COX5A (Cytochrome c oxidase subunit Va) is a mitochondrial protein essential for cellular respiration as part of the cytochrome c oxidase (COX) complex, the terminal enzyme of the electron transport chain . It facilitates proton gradient formation for ATP synthesis and regulates mitochondrial energy metabolism . COX5A antibodies are tools for detecting and studying this protein in human, mouse, rat, and other species via techniques like Western blot (WB), immunohistochemistry (IHC), immunoprecipitation (IP), and immunofluorescence (IF) .
Mechanism: COX5A downregulation in aged hippocampus correlates with reduced BDNF/ERK1/2 signaling, impairing dendritic branching and spatial memory .
Intervention: Transgenic mice with COX5A overexpression (51% increase) showed improved hippocampal mitochondrial activity, ATP levels, and memory performance .
Key Finding: ERK1/2 inhibitor PD98059 blocked COX5A’s neuroprotective effects, confirming BDNF/ERK1/2 pathway dependency .
Protective Role: COX5A overexpression in cardiomyocytes reduced oxidative stress (ROS), mitochondrial dysfunction, and apoptosis via PI3K/Akt signaling .
Clinical Relevance: Human end-stage dilated cardiomyopathy (DCM) samples showed diminished COX5A expression, suggesting therapeutic potential .
OxPhos Signature: COX5A is a hub gene in SLE T cells, correlating with disease activity, skin/kidney involvement, and interferon response .
Biomarker Potential: Elevated COX5A expression in effector T cells predicts organ damage severity .