Evidence map›Paper›PMID 22291026›Full record

ArticleThe Journal of biological chemistry2012

On potential interactions between non-selective cation channel TRPM4 and sulfonylurea receptor SUR1.

Monica Sala-Rabanal, Shizhen Wang, Colin G Nichols

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. TRP Channels in Stroke.Neuroscience bulletin · 2024
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Pulmonary Hypertension and ATP-Sensitive Potassium Channels.Hypertension (Dallas, Tex. : 1979) · 2019
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Sulfonylurea receptor 1 in central nervous system injury: a focused review.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012
    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

3 authors at 1 institution in 1 country.

Monica Sala-RabanalDepartment of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Shizhen Wang
Colin G Nichols
Washington University in St. Louis · US

Funding

SUR1 (ABCC8) AND ATRIAL KATP CHANNELSR01HL095010 · NHLBI · WASHINGTON UNIVERSITY · PI NICHOLS, COLIN G · 2009 to 2017
$3.4M
NHLBI NIH HHS HL95010NHLBI NIH HHS R01 HL095010
6 · The paper itself

Abstract

The sulfonylurea receptor SUR1 associates with Kir6.2 or Kir6.1 to form K(ATP) channels, which link metabolism to excitability in multiple cell types. The strong physical coupling of SUR1 with Kir6 subunits appears exclusive, but recent studies argue that SUR1 also modulates TRPM4, a member of the transient receptor potential family of non-selective cation channels. It has been reported that, following stroke, brain, or spinal cord injury, SUR1 is increased in neurovascular cells at the site of injury. This is accompanied by up-regulation of a non-selective cation conductance with TRPM4-like properties and apparently sensitive to sulfonylureas, leading to the postulation that post-traumatic non-selective cation currents are determined by TRPM4/SUR1 channels. To investigate the mechanistic hypothesis for the coupling between TRPM4 and SUR1, we performed electrophysiological and FRET studies in COSm6 cells expressing TRPM4 channels with or without SUR1. TRPM4-mediated currents were Ca(2+)-activated, voltage-dependent, underwent desensitization, and were inhibited by ATP but were insensitive to glibenclamide and tolbutamide. These properties were not affected by cotransfection with SUR1. When the same SUR1 was cotransfected with Kir6.2, functional K(ATP) channels were formed. In cells cotransfected with Kir6.2, SUR1, and TRPM4, we measured K(ATP)-mediated K(+) currents and Ca(2+)-activated, sulfonylurea-insensitive Na(+) currents in the same patch, further showing that SUR1 controls K(ATP) channel activity but not TRPM4 channels. FRET signal between fluorophore-tagged TRPM4 subunits was similar to that between Kir6.2 and SUR1, whereas there was no detectable FRET efficiency between TRPM4 and SUR1. Our data suggest that functional or structural association of TRPM4 and SUR1 is unlikely.

Indexed as

Amino Acid MotifsAnimalsATP-Binding Cassette TransportersCell LineKineticsMicePotassium ChannelsPotassium Channels, Inwardly RectifyingProtein BindingReceptors, DrugSulfonylurea ReceptorsTRPM Cation ChannelsAbcc8 protein, mouseATP-Binding Cassette TransportersPotassium ChannelsPotassium Channels, Inwardly RectifyingReceptors, DrugSulfonylurea ReceptorsTRPM4 protein, mouseTRPM Cation Channels

Identifiers

PMID22291026
PMCPMC3308803
OpenAlexW2148922748

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.