Target intelligence / Profile preview

V-type proton ATPase subunit G1 (ATP6V1G1)

Target
ATP6V1G1
Molecular classification
Enzyme, Transporter (specifically, ATPase; subunit of vacuolar (V-type) ATPase proton pump)
01

Overview

V-type proton ATPase subunit G1 (ATP6V1G1) is a core component of the V1 domain of the vacuolar-type H^(+)-ATPase (V-ATPase), a multisubunit enzyme transporter complex responsible for the acidification of eukaryotic intracellular organelles such as lysosomes, endosomes, and synaptic vesicles. This acidification is crucial for processes including protein degradation, receptor-mediated endocytosis, protein sorting, and neurotransmitter loading into vesicles. Dysregulation or mutation of ATP6V1G1 is associated with human disease, notably optic atrophy 6; the V-ATPase complex has broader implications in pathologies including neurodegeneration and cancer. ATP6V1G1 does not have specific approved drugs but is researched as part of the V-ATPase complex, especially using inhibitors like bafilomycin A1.

Other names
ATPase H+ transporting V1 subunit G1ATP6GATP6G1ATP6GLATP6JVma10Vacuolar ATP synthase subunit M16V-ATPase subunit G1Vacuolar proton pump subunit G1Vacuolar proton pump subunit M16DKFZp547P234ATPase, H+ transporting, lysosomal (vacuolar proton pump), member JATPase, H+ transporting, lysosomal 13kDa, V1 subunit G1V-ATPase 13 kDa subunit 1Vacuolar H(+)-ATPase subunit G1
02

Mechanism of action

Inhibition of proton transport/acidification by V-ATPase; can impact cellular pH, lysosomal function, and vesicle trafficking

03

Biological functions

Organelle acidificationATP hydrolysisProton transportProtein sortingZymogen activationReceptor-mediated endocytosisSynaptic vesicle proton gradient generationIntracellular iron homeostasis
04

Disease associations

Optic atrophy (specifically Optic Atrophy 6)potential roles in cancerneurodegenerative diseasesdisorders involving lysosomal or vesicular dysfunction
05

Safety considerations

Systemic inhibition of V-ATPase causes widespread cellular dysfunction, resulting in toxicity including impaired lysosomal function, disrupted pH homeostasis, and possible adverse neurological or developmental effectslimited therapeutic window
06

Interacting drugs

Bafilomycin A1
07

Biomarkers

No established clinical biomarkers specific for ATP6V1G1Mutations may be considered for genetic diagnosis of optic atrophy subtypes

Beyond the preview

Go deeper on V-type proton ATPase subunit G1 (ATP6V1G1).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on V-type proton ATPase subunit G1 (ATP6V1G1).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call