CAP2 Recombinant Rabbit mAb (S-4359-62)

Adenylyl cyclase-associated protein 2 (CAP2) is a highly evolutionarily conserved actin-binding protein of the CAP protein family, whose core function lies in precisely remodeling the dynamic structure of the cytoskeleton through coordinated regulation of actin polymerization and depolymerization kinetics. At the molecular level, CAP2 not only directly binds globular actin (G-actin) via its C-terminal actin-binding domain to promote polymerization, but also interacts with adenylyl cyclase through its N-terminal domain, tightly coupling signal transduction with cytoskeletal reorganization. Crucially, CAP2 facilitates Cofilin-mediated actin depolymerization through its unique β-fold domain, playing a dual regulatory role in maintaining the steady-state pool of polymerizable actin monomers within the cell. In terms of tissue distribution, CAP2 expression is highly selective, being predominantly enriched in the central nervous system (especially the hippocampus and cerebral cortex), as well as in skeletal muscle, cardiac muscle, and adipose tissue, suggesting its important roles in neuronal synaptic plasticity and muscle contractile function—indeed, in mouse model studies, CAP2 knockout leads to abnormal dendritic spine morphogenesis, impaired long-term potentiation (LTP), and significant deficits in spatial memory and learning abilities. In clinical pathology, CAP2 dysfunction is closely associated with multiple diseases: recessive mutations in the CAP2 gene have been confirmed to cause dilated cardiomyopathy and skeletal myopathy; in the field of neurodegenerative diseases, CAP2 protein levels are significantly elevated in the cerebrospinal fluid of patients with Alzheimer's disease and amyotrophic lateral sclerosis, and are highly positively correlated with Tau pathology and the degree of cognitive decline, positioning it as a novel candidate biomarker for assessing early synaptic dysfunction and neurodegenerative progression. Furthermore, recent studies have revealed that CAP2 is aberrantly overexpressed in various tumor tissues (such as lung cancer, liver cancer, and colon cancer) and influences tumor cell migration, invasion, and epithelial–mesenchymal transition (EMT) through regulating actin dynamics, making it a potential prognostic marker and therapeutic intervention target in oncology. Taken together, CAP2, as a pleiotropic molecule integrating signal coupling, actin regulation, and pathological biomarker functions, is advancing from fundamental cell biology toward the forefront of translational clinical research.