Evidence map›Paper›PMID 27348301›Full record

ArticleeLife2016

Atypical calcium regulation of the PKD2-L1 polycystin ion channel.

Paul G DeCaen, Xiaowen Liu, Sunday Abiria, David E Clapham

Open access · goldAbstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
7.5field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Gene expression regulation by CaCellular & molecular biology letters · 2026
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. 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
  8. Article
  9. A synthetic method to assay polycystin channel biophysics.bioRxiv : the preprint server for biology · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Polycystin Channel Complexes.Annual review of physiology · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Disrupting polycystin-2 EF hand CaJournal of cell science · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Paul G DeCaenDepartment of Cardiology, Howard Hughes Medical Institute, Boston Children's Hospital, Boston, United States.
Xiaowen LiuDepartment of Cardiology, Howard Hughes Medical Institute, Boston Children's Hospital, Boston, United States.
Sunday AbiriaDepartment of Cardiology, Howard Hughes Medical Institute, Boston Children's Hospital, Boston, United States.
David E ClaphamDepartment of Cardiology, Howard Hughes Medical Institute, Boston Children's Hospital, Boston, United States.ORCID 0000-0002-4459-9428
Boston Children's Hospital · US

Funding

RESEARCH METHODS IN PEDIATRICS HEART DISEASET32HL007572 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI Sarah D DE FERRANTI, Jane W. Newburger · 1985 to 2026
$13.0M
The genetic identity of the primary cilia ion channels of kidney collecting duct cells and their regulation by internal calciumR00DK106655 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DECAEN, PAUL GREGORY · 2017 to 2019
$742k
Howard Hughes Medical InstituteNHLBI NIH HHS T32 HL007572NIDDK NIH HHS R00 DK106655
6 · The paper itself

Abstract

Native PKD2-L1 channel subunits are present in primary cilia and other restricted cellular spaces. Here we investigate the mechanism for the channel's unusual regulation by external calcium, and rationalize this behavior to its specialized function. We report that the human PKD2-L1 selectivity filter is partially selective to calcium ions (Ca(2+)) moving into the cell, but blocked by high internal Ca(2+)concentrations, a unique feature of this transient receptor potential (TRP) channel family member. Surprisingly, we find that the C-terminal EF-hands and coiled-coil domains do not contribute to PKD2-L1 Ca(2+)-induced potentiation and inactivation. We propose a model in which prolonged channel activity results in calcium accumulation, triggering outward-moving Ca(2+) ions to block PKD2-L1 in a high-affinity interaction with the innermost acidic residue (D523) of the selectivity filter and subsequent long-term channel inactivation. This response rectifies Ca(2+) flow, enabling Ca(2+) to enter but not leave small compartments such as the cilium.

Indexed as

Gene Expression RegulationCalciumEF Hand MotifsHumansIon TransportMembrane ProteinsModels, BiologicalCalciumMembrane ProteinsPKD1L1 protein, humanbiophysicscalcium signalingcell biologychannel desensitizationhumanion channel biophysicsion selectivitypolycystic kidney diseasestructural biologyTRP channels

Identifiers

PMID27348301
PMCPMC4922860
OpenAlexW2461025464

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.