TXLNB (taxilin beta) is a cardiomyocyte and skeletal muscle-enriched centrosomal adapter protein that functions as a regulator of cellular proteostasis. Structurally, TXLNB localizes to perinuclear centrosomal compartments where it bridges centrosomal and ubiquitin-proteasome system (UPS) machinery 1. At the molecular level, TXLNB interacts with cytoskeletal and microtubule-associated proteins while promoting proteasomal activity and reducing ubiquitinated protein accumulation 2. In myogenesis, TXLNB participates in myoblast differentiation by suppressing dysbindin function to regulate myotube formation 3. In cardiac tissue, TXLNB dysfunction has significant pathological consequences. Loss of TXLNB causes proteasomal insufficiency, increased ubiquitinated protein accumulation, and altered cardiac growth with aging 1. TXLNB knockout mice exhibit exacerbated heart failure phenotypes in models of cardiac proteotoxicity and pressure overload, including reduced ejection fraction and increased heart mass 1. Conversely, TXLNB overexpression enhances proteasomal function during cardiac hypertrophy 2. These findings establish TXLNB as a critical regulator of cardiac proteostasis with therapeutic implications for cardiomyopathies associated with protein quality control defects. Additionally, TXLNB has been identified as a differentially expressed lncRNA in ovarian tumors 4.