ArticleAmerican journal of physiology. Renal physiology2018
Targeted deletion of the Ncoa7 gene results in incomplete distal renal tubular acidosis in mice.
Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- TLDc proteins: Stress-responsive nexus regulators of redox signaling, V-ATPase dynamics, and organellar crosstalk in neurodegeneration.Redox biology · 2026Review
- NCOA7 inhibits renal cancer progression by inducing autophagy and lipid metabolism through V-ATPase interaction.Cell death discovery · 2025Article
- Knockout of the V-ATPase interacting protein Tldc2 in B-type kidney intercalated cells impairs urine alkalinization.American journal of physiology. Renal physiology · 2025Article
- Interaction of yeast V-ATPase with TLDc protein Rtc5p.bioRxiv : the preprint server for biology · 2025Article
- Lysosomal dysfunction and inflammatory sterol metabolism in pulmonary arterial hypertension.Science (New York, N.Y.) · 2025Article
- Human V-ATPase function is positively and negatively regulated by TLDc proteins.Structure (London, England : 1993) · 2024Article
- Dmxl1 Is an Essential Mammalian Gene that Is Required for V-ATPase Assembly and Function In Vivo.Function (Oxford, England) · 2024Article
- Molecular mechanism of Oxr1p mediated disassembly of yeast V-ATPase.EMBO reports · 2024Article
- Integration of genetic fine-mapping and multi-omics data reveals candidate effector genes for hypertension.American journal of human genetics · 2023Article
- NCOA7 Regulates Growth and Metastasis of Clear Cell Renal Cell Carcinoma via MAPK/ERK Signaling Pathway.International journal of molecular sciences · 2023Article
- Tender love and disassembly: How a TLDc domain protein breaks the V-ATPase.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Article
- Oxidative stress protein Oxr1 promotes V-ATPase holoenzyme disassembly in catalytic activity-independent manner.The EMBO journal · 2022Article
- The evolutionary conserved TLDc domain defines a new class of (HScientific reports · 2021Article
- The Ncoa7 locus regulates V-ATPase formation and function, neurodevelopment and behaviour.Cellular and molecular life sciences : CMLS · 2021Article
- The HAmerican journal of physiology. Cell physiology · 2021Review
- DOORS syndrome and a recurrent truncating ATP6V1B2 variant.Genetics in medicine : official journal of the American College of Medical Genetics · 2021Article
- Loss of Oxidation Resistance 1, OXR1, Is Associated with an Autosomal-Recessive Neurological Disease with Cerebellar Atrophy and Lysosomal Dysfunction.American journal of human genetics · 2019Article
- The interferon-inducible isoform of NCOA7 inhibits endosome-mediated viral entry.Nature microbiology · 2018Article
- Improving outcomes for patients with distal renal tubular acidosis: recent advances and challenges ahead.Pediatric health, medicine and therapeutics · 2018Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
We recently reported that nuclear receptor coactivator 7 (Ncoa7) is a vacuolar proton pumping ATPase (V-ATPase) interacting protein whose function has not been defined. Ncoa7 is highly expressed in the kidney and partially colocalizes with the V-ATPase in collecting duct intercalated cells (ICs). Here, we hypothesized that targeted deletion of the Ncoa7 gene could affect V-ATPase activity in ICs in vivo. We tested this by analyzing the acid-base status, major electrolytes, and kidney morphology of Ncoa7 knockout (KO) mice. We found that Ncoa7 KO mice, similar to Atp6v1b1 KOs, did not develop severe distal renal tubular acidosis (dRTA), but they exhibited a persistently high urine pH and developed hypobicarbonatemia after acid loading with ammonium chloride. Conversely, they did not develop significant hyperbicarbonatemia and alkalemia after alkali loading with sodium bicarbonate. We also found that ICs were larger and with more developed apical microvilli in Ncoa7 KO compared with wild-type mice, a phenotype previously associated with metabolic acidosis. At the molecular level, the abundance of several V-ATPase subunits, carbonic anhydrase 2, and the anion exchanger 1 was significantly reduced in medullary ICs of Ncoa7 KO mice, suggesting that Ncoa7 is important for maintaining high levels of these proteins in the kidney. We conclude that Ncoa7 is involved in IC function and urine acidification in mice in vivo, likely through modulating the abundance of V-ATPase and other key acid-base regulators in the renal medulla. Consequently, mutations in the NCOA7 gene may also be involved in dRTA pathogenesis in humans.
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