Gbp2, short for guanylate binding protein 2, is a member of the GTPase family. It is an interferon-inducible large GTPase crucial to host immunity against pathogens. It is involved in multiple pathways, such as the notch1 signaling pathway, IFN-γ signaling pathway, and is associated with biological processes like macrophage polarization, immune cell infiltration, and angiogenesis [1,2]. Genetic models, especially KO/CKO mouse models, could potentially provide in-depth insights into its functions.

In diabetic nephropathy, Gbp2 promotes M1 macrophage polarization by activating the notch1 signaling pathway, which may influence the progression of the disease [1]. In microsatellite stability colorectal cancer, lower Gbp2 expression is related to poor prognosis and metastasis, and it is highly associated with the IFN-γ signaling pathway and CD8 +T cell infiltration [2]. In septic lung injury, Gbp2 upregulated in LPS-stimulated macrophages-derived exosomes accelerates the injury by activating epithelial cell NLRP3 signaling [3]. In glioblastoma, Gbp2 enhances invasion through the Stat3/fibronectin pathway [4]. In glioma, it facilitates progression via the regulation of KIF22/EGFR signaling [5]. In pancreatic adenocarcinoma, its overexpression is correlated with an advanced T stage and poor overall survival [6]. In triple-negative breast cancer, Gbp2 enhances paclitaxel sensitivity by promoting autophagy and inhibiting the PI3K/AKT/mTOR pathway [7]. In gastric cancer, it is highly expressed in tumor tissues, associated with a poor prognosis and an immune-hot phenotype, and can predict immunotherapeutic responses [8].

In conclusion, Gbp2 plays diverse and significant roles in various biological processes and disease conditions. Studies using KO/CKO mouse models, though not explicitly detailed in the provided references, could further clarify its functions. It is involved in macrophage-related immune responses, cancer progression, and response to therapies, making it a potential biomarker and therapeutic target for multiple diseases.