Ripk4-flox Mouse

Ripk4, short for receptor-interacting protein kinase 4, is a member of the RIPK family. It was initially described as an interaction partner of protein kinase C (PKC) β and PKCδ. Ripk4 is a key regulator in multiple biological processes. It can regulate signaling pathways such as NF-κB, Wnt/β-catenin, and RAF/MEK/ERK, and is important for keratinocyte differentiation, cutaneous inflammation, and cutaneous wound repair [3].

Specific ablation of Ripk4 in kidney proximal tubules protects mice from acute kidney injury induced by cisplatin and renal ischemia/reperfusion, suggesting its role in oxidative stress and ferroptotic death [1]. In ovarian cancer, Ripk4 silencing inhibits intraperitoneal tumor growth, invasion, and vascular mimicry, and downregulation of Ripk4 inhibits the epithelial-mesenchymal transition. This indicates that Ripk4 may function as an oncogene in ovarian cancer [2]. In cutaneous squamous cell carcinoma, depletion of Ripk4 parallels higher malignancy potential, although it does not reverse radiation resistance in vitro [4].

In conclusion, Ripk4 is a crucial regulator in various biological processes and diseases. Gene-knockout mouse models have revealed its role in acute kidney injury, ovarian cancer, and cutaneous squamous cell carcinoma, among others. Understanding Ripk4 provides insights into the mechanisms of these diseases and may offer potential therapeutic targets.