Evidence map›Paper›PMID 18001767›Full record

ArticleJournal of molecular and cellular cardiology2008

Cardiac sulfonylurea receptor short form-based channels confer a glibenclamide-insensitive KATP activity.

Jie-Lin Pu, Bin Ye, Stacie L Kroboth, Elizabeth M McNally, Jonathan C Makielski, Nian-Qing Shi

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 42 citations in OpenAlex.

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  8. Review
  9. Abcc9 is required for the transition to oxidative metabolism in the newborn heart.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
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  17. Vasodilation induced by oxygen/glucose deprivation is attenuated in cerebral arteries of SUR2 null mice.American journal of physiology. Heart and circulatory physiology · 2011
    Article
  18. Hydrogen sulfide dilates cerebral arterioles by activating smooth muscle cell plasma membrane KATP channels.American journal of physiology. Heart and circulatory physiology · 2011
    Article
  19. Article
  20. The mitochondrial bioenergetic phenotype for protection from cardiac ischemia in SUR2 mutant mice.American journal of physiology. Heart and circulatory physiology · 2010
    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

6 authors at 1 institution in 1 country.

Jie-Lin PuDepartment of Medicine, University of Wisconsin, 1300, University Ave., Room 24, SMI Building, Madison, WI 53706, USA.
Bin Ye
Stacie L Kroboth
Elizabeth M McNally
Jonathan C Makielski
Nian-Qing Shi
University of Chicago · US

Funding

Molecular Regulation of Cardiac KATP Channels in IschemiaR01HL057414 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MAKIELSKI, JONATHAN C · 1997 to 2012
$3.8M
NHLBI NIH HHS 2R01HL-57414NHLBI NIH HHS R01 HL057414
6 · The paper itself

Abstract

The cardiac sarcolemmal ATP-sensitive potassium channel (K(ATP)) consists of a Kir6.2 pore and an SUR2 regulatory subunit, which is an ATP-binding cassette (ABC) transporter. K(ATP) channels have been proposed to play protective roles during ischemic preconditioning. An SUR2 mutant mouse was previously generated by disrupting the first nucleotide-binding domain (NBD1), where a glibenclamide action site was located. In the mutant ventricular myocytes, a non-conventional glibenclamide-insensitive (10 microM), ATP-sensitive current (I(KATPn)) was detected in 33% of single-channel recordings with an average amplitude of 12.3+/-5.4 pA per patch, an IC(50) to ATP inhibition at 10 microM and a mean burst duration at 20.6+/-1.8 ms. Newly designed SUR2 isoform- or variant-specific antibodies identified novel SUR2 short forms in the sizes of 28 and 68 kDa in addition to a 150-kDa long form in the sarcolemmal membrane of wild-type (WT) heart. We hypothesized that channels constituted by these short forms that lack NBD1 confer I(KATPn). The absence of the long form in the mutant corresponded to loss of the conventional glibenclamide-sensitive K(ATP) currents (I(KATP)) in isolated cardiomyocytes and vascular smooth muscle cells but the SUR2 short forms remained intact. Nested exonic RT-PCR in the mutant indicated that the short forms lacked NBD1 but contained NBD2. The SUR2 short forms co-immunoprecipitated with Kir6.1 or Kir6.2 suggesting that the short forms may function as hemi-transporters reported in other eukaryotic ABC transporter subgroups. Our results indicate that different K(ATP) compositions may co-exist in cardiac sarcolemmal membrane.

Indexed as

AnimalsAntibodiesAntibody SpecificityATP-Binding Cassette TransportersBlotting, WesternCell LineGlyburideImmunoprecipitationIon Channel GatingKATP ChannelsKcnj11 ChannelKineticsMembrane PotentialsMiceMutant ProteinsMyocardiumAbcc9 protein, ratAntibodiesATP-Binding Cassette TransportersGlyburideKATP ChannelsKcnj11 ChannelMutant ProteinsPotassium ChannelsPotassium Channels, Inwardly RectifyingProtein IsoformsReceptors, DrugSulfonylurea ReceptorsuK-ATP-1 potassium channel

Identifiers

PMID18001767
PMCPMC2276634
OpenAlexW2040681679

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.