Evidence map›Paper›PMID 22334691›Full record

ArticleThe Journal of biological chemistry2012

Rapid aquaporin translocation regulates cellular water flow: mechanism of hypotonicity-induced subcellular localization of aquaporin 1 water channel.

Matthew T Conner, Alex C Conner, Charlotte E Bland, Luke H J Taylor, James E P Brown, H Rheinallt Parri, Roslyn M Bill

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

53 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Aquaporin-1 and Osmosis: From Physiology to Precision in Peritoneal Dialysis.Journal of the American Society of Nephrology : JASN · 2024
    Review
  8. Review
  9. Osmotic Pressure and Its Biological Implications.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Article
  12. Anomalous Oligomerization Behavior ofInternational journal of molecular sciences · 2023
    Article
  13. Evolutionary Overview of Aquaporin Superfamily.Advances in experimental medicine and biology · 2023
    Article
  14. Protein Structure and Modification of Aquaporins.Advances in experimental medicine and biology · 2023
    Article
  15. Article
  16. Aquaporin Gating: A New Twist to Unravel Permeation through Water Channels.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Molecular mechanisms governing aquaporin relocalisation.Biochimica et biophysica acta. Biomembranes · 2022
    Review
  19. Emerging roles for AQP in mammalian extracellular vesicles.Biochimica et biophysica acta. Biomembranes · 2022
    Review
  20. Review
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

7 authors at 2 institutions in 1 country.

Matthew T ConnerSchool of Life & Health Sciences and Aston Research Centre for Healthy Ageing, Aston University, Aston Triangle, Birmingham B4 7ET, United Kingdom.
Alex C Conner
Charlotte E Bland
Luke H J Taylor
James E P Brown
H Rheinallt Parri
Roslyn M Bill
Aston University · GBUniversity of Warwick · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The control of cellular water flow is mediated by the aquaporin (AQP) family of membrane proteins. The structural features of the family and the mechanism of selective water passage through the AQP pore are established, but there remains a gap in our knowledge of how water transport is regulated. Two broad possibilities exist. One is controlling the passage of water through the AQP pore, but this only has been observed as a phenomenon in some plant and microbial AQPs. An alternative is controlling the number of AQPs in the cell membrane. Here, we describe a novel pathway in mammalian cells whereby a hypotonic stimulus directly induces intracellular calcium elevations through transient receptor potential channels, which trigger AQP1 translocation. This translocation, which has a direct role in cell volume regulation, occurs within 30 s and is dependent on calmodulin activation and phosphorylation of AQP1 at two threonine residues by protein kinase C. This direct mechanism provides a rationale for the changes in water transport that are required in response to constantly changing local cellular water availability. Moreover, because calcium is a pluripotent and ubiquitous second messenger in biological systems, the discovery of its role in the regulation of AQP translocation has ramifications for diverse physiological and pathophysiological processes, as well as providing an explanation for the rapid regulation of water flow that is necessary for cell homeostasis.

Indexed as

OsmosisAnimalsAquaporin 1AstrocytesCalciumCalmodulinCell SizeHEK293 CellsHomeostasisHumansIntracellular SpaceKineticsPhosphorylationProtein Kinase CProtein TransportRatsAquaporin 1CalciumCalmodulinProtein Kinase CTRPC Cation ChannelsWater

Identifiers

PMID22334691
PMCPMC3322852
OpenAlexW2150727193

What OpenQuestion holds

Textmetadata
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.