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F-actin-capping protein subunit alpha-2 (CAPZA2) is a structural protein that forms part of the CapZ complex, an α/β heterodimer that binds the barbed (fast-growing) end of actin filaments in a Ca2+-independent manner, preventing addition or loss of actin monomers at this site[1][2][3][4]. CapZ plays a crucial role in organizing myofilaments during muscle development and maintenance, especially at the Z-discs of sarcomeres[1][3]. CAPZA2 is widely expressed in muscle and neuronal tissues, and its proper function is essential for cytoskeletal regulation, muscle contraction, and cellular development; loss-of-function or pathogenic mutations in this gene are associated with severe neurodevelopmental disorders such as global developmental delay, intellectual disability, and hypotonia[2]. Unlike some actin-capping proteins, CapZ does not sever actin filaments[3][4]. CAPZA2 is not a typical drug target, and there are currently no established interacting drugs or biomarker or therapeutic uses directly involving this protein; however, its essentiality for cellular structure and organ development has made it relevant in studies of muscle pathology, genetics, and developmental biology[2][3].
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