Angiomotin (Amot), a membrane protein, is involved in multiple biological processes. It plays roles in the Hippo signaling pathway, and is important for processes such as cell growth, polarity, and contact inhibition. Genetic models, like gene-knockout (KO) mouse models, are valuable for studying its functions [1,2,4,5].

In a mouse model with endothelial-specific deletion of Amot, it was found that Amot is required for the migration and expansion of the physiological and pathological vascular network, as well as tip cell migration and filopodia extension. It binds Talin and is essential for relaying forces between fibronectin and the cytoskeleton, integrating spatial cues from the extracellular matrix to form a functional vascular network [3].

Conditional deletion of Amot and Yap1 in neurons led to a decrease in the complexity of Purkinje cell dendritic trees, abnormal cerebellar morphology, and impairments in motor coordination, indicating Amot's role in dendritic morphogenesis [4].

In the context of diffuse large B-cell lymphoma (DLBCL), Amot expression was reduced in biopsy sections, and overexpression of Amot in human DLBCL cells inhibited cell viability, increased chemosensitivity, and reduced activation of key kinases for the DNA damage response, suggesting it acts as a tumor suppressor [1].

In conclusion, Amot is crucial for various biological functions, including vascular development, neuronal dendrite growth, and in influencing tumor progression in DLBCL. Mouse models, especially KO and conditional knockout (CKO) models, have been instrumental in revealing these functions, providing insights into its roles in specific disease areas like lymphoma and potentially guiding therapeutic strategies.