.