Evidence map›Paper›PMID 19641096›Full record

ArticleAmerican journal of physiology. Cell physiology2009

Regulation of Kir channels in bovine retinal pigment epithelial cells by phosphatidylinositol 4,5-bisphosphate.

Bikash R Pattnaik, Bret A Hughes

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

25 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Inward rectifier potassium (Kir) channels in the retina: living our vision.American journal of physiology. Cell physiology · 2022
    Review
  8. Article
  9. Kir7.1 disease mutant T153I within the inner pore affects KAmerican journal of physiology. Cell physiology · 2022
    Article
  10. Article
  11. Retinal Development and Pathophysiology in Kcnj13 Knockout Mice.Frontiers in cell and developmental biology · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

2 authors at 1 institution in 1 country.

Bikash R PattnaikDepartment of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, Michigan 48105, USA.
Bret A Hughes
University of Michigan–Ann Arbor · US

Funding

VIVARIUM MODULEP30EY007003 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI David Antonetti · 1987 to 2026
$17.6M
ION CONDUCTANCES IN THE RETINAL PIGMENT EPITHELIUMR01EY008850 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HUGHES, BRET A · 1991 to 2017
$6.8M
NEI NIH HHS EY-07003NEI NIH HHS EY-08850NEI NIH HHS P30 EY007003NEI NIH HHS R01 EY008850
6 · The paper itself

Abstract

The inwardly rectifying K+ (Kir) current in mammalian retinal pigment epithelial (RPE) cells, which is largely mediated by Kir7.1 channels, is stable in cells dialyzed with MgATP but runs down when intracellular ATP is depleted. A potential mechanism for this rundown is a decrease in phosphatidylinositol 4,5-bisphosphate (PIP2) regeneration by ATP-dependent lipid kinases. Here, we used the whole cell voltage-clamp technique to investigate the membrane PIP2 dependence of Kir channels in isolated bovine RPE cells. When RPE cells were dialyzed with ATP-free solution containing PIP2 (25-50 microM), rundown persisted but was markedly reduced. Removal of Mg2+ from the pipette solution also slowed rundown, indicating that elevated intracellular Mg2+ concentration contributes to rundown. Cell dialysis with the PIP2 scavenger neomycin in MgATP solution diminished Kir current in a voltage-dependent manner, suggesting that it acted at least in part by blocking the Kir channel. Kir current in MgATP-loaded cells was partially inhibited by bath application of quercetin (100 microM), phenylarsine oxide (100 microM), or wortmannin (50 microM), inhibitors of phosphatidylinositol (PI) kinases, and was completely inhibited by cell dialysis with 2 mM adenosine, a PI4 kinase inhibitor. Both LY-294002 (100 microM), an inhibitor of PI3 kinases, and its inactive analog LY-303511 (100 microM) rapidly and reversibly inhibited Kir current, suggesting that these compounds act as direct channel blockers. We conclude that the activity of Kir channels in the RPE is critically dependent on the regeneration of membrane PIP2 by PI4 kinases and that this may explain the dependence of these channels on hydrolyzable ATP.

Indexed as

1-Phosphatidylinositol 4-KinaseAdenosine TriphosphateAndrostadienesAnimalsCattleChromonesIon Channel GatingMagnesiumMorpholinesNeomycinPatch-Clamp TechniquesPhosphatidylinositol 3-KinasesPhosphatidylinositol 4,5-DiphosphatePhosphatidylinositolsPhosphoinositide-3 Kinase InhibitorsPigment Epithelium of Eye1-Phosphatidylinositol 4-Kinase2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAdenosine TriphosphateAndrostadienesChromonesKir7.1 channelLY 303511MagnesiumMorpholinesNeomycinPhosphatidylinositol 3-KinasesPhosphatidylinositol 4,5-DiphosphatePhosphatidylinositolsPhosphoinositide-3 Kinase InhibitorsPiperazinesPotassium Channels, Inwardly RectifyingWortmannin

Identifiers

PMID19641096
PMCPMC2770741
OpenAlexW2115101062

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.