Evidence map›Paper›PMID 16166157›Full record

ArticleThe Journal of physiology2005

ATP sensitivity of ATP-sensitive K+ channels: role of the gamma phosphate group of ATP and the R50 residue of mouse Kir6.2.

Scott A John, James N Weiss, Bernard Ribalet

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. KATP Channels in the Cardiovascular System.Physiological reviews · 2016
    Review
  3. Article
  4. Review
  5. Article
  6. Functional analysis of six Kir6.2 (KCNJ11) mutations causing neonatal diabetes.Pflugers Archiv : European journal of physiology · 2006
    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

3 authors at 1 institution in 1 country.

Scott A JohnUCLA Cardiovascular Research Laboratory, Department of Medicine (Cardiology), UCLA School of Medicine, Los Angeles, CA 90095, USA.
James N Weiss
Bernard Ribalet
University of California, Los Angeles · US

Funding

SYMPATHETIC RESPONSES DURING VENTRICULAR TACHYCARDIAP50HL052319 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WEISS, JAMES N · 1995 to 2004
$6.2M
PROPERTIES OF INWARD RECTIFIER K CHANNELSR37HL060025 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WEISS, JAMES N · 1998 to 2007
$2.8M
NHLBI NIH HHS P50 HL052319NHLBI NIH HHS P50 HL52319NHLBI NIH HHS R37 HL060025NHLBI NIH HHS R37HL60025
6 · The paper itself

Abstract

ATP-sensitive K (K(ATP)) channels are composed of Kir6, the pore-forming protein, and the sulphonylurea receptor SUR, a regulatory protein. We and others have previously shown that positively charged residues in the C terminus of Kir6.2, including R201 and K185, interact with the alpha and beta phosphate groups of ATP, respectively, to induce channel closure. A positively charged residue in the N terminus, R50, is also important, and has been proposed to interact with either the gamma or beta phosphate group of ATP. To examine this issue, we systematically mutated R50 to residues of different size, charge and hydropathy, and examined the effects on adenine nucleotide sensitivity in the absence and presence of SUR1. In the absence of SUR1, only the size of residue 50 significantly altered ATP sensitivity, with smaller side chains decreasing ATP sensitivity. In the presence of SUR1, however, hydrophathy and charge also played a role. Hydrophilic residues decreased ATP sensitivity more than hydrophobic residues for small size residues, and, surprisingly, negatively charged residues E and D preserved ATP sensitivity and increased ADP sensitivity relative to the wild-type residue R. These observations suggest that a negative charge near position 50, due to either mutation of R50 or the interaction of the gamma phosphate group of ATP with R50, facilitates closure of the ATP-dependent gate. Mutation of the nearby positively charged residue R54, known to be involved in stabilizing channel opening via electrostatic interactions with phosphatidylinositol 4,5-bisphosphate (PIP2), also caused increased ADP sensitivity as compared with ATP, suggesting a loss of function of ATP's gamma phosphate. Based on these results, we propose that a phosphate group or a negative charge at position 50 initiates channel closure by destabilizing the electrostatic interactions between negative phosphate groups of PIP2 and residues such as R54.

Indexed as

Adenosine TriphosphateAnimalsBinding SitesCell LineDose-Response Relationship, DrugHumansIon Channel GatingKcnj11 ChannelKidneyMicePhosphatesPotassium Channels, Inwardly RectifyingProtein BindingStructure-Activity RelationshipAdenosine TriphosphateKcnj11 ChannelPhosphatesPotassium Channels, Inwardly Rectifying

Identifiers

PMID16166157
PMCPMC1464185
OpenAlexW1520750690

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.