ATP6V0C Membrane Protein Introduction

Introduction of ATP6V0C

V-type proton ATPase 16 kDa proteolipid subunit (ATP6V0C) is encoded by ATP6V0C gene, which is mapped to chromosome 16p13.3. ATP6V0C is the bafilomycin A1-binding subunit of vacuolar ATPase (V-ATPase), an enzyme complex that critically regulates the eukaryotic intracellular organelles acidification. V-ATPase is organized into two coordinately operating multi-subunit domains: a peripheral V1 domain where ATP hydrolysis provides energy for proton movement, and an integral membrane V0 domain where proton translocation takes place. ATP6V0C is the c subunit of the V0 domain. ATP6V0C is most abundant in brain and kidney.

Basic Information of ATP6V0C
Protein Name V-type proton ATPase 16 kDa proteolipid subunit
Gene Name ATP6V0C
Aliases Vacuolar proton pump 16 kDa proteolipid subunit
Organism Homo sapiens (Human)
UniProt ID P27449
Transmembrane Times 4
Length (aa) 155

Function of ATP6V0C Membrane Protein

Localized to many different membranes of eukaryotic cells including lysosomes, endosomes, Golgi-derived vesicles, ANF secretory vesicles, V-ATPase has well documented functions, including vesicle fusion with vacuoles and the acidification of eukaryotic intracellular organelles, that is essential for many intracellular processes, such as protein sorting, zymogen activation, synaptic vesicle proton gradient generation, and receptor-mediated endocytosis. ATP6V0C acts as a part of the proton channel of V-ATPases and is indispensable for the V-ATPase assembly and functions. It has been shown that ATP6V0C knockdown can inhibit vesicular acidification and sensitize cells to stress-induced cell death. In addition, knockdown of ATP6V0C in neuronal cells is shown to adversely affect autophagy-lysosome pathway function and cause the abnormal accumulation of ALP-associated substrates including α-syn and APP-CTFs, suggesting the relevance of ATP6V0C to age-related neurodegenerative disease. ATP6V0C can be degraded via the ubiquitin-proteasome pathway after being ubiquitinated by RNF182.

The predicted structure of ATP6V0C. Fig.1 The predicted structure of ATP6V0C. (Bienert, 2017)

Application of ATP6V0C Membrane Protein in Literature

  1. Mangieri L.R., et al. ATP6V0C knockdown in neuroblastoma cells alters autophagy-lysosome pathway function and metabolism of proteins that accumulate in neurodegenerative disease. PLoS One. 2014, 9(4): e93257. PubMed ID: 24695574

    This article indicates that ATP6V0C may be associated with keeping constitutive and stress-induced alkaline phosphatase function, in particular, the metabolism of substrates which accumulate in age-related neurodegenerative disease. Additionally, it may be associated with disease pathogenesis.

  2. Pavelin J., et al. Systematic microRNA analysis identifies ATP6V0C as an essential host factor for human cytomegalovirus replication. PLoS Pathog. 2013, 9(12): e1003820. PubMed ID: 24385903

    This article finds that siRNA knockdown of ATP6V0C leads to almost complete loss of infectious virus production, suggesting that an HCMV microRNA can target a critical cellular factor required for virus replication.

  3. Lim J.H., et al. ATP6V0C competes with von Hippel-Lindau protein in hypoxia-inducible factor 1alpha (HIF-1alpha) binding and mediates HIF-1alpha expression by bafilomycin A1. Mol Pharmacol. 2007, 71(3):942-8. PubMed ID: 17178925

    This article suggests that a novel regulator of HIF-1alpha, ATP6V0C, regulates HIF-1alpha expression by bafilomycin.

  4. Liu Q.Y., et al. A novel brain-enriched E3 ubiquitin ligase RNF182 is up-regulated in the brains of Alzheimer's patients and targets ATP6V0C for degradation. Mol Neurodegener. 2008, 3: 4. PubMed ID: 18298843

    This article confirms that a novel brain-enriched RING finger E3 ligase interacts with ATP6V0C protein, suggesting that it may have an influence in controlling the turnover of an essential component of neurotransmitter release machinery.

  5. Jin D., et al. Dopamine release via the vacuolar ATPase V0 sector c-subunit, confirmed in N18 neuroblastoma cells, results in behavioral recovery in hemiparkinsonian mice. Neurochem Int. 2012, 61(6): 907-12. PubMed ID: 22265874

    This article indicates that ATP6V0C regulates dopamine release from gene-transferred striatal cells of parkinsonian mice and from nerve terminals in the striatum of dopamine neurons of normal mice, suggesting that it may be helpful as a rescue molecule in addition to endogenous dopamine synthetic enzymes in the gene therapy of Parkinson's disease.

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  1. Bienert S, et al. (2017). The SWISS-MODEL Repository - new features and functionality. Nucleic Acids Res. 45: D313-D319.

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