Evidence map›Paper›PMID 26239621›Full record

ArticleScientific reports2015

A Systems Level Analysis of Vasopressin-mediated Signaling Networks in Kidney Distal Convoluted Tubule Cells.

Lei Cheng, Qi Wu, Marleen L A Kortenoeven, Trairak Pisitkun, Robert A Fenton

Abstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Neddylation steers the fate of cellular receptors.Experimental & molecular medicine · 2024
    Review
  2. Review
  3. Review
  4. Article
  5. Arginine vasopressin regulates the renal NaAmerican journal of physiology. Renal physiology · 2024
    Article
  6. Review
  7. Review
  8. Article
  9. Targeting the Trafficking of Kidney Water Channels for Therapeutic Benefit.Annual review of pharmacology and toxicology · 2020
    Review
  10. AMPK phosphorylation of the βAmerican journal of physiology. Renal physiology · 2019
    Article
  11. Article
  12. Article
  13. Review
  14. CHIP Regulates Aquaporin-2 Quality Control and Body Water Homeostasis.Journal of the American Society of Nephrology : JASN · 2018
    Article
  15. Regulation of renal Na-(K)-Cl cotransporters by vasopressin.Pflugers Archiv : European journal of physiology · 2017
    Review
  16. Molecular mechanisms regulating aquaporin-2 in kidney collecting duct.American journal of physiology. Renal physiology · 2016
    Review
  17. Article
  18. Article
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

5 authors.

Lei ChengCenter for Interactions of Proteins in Epithelial Transport, Department of Biomedicine, Aarhus University, 8000, Aarhus, Denmark.
Qi WuCenter for Interactions of Proteins in Epithelial Transport, Department of Biomedicine, Aarhus University, 8000, Aarhus, Denmark.
Marleen L A KortenoevenCenter for Interactions of Proteins in Epithelial Transport, Department of Biomedicine, Aarhus University, 8000, Aarhus, Denmark.
Trairak PisitkunCenter for Interactions of Proteins in Epithelial Transport, Department of Biomedicine, Aarhus University, 8000, Aarhus, Denmark.
Robert A FentonCenter for Interactions of Proteins in Epithelial Transport, Department of Biomedicine, Aarhus University, 8000, Aarhus, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The kidney distal convoluted tubule (DCT) plays an essential role in maintaining body sodium balance and blood pressure. The major sodium reabsorption pathway in the DCT is the thiazide-sensitive NaCl cotransporter (NCC), whose functions can be modulated by the hormone vasopressin (VP) acting via uncharacterized signaling cascades. Here we use a systems biology approach centered on stable isotope labeling by amino acids in cell culture (SILAC) based quantitative phosphoproteomics of cultured mouse DCT cells to map global changes in protein phosphorylation upon acute treatment with a VP type II receptor agonist 1-desamino-8-D-arginine vasopressin (dDAVP). 6330 unique proteins, containing 12333 different phosphorylation sites were identified. 185 sites were altered in abundance following dDAVP. Basophilic motifs were preferential targets for upregulated sites upon dDAVP stimulation, whereas proline-directed motifs were prominent for downregulated sites. Kinase prediction indicated that dDAVP increased AGC and CAMK kinase families' activities and decreased activity of CDK and MAPK families. Network analysis implicated phosphatidylinositol-4,5-bisphosphate 3-kinase or CAMKK dependent pathways in VP-mediated signaling; pharmacological inhibition of which significantly reduced dDAVP induced increases in phosphorylated NCC at an activating site. In conclusion, this study identifies unique VP signaling cascades in DCT cells that may be important for regulating blood pressure.

Indexed as

Gene Regulatory NetworksSignal TransductionAnimalsBlood PressureCalciumCalcium-Calmodulin-Dependent Protein Kinase KinaseCell LineDeamino Arginine VasopressinEpithelial Sodium ChannelsGene Expression RegulationIon TransportIsotope LabelingKidney Tubules, DistalMaleMiceMice, Inbred C57BLCalciumCalcium-Calmodulin-Dependent Protein Kinase KinaseDeamino Arginine VasopressinEpithelial Sodium ChannelsReceptors, VasopressinScnn1a protein, mouseScnn1b protein, mouseSlc12a3 protein, mouseSodiumSolute Carrier Family 12, Member 3ThiazidesVasopressins

Identifiers

PMID26239621
PMCPMC4523861

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Registered trials

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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.