ArticleTrends in pharmacological sciences2022
GPR35, ally of the anti-ischemic ATPIF1-ATP synthase interaction.
Article in Trends in pharmacological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Proline-Mediated Inhibition of ATPIF1-mTOR Signaling Alleviates Radiation-Induced Macrophage Polarization and Colon Inflammation.Inflammation · 2026Article
- Receptor-Mitochondria Crosstalk in the Kynurenine Metabolic Pathway: Integrating Metabolomics and Clinical Mass Spectrometry.Antioxidants (Basel, Switzerland) · 2026Review
- The Mitochondrial ATP Synthase/IF1 Axis in Cancer Progression: Targets for Therapeutic Intervention.Cancers · 2023Review
- IF1 ablation prevents ATP synthase oligomerization, enhances mitochondrial ATP turnover and promotes an adenosine-mediated pro-inflammatory phenotype.Cell death & disease · 2023Article
- Recent advances in GPR35 pharmacology; 5-HIAA serotonin metabolite becomes a ligand.Archives of pharmacal research · 2023Review
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1 author at 1 institution in 1 country.
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Abstract
Mitochondrial ATP synthase synthesizes ATP for cellular functions; however, under various conditions, including ischemia, it hydrolyzes ATP, primarily to re-energize the mitochondria. ATP synthase inhibitory factor 1 (ATPIF1) inhibits hydrolysis of ATP by ATP synthase. Wyant and colleagues recently demonstrated that G-protein-coupled receptor 35 (GPR35) is involved in this process. This finding provides an additional framework for the novel discovery of potential therapeutic molecules against ischemia/reperfusion (I/R) injury.
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