Txlnb, also known as β -taxilin, is a cardiomyocyte-enriched protein belonging to a family of centrosome adapter proteins involved in protein quality control. It is associated with the ubiquitin-proteasome system (UPS) and centrosome-related processes, playing a potential role in maintaining proteostasis. Genetic models, such as gene knockout mouse models, are valuable for studying its functions [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 mouse models of cardiac proteotoxicity (CryAB-R120G mice) and pressure overload (transverse aortic constriction, TAC), loss of Txlnb worsens heart phenotypes, including lower ejection fractions, increased heart mass, and elevated ubiquitinated protein accumulation. Txlnb-KO also leads to up-regulation of Txlna and several centrosomal proteins, suggesting altered centrosomal dynamics [1,2].

In conclusion, Txlnb is a key regulator of cardiac proteostasis, revealed through KO mouse models. Its role in maintaining proteostasis in cardiomyocytes is crucial, and understanding its functions provides insights into cardiac-related disease mechanisms, such as heart failure and cardiac proteotoxicity.