Rab11b, a member of the Rab family of small GTPases, plays crucial roles in membrane trafficking, especially in the recycling of various proteins. It is involved in pathways related to vesicular transport, which is essential for maintaining normal cellular functions. Genetic models, such as KO/CKO mouse models, are valuable tools for studying its functions [1,2,3,4,5].

In an alcohol-associated liver disease (ALD) mouse model, knockdown of Rab11b in macrophages alleviated alcohol-induced liver inflammation, injury, and steatosis. Rab11b activated the NLRP3 inflammasome to induce M1 macrophage polarization and inhibited autophagic flux, suppressing LC3B-mediated NLRP3 degradation [1]. In breast cancer brain metastasis (BCBM) studies, RNA-sequencing and genetic screen in Drosophila melanogaster identified Rab11b as a mediator of metastatic adaptation. It controls integrin β1 recycling, enabling efficient interaction with the brain extracellular matrix and promoting survival. Lipophilic statins, which prevent Rab11b membrane association, can prevent BCBM [2]. In intestinal epithelial progenitor cells, compound ablation of Rab11a and Rab11b in mice led to defective cell cycle entry, mitotic arrest, and apoptosis. Ex vivo, enteroids showed abnormal mitotic spindle formation and cell death. Rab11a and Rab11b share an interactome containing mitotic spindle microtubule regulators [3].

In conclusion, Rab11b is essential for membrane trafficking-related processes. Through model-based research, it has been revealed to be involved in multiple disease-related processes, such as ALD, BCBM, and intestinal epithelial renewal. These findings highlight the significance of Rab11b in understanding disease mechanisms and potentially developing therapeutic strategies.