ArticleProceedings of the National Academy of Sciences of the United States of America2005
The B1-subunit of the H(+) ATPase is required for maximal urinary acidification.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.
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Who cites it
73 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.
- Role of ROS-Induced NLRP3 Inflammasome Activation in the Formation of Calcium Oxalate Nephrolithiasis.Frontiers in immunology · 2022Pooled it
- The kidney and the balance of sulfur and nitrogen as fundamental components of pH homeostasis.Physiological reports · 2026Review
- STAT3-Dependent Regulation of CFTR and Ciliogenesis Is Essential for Mucociliary Clearance and Innate Airway Defense in Hyper-IgE Syndrome.American journal of respiratory and critical care medicine · 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
- Transcriptome and Metabolome Analyses Reveal High-Altitude Adaptation Mechanism of Epididymis Sperm Maturation in Tibetan Sheep.Animals : an open access journal from MDPI · 2024Article
- Dmxl1 Is an Essential Mammalian Gene that Is Required for V-ATPase Assembly and Function In Vivo.Function (Oxford, England) · 2024Article
- pH Homeodynamics and Male Fertility: A Coordinated Regulation of Acid-Based Balance during Sperm Journey to Fertilization.Biomolecules · 2024Review
- New functions and roles of the NaPflugers Archiv : European journal of physiology · 2024Review
- State of knowledge on ammonia handling by the kidney.Pflugers Archiv : European journal of physiology · 2024Review
- Urinary Acidification Does Not Explain the Absence of Nephrocalcinosis in a Mouse Model of Familial Hypomagnesaemia with Hypercalciuria and Nephrocalcinosis (FHHNC).International journal of molecular sciences · 2024Article
- The pathophysiology of distal renal tubular acidosis.Nature reviews. Nephrology · 2023Review
- Mechanistic insights into the primary and secondary alterations of renal ion and water transport in the distal nephron.Journal of internal medicine · 2023Review
- NHE3 in the thick ascending limb is required for sustained but not acute furosemide-induced urinary acidification.American journal of physiology. Renal physiology · 2022Article
- A role for tubular NaAmerican journal of physiology. Renal physiology · 2020Article
- The Renal Physiology of Pendrin-Positive Intercalated Cells.Physiological reviews · 2020Review
- Effect of renal tubule-specific knockdown of the NaAmerican journal of physiology. Renal physiology · 2019Article
- Sex-dependent differences in water homeostasis in wild-type and V-ATPase B1-subunit deficient mice.PloS one · 2019Article
- HAmerican journal of physiology. Renal physiology · 2018Article
- Adenylyl cyclase 6 is required for maintaining acid-base homeostasis.Clinical science (London, England : 1979) · 2018Article
- Pathophysiology, diagnosis and treatment of inherited distal renal tubular acidosis.Journal of nephrology · 2018Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The multisubunit vacuolar-type H(+)ATPases mediate acidification of various intracellular organelles and in some tissues mediate H(+) secretion across the plasma membrane. Mutations in the B1-subunit of the apical H(+)ATPase that secretes protons in the distal nephron cause distal renal tubular acidosis in humans, a condition characterized by metabolic acidosis with an inappropriately alkaline urine. To examine the detailed cellular and organismal physiology resulting from this mutation, we have generated mice deficient in the B1-subunit (Atp6v1b1(-/-) mice). Urine pH is more alkaline and metabolic acidosis is more severe in Atp6v1b1(-/-) mice after oral acid challenge, demonstrating a failure of normal urinary acidification. In Atp6v1b1(-/-) mice, the normal urinary acidification induced by a lumen-negative potential in response to furosemide infusion is abolished. After an acute intracellular acidification, Na(+)-independent pH recovery rates of individual Atp6v1b1(-/-) intercalated cells of the cortical collecting duct are markedly reduced and show no further decrease after treatment with the selective H(+)ATPase inhibitor concanamycin. Apical expression of the alternative B-subunit isoform, B2, is increased in Atp6v1b1(-/-) medulla and colocalizes with the H(+)ATPase E-subunit; however, the greater severity of metabolic acidosis in Atp6v1b1(-/-) mice after oral acid challenge indicates that the B2-subunit cannot fully functionally compensate for the loss of B1. Our results indicate that the B1 isoform is the major B-subunit isoform that incorporates into functional, plasma membrane H(+)ATPases in intercalated cells of the cortical collecting duct and is required for maximal urinary acidification.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.