Evidence map›Paper›PMID 18276733›Full record

ArticleThe Journal of physiology2008

Phosphatidylinositol-4,5-bisphosphate (PIP2) regulation of strong inward rectifier Kir2.1 channels: multilevel positive cooperativity.

Lai-Hua Xie, Scott A John, Bernard Ribalet, James N Weiss

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

52 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Ectopic mouse TMC1 and TMC2 alone form mechanosensitive channels that are potently modulated by TMIE.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. The network of cardiac KNaunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
  6. Coordination of bilayer properties by an inward-rectifier KJournal of structural biology: X · 2024
    Article
  7. Cooperative Gating of a KJournal of the American Chemical Society · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. From Crosstalk to Synergism: The Combined Effect of Cholesterol and PI(4,5)PAdvances in experimental medicine and biology · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. PIPFunction (Oxford, England) · 2021
    Article
  17. Review
  18. Phosphatidylinositol 4,5-bisphosphate (PIPThe Journal of biological chemistry · 2019
    Article
  19. Review
  20. 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

4 authors at 2 institutions in 2 countries.

Lai-Hua XieCardiovascular Research Laboratory, Rm 3645 MRL Building, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA. lxie@mednet.ucla.edu
Scott A John
Bernard Ribalet
James N Weiss
University of California, Los Angeles · USInstitute of Cardiology · PL

Funding

PROPERTIES OF INWARD RECTIFIER K CHANNELSR37HL060025 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WEISS, JAMES N · 1998 to 2007
$2.8M
NHLBI NIH HHS R37 HL060025NHLBI NIH HHS R37 HL60025
6 · The paper itself

Abstract

Inwardly rectifying potassium (Kir) channels are gated by the interaction of their cytoplasmic regions with membrane-bound phosphatidylinositol-4,5-bisphosphate (PIP(2)). In the present study, we examined how PIP(2) interaction regulates channel availability and channel openings to various subconductance levels (sublevels) as well as the fully open state in the strong inward rectifier Kir2.1 channel. Various Kir2.1 channel constructs were expressed in Xenopus oocytes and single channel or macroscopic currents were recorded from inside-out patches. The wild-type (WT) channel rarely visited the subconductance levels under control conditions. However, upon reducing Kir2.1 channel interaction with PIP(2) by a variety of interventions, including PIP(2) antibodies, screening PIP(2) with neomycin, or mutating PIP(2) binding sites (e.g. K188Q), visitation to the sublevels was markedly increased before channels were converted to an unavailable mode in which they did not open. No channel activity was detected in channels with the double mutation K188A/R189A, a mutant which exhibits extremely weak interaction with PIP(2). By linking subunits together in tandem dimers or tetramers containing mixtures of WT and K188A/R189A subunits, we demonstrate that one functional PIP(2)-interacting WT subunit is sufficient to convert channels from the unavailable to the available mode with a high open probability dominated by the fully open state, with similar kinetics as tetrameric WT channels. Occasional openings to sublevels become progressively less frequent as the number of WT subunits increases. Quantitative analysis reveals that the interaction of PIP(2) with WT subunits exerts strong positive cooperativity in both converting the channels from the unavailable to the available mode, and in promoting the fully open state over sublevels. We conclude that the interaction of PIP(2) with only one Kir2.1 subunit is sufficient for the channel to become available and to open to its full conductance state. Interaction with additional subunits exerts positive cooperativity at multiple levels to further enhance channel availability and promote the fully open state.

Indexed as

AnimalsAntibodiesFemaleMiceModels, StructuralMutationNeomycinOocytesPatch-Clamp TechniquesPhosphatidylinositol 4,5-DiphosphatePotassium Channels, Inwardly RectifyingProtein ConformationProtein SubunitsProtein Synthesis InhibitorsXenopus laevisAntibodiesKir2.1 channelNeomycinPhosphatidylinositol 4,5-DiphosphatePotassium Channels, Inwardly RectifyingProtein SubunitsProtein Synthesis Inhibitors

Identifiers

PMID18276733
PMCPMC2375719
OpenAlexW1599430377

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.