Evidence map›Paper›PMID 27613772›Full record

ArticleJournal of the American Heart Association2016

Protein Carbonylation of an Amino Acid Residue of the Na/K-ATPase α1 Subunit Determines Na/K-ATPase Signaling and Sodium Transport in Renal Proximal Tubular Cells.

Yanling Yan, Anna P Shapiro, Brahma R Mopidevi, Muhammad A Chaudhry, Kyle Maxwell, Steven T Haller, Christopher A Drummond, David J Kennedy, Jiang Tian, Deepak Malhotra and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 40 citations in OpenAlex.

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  10. Protein carbonylation causes sarcoplasmic reticulum CaPflugers Archiv : European journal of physiology · 2024
    Article
  11. NaInternational journal of molecular sciences · 2024
    Review
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  19. NaMolecules (Basel, Switzerland) · 2021
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 1 country.

Yanling YanDepartment of Pharmacology, Physiology and Toxicology, JCE School of Medicine, Marshall University, Huntington, WV.
Anna P ShapiroDepartment of Medicine, University of Toledo College of Medicine, Toledo, OH.
Brahma R MopideviDepartment of Medicine, University of Toledo College of Medicine, Toledo, OH.
Muhammad A ChaudhryDepartment of Pharmacology, Physiology and Toxicology, JCE School of Medicine, Marshall University, Huntington, WV.
Kyle MaxwellDepartment of Pharmacology, Physiology and Toxicology, JCE School of Medicine, Marshall University, Huntington, WV.
Steven T HallerDepartment of Medicine, University of Toledo College of Medicine, Toledo, OH.
Christopher A DrummondDepartment of Medicine, University of Toledo College of Medicine, Toledo, OH.
David J KennedyDepartment of Medicine, University of Toledo College of Medicine, Toledo, OH.
Jiang TianDepartment of Medicine, University of Toledo College of Medicine, Toledo, OH.
Deepak MalhotraDepartment of Medicine, University of Toledo College of Medicine, Toledo, OH.
Zi-Jian XieMarshall Institute for Interdisciplinary Research, Marshall University, Huntington, WV.
Joseph I ShapiroDepartment of Pharmacology, Physiology and Toxicology, JCE School of Medicine, Marshall University, Huntington, WV Department of Medicine, University of Toledo College of Medicine, Toledo, OH.
Jiang LiuDepartment of Pharmacology, Physiology and Toxicology, JCE School of Medicine, Marshall University, Huntington, WV Marshall Institute for Interdisciplinary Research, Marshall University, Huntington, WV liuj@marshall.edu.
University of Toledo · USMarshall University · US

Funding

CORAL: Clinical Coordinating CenterU01HL071556 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI COOPER, CHRISTOPHER J · 2004 to 2013
$19.3M
Receptor Na/K-ATPase Antagonists As Novel Therapeutics For Renal/Cardiac DiseasesR01HL109015 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI SHAPIRO, JOSEPH ISAAC, XIE, ZIJIAN · 2011 to 2014
$2.2M
Na/K-ATPase Reduction in Renal Disease-Related Cardiac DysfunctionR01HL105649 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI TIAN, JIANG · 2012 to 2016
$1.8M
The Role of Oxidative Signaling through Na/K-ATPase in Salt-Sensitive HypertensionR15DK106666 · NIDDK · MARSHALL UNIVERSITY · PI LIU, JIANG · 2016 to 2016
$435k
Evaluating the role of Exogenous administration of micro RNA 29b in preventing Chronic Kidney Disease induced cardiac FibrosisF32DK104615 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI DRUMMOND, CHRISTOPHER ANSON · 2014 to 2016
$134k
NHLBI NIH HHS R01 HL105649NHLBI NIH HHS R01 HL109015NHLBI NIH HHS U01 HL071556NIDDK NIH HHS F32 DK104615NIDDK NIH HHS R15 DK106666
6 · The paper itself

Abstract

backgroundWe have demonstrated that cardiotonic steroids, such as ouabain, signaling through the Na/K-ATPase, regulate sodium reabsorption in the renal proximal tubule. By direct carbonylation modification of the Pro222 residue in the actuator (A) domain of pig Na/K-ATPase α1 subunit, reactive oxygen species are required for ouabain-stimulated Na/K-ATPase/c-Src signaling and subsequent regulation of active transepithelial (22)Na(+) transport. In the present study we sought to determine the functional role of Pro222 carbonylation in Na/K-ATPase signaling and sodium handling. METHODS AND

resultsStable pig α1 knockdown LLC-PK1-originated PY-17 cells were rescued by expressing wild-type rat α1 and rat α1 with a single mutation of Pro224 (corresponding to pig Pro222) to Ala. This mutation does not affect ouabain-induced inhibition of Na/K-ATPase activity, but abolishes the effects of ouabain on Na/K-ATPase/c-Src signaling, protein carbonylation, Na/K-ATPase endocytosis, and active transepithelial (22)Na(+) transport.

conclusionsDirect carbonylation modification of Pro224 in the rat α1 subunit determines ouabain-mediated Na/K-ATPase signal transduction and subsequent regulation of renal proximal tubule sodium transport.

Indexed as

Protein CarbonylationAnimalsAnimals, Genetically ModifiedCells, CulturedCSK Tyrosine-Protein KinaseGene Knockdown TechniquesKidney Tubules, ProximalMutationOuabainRatsSignal TransductionSodiumSodium-Potassium-Exchanging ATPasesrc-Family KinasesSwineAtp1a1 protein, ratCSK Tyrosine-Protein KinaseOuabainSodiumSodium-Potassium-Exchanging ATPasesrc-Family KinasesNa/K‐ATPaseprotein carbonylationprotein traffickingreactive oxygen speciessignalingsodium transport

Identifiers

PMID27613772
PMCPMC5079028
OpenAlexW2510330873

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.