Evidence map›Paper›PMID 27760766›Full record

ArticleAmerican journal of physiology. Renal physiology2017

The native TRPP2-dependent channel of murine renal primary cilia.

Steven J Kleene, Nancy K Kleene

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
9.3field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 94 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Pathogenic variants in the polycystin pore helix cause distinct forms of channel dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Article
  11. Article
  12. Hyperosmolality activates polycystin-2 and TRPM4 in renal primary cilium.Pflugers Archiv : European journal of physiology · 2025
    Article
  13. Article
  14. Review
  15. A synthetic method to assay polycystin channel biophysics.bioRxiv : the preprint server for biology · 2024
    Article
  16. Calcium signalling and transport in the kidney.Nature reviews. Nephrology · 2024
    Review
  17. Article
  18. Review
  19. Article
  20. Molecular and structural basis of the dual regulation of the polycystin-2 ion channel by small-molecule ligands.Proceedings of the National Academy of Sciences of the United States of America · 2024
    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

2 authors at 1 institution in 1 country.

Steven J KleeneDepartment of Molecular and Cellular Physiology, University of Cincinnati, Cincinnati, Ohio steve@syrano.acb.uc.edu.ORCID 0000-0001-7663-3590
Nancy K KleeneDepartment of Molecular and Cellular Physiology, University of Cincinnati, Cincinnati, Ohio.
University of Cincinnati · US

Funding

Research BaseP30DK090868 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI WATNICK, TERRY J · 2010 to 2019
$11.1M
Chemosensory Transduction in a Primary CiliumR21DK091917 · NIDDK · UNIVERSITY OF CINCINNATI · PI KLEENE, STEVEN J · 2011 to 2012
$432k
NIDDK NIH HHS P30 DK090868NIDDK NIH HHS R21 DK091917
6 · The paper itself

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is the most common life-threatening monogenic renal disease. ADPKD results from mutations in either of two proteins: polycystin-1 (also known as PC1 or PKD1) or transient receptor potential cation channel, subfamily P, member 2 (TRPP2, also known as polycystin-2, PC2, or PKD2). Each of these proteins is expressed in the primary cilium that extends from many renal epithelial cells. Existing evidence suggests that the cilium can promote renal cystogenesis, while PC1 and TRPP2 counter this cystogenic effect. To better understand the function of TRPP2, we investigated its electrophysiological properties in the native ciliary membrane. We recorded directly from the cilia of mIMCD-3 cells, a murine cell line of renal epithelial origin. In one-third of cilia examined, a large-conductance channel was observed. The channel was not permeable to Cl¯ but conducted cations with permeability ratios P

Indexed as

AnimalsCalciumCell LineCiliaCytoplasmEpithelial CellsGene Knockout TechniquesKidneyMicePolycystic Kidney, Autosomal DominantTRPP Cation ChannelsCalciumTRPP Cation ChannelsPC2polycystic kidney diseasepolycystinprimary ciliumTRPP2

Identifiers

PMID27760766
PMCPMC5283891
OpenAlexW2539249355

What OpenQuestion holds

Textmetadata
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.