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Vacuolar ATPase subunit B2 (ATP6V1B2) is a non-catalytic component of the V1 sector of the V-ATPase complex, a multi-subunit enzyme responsible for acidifying intracellular compartments including lysosomes, endosomes, and synaptic vesicles[1][3]. The V-ATPase is vital for such processes as protein degradation, receptor-mediated endocytosis, neurotransmitter storage, and autophagy. ATP6V1B2 is ubiquitously expressed, with important roles in the brain, osteoclasts, and inner ear. Mutations in ATP6V1B2 can cause syndromic deafness and developmental disorders due to impaired lysosomal acidification and subsequent disruption of cellular degradation pathways, leading to cellular apoptosis, especially in neurons[1][3]. The protein is an established research target for pharmacological inhibition in studies of cell biology and disease, but no clinically approved drugs target this subunit directly.
Inhibition of proton translocation (by V-ATPase inhibitors, preventing ATP-driven proton pumping and organellar acidification)
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