Txlnb-KO Mouse

Txlnb, also known as β -taxilin, is a cardiomyocyte-enriched protein belonging to a family of centrosome adapter proteins implicated in protein quality control. It is involved in cytoskeletal, microtubule, and the ubiquitin-proteasome system (UPS) processes, especially those related to centrosome functions. The centrosome-proteasome axis, in which Txlnb may play a bridging role, is potentially important for proteostasis in cardiomyocytes [1,2].

In Txlnb-knockout (KO) mouse models, there is proteasomal insufficiency and altered cardiac growth. Ubiquitinated protein accumulates, 26Sβ5 proteasome activity decreases, and cardiac mass lowers with age. In models of cardiac proteotoxicity (CryAB-R120G mice) and pressure overload (transverse aortic constriction, TAC), loss of Txlnb worsens heart phenotypes, such as reduced ejection fraction and increased heart mass [1,2]. In C2C12 cells, knockdown of β -taxilin (Txlnb) impairs the fusion of myoblasts into myotubes and decreases myotube diameter, indicating its role in myogenesis [3].

In conclusion, Txlnb plays a crucial role in cardiac proteostasis and myogenesis. The Txlnb KO mouse models and cell-based knockdown experiments have revealed its significance in cardiac-related diseases and muscle development, highlighting the importance of the centrosome-proteasome connection in cardiomyocytes and the role of Txlnb in myoblast differentiation.