ArticleThe Journal of clinical investigation1991
Dissociation and redistribution of Na+,K(+)-ATPase from its surface membrane actin cytoskeletal complex during cellular ATP depletion.
Article in The Journal of clinical investigation, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 148 citations in OpenAlex.
- Therapeutic Approaches Involving Mitochondria in the Treatment of Acute Kidney Injury.Seminars in nephrology · 2026Review
- Ameliorating Acute Kidney Injury Induced by Ischemia-Reperfusion by Targeting Purine Metabolism.International journal of molecular sciences · 2025Article
- Electrical Stimulation Therapy - Dedicated to the Perfect Plastic Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Xanthine oxidase inhibitor ameliorates postischemic renal injury in mice by promoting resynthesis of adenine nucleotides.JCI insight · 2019Article
- Influenza A Virus Infection Induces Apical Redistribution of NaAmerican journal of respiratory cell and molecular biology · 2019Article
- Hyperuricemia Induces Wnt5a/Ror2 Gene Expression, Epithelial-Mesenchymal Transition, and Kidney Tubular Injury in Mice.Iranian journal of medical sciences · 2018Article
- Akt Substrate of 160 kD Regulates Na+,K+-ATPase Trafficking in Response to Energy Depletion and Renal Ischemia.Journal of the American Society of Nephrology : JASN · 2015Article
- Role of Toll-like receptor-4 in renal graft ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2014Review
- Pathophysiology of acute kidney injury.Comprehensive Physiology · 2012Review
- Preactivation of AMPK by metformin may ameliorate the epithelial cell damage caused by renal ischemia.American journal of physiology. Renal physiology · 2011Article
- Pathophysiology of ischemic acute kidney injury.Nature reviews. Nephrology · 2011Review
- The sodium pump alpha1 sub-unit: a disease progression-related target for metastatic melanoma treatment.Journal of cellular and molecular medicine · 2009Article
- The sodium pump alpha1 subunit as a potential target to combat apoptosis-resistant glioblastomas.Neoplasia (New York, N.Y.) · 2008Review
- Na+/K+ -ATPase stabilization by Hsp70 in the outer stripe of the outer medulla in rats during recovery from a low-protein diet.Cell stress & chaperones · 2008Article
- Altered renal tubular expression of the complement inhibitor Crry permits complement activation after ischemia/reperfusion.The Journal of clinical investigation · 2006Article
- Heat-shock protein 70: molecular supertool?Pediatric nephrology (Berlin, Germany) · 2005Review
- Sex differences in the alterations of Na(+), K(+)-ATPase following ischaemia-reperfusion injury in the rat kidney.The Journal of physiology · 2004Article
- Structural and functional lesions in brush border of human polarized intestinal Caco-2/TC7 cells infected by members of the Afa/Dr diffusely adhering family of Escherichia coli.Infection and immunity · 2000Article
- Potentiation of a voltage-gated proton current in acidosis-induced swelling of rat microglia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Polycystin-1, the PKD1 gene product, is in a complex containing E-cadherin and the catenins.The Journal of clinical investigation · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Establishment and maintenance of a polar distribution of Na+,K(+)-ATPase is essential for efficient Na+ reabsorption by proximal tubule cells and is dependent upon the formation of a metabolically stable, detergent-insoluble complex of Na+,K(+)-ATPase with the actin membrane cytoskeleton. The present studies show that cellular ATP depletion results in a rapid duration-dependent dissociation of Na+,K(+)-ATPase from the actin cytoskeleton and redistribution of Na+,K(+)-ATPase to the apical membrane. During ATP depletion, total cellular Na+,K(+)-ATPase activity was unaltered, but the Triton-X-100-insoluble fraction (cytoskeleton associated) of Na+,K(+)-ATPase activity decreased (P less than 0.01), with a corresponding increase in the detergent-soluble fraction of Na+,K(+)-ATPase (P less than 0.01). Indirect immunofluorescent studies of cells with depleted ATP revealed a redistribution of Na+,K(+)-ATPase from the basolateral membrane into the apical membrane and throughout the cytoplasm. ATP depletion also resulted in the redistribution of F-actin from a primarily cortical concentration to a perinuclear location. There was also a rapid, duration-dependent conversion of monomeric G-actin to F-actin starting during the first 5 min of ATP depletion. Taken together, these data suggest that ATP depletion causes profound alterations in cell polarity by inducing major changes in the actin cytoskeletal architecture.
Indexed as
Identifiers
What OpenQuestion holds
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.