Lats2

Large tumor suppressor kinase 2 (LATS2) is a core serine/threonine kinase of the Hippo signaling pathway that restricts cell proliferation and supports tumor suppression through phosphorylation-dependent inhibition of the transcriptional coactivators YAP and TAZ, thereby regulating organ size, cell survival, and apoptosis[1][2]. Mechanistically, LATS2 functions downstream of the Hippo kinase cascade and serves as a major effector that converts upstream growth-suppressive signals into transcriptional repression of YAP/TAZ-dependent programs[1][2]. Beyond canonical Hippo signaling, LATS2 contributes to genomic stability, centrosome regulation, mitotic fidelity, and cell-cycle control, linking growth regulation with maintenance of cellular integrity[1][3]. LATS2 also interacts functionally with the p53 tumor suppressor network, where it contributes to p53 stabilization and activation, establishing a positive regulatory connection between the Hippo and p53 pathways during cellular stress responses and tumor suppression[1][4]. In disease contexts, reduced LATS2 expression has been reported in multiple cancers, and experimental studies support its role as a tumor suppressor whose loss can facilitate malignant progression[1][5]. Compared with the closely related isoform LATS1, LATS2 exhibits distinct biological functions and tissue-specific activities despite substantial structural similarity, indicating nonredundant roles in tumor biology and stress-response pathways[1][5]. In experimental models, LATS2 has been shown to regulate DNA damage responses through direct inhibition of c-Abl kinase activity, thereby influencing apoptosis decisions following genotoxic stress and providing a useful framework for investigating Hippo pathway-mediated cell fate regulation[6].