SCUBA

ATP6V0D1 — ATPase H+ transporting V0 subunit d1

ATP6V0D1 belongs to a gene co-expression module in 3 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

ATP6V0D1's module in each cell type

Cell typeModuleShares the module with
CD19⁺ B cellsOxidative/ER stress
Stress
ASAH1, B4GALT1, FAM210A, FOSL2, GEM, GZF1, HIC1, MAFG +6 moreView in SCUBA
Innate lymphoid cellsTRiC Chaperonin Folding
Protein processing & ER
CACYBP, CCT2, CCT3, CCT4, CCT5, EIF5A, ELOC, FAM162A +9 moreView in SCUBA
MacrophagesProtein Biogenesis
Housekeeping
B3GAT3, BUD23, C11orf58, CHD4, CNPY2, DAZAP1, DDX46, DNAJA2 +23 moreView in SCUBA

About the gene

SynonymsATP6D, ATP6DV, P39, VATX, Vma6, VPATPD
Chromosome16: 67438014-67481181
Predicted locationIntracellular
Essential geneYes
Protein classEssential proteins, Metabolic proteins, Plasma proteins, Predicted intracellular proteins, Transporters
Biological processCilium biogenesis/degradation, Hydrogen ion transport, Ion transport, Transport

Function

Subunit of the V0 complex of vacuolar(H+)-ATPase (V-ATPase), a multisubunit enzyme composed of a peripheral complex (V1) that hydrolyzes ATP and a membrane integral complex (V0) that translocates protons. V-ATPase is responsible for acidifying and maintaining the pH of intracellular compartments and in some cell types, is targeted to the plasma membrane, where it is responsible for acidifying the extracellular environment. May play a role in coupling of proton transport and ATP hydrolysis (By similarity). In aerobic conditions, involved in intracellular iron homeostasis, thus triggering the activity of Fe(2+) prolyl hydroxylase (PHD) enzymes, and leading to HIF1A hydroxylation and subsequent proteasomal degradation. May play a role in cilium biogenesis through regulation of the transport and the localization of proteins to the cilium (By similarity).

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.