Evidence map›Paper›PMID 11325720›Full record

ArticleBiophysical journal2001

Actin modifies Ca2+ block of epithelial Na+ channels in planar lipid bilayers.

B K Berdiev, R Latorre, D J Benos, I I Ismailov

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

12 citing papers in PubMed, 31 citations in OpenAlex.

  1. Lipidomic and proteomic analysis of exosomes from mouse cortical collecting duct cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  2. Article
  3. Article
  4. Regulation of epithelial sodium transport via epithelial Na+ channel.Journal of biomedicine & biotechnology · 2011
    Review
  5. Review
  6. Article
  7. Review
  8. Liquid movement across the surface epithelium of large airways.Respiratory physiology & neurobiology · 2007
    Review
  9. Review
  10. Article
  11. Article
  12. 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.

B K BerdievDepartment of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama 35294-0005, USA.
R Latorre
D J Benos
I I Ismailov
University of Alabama at Birmingham · USUniversity of Chile · CL

Funding

SODIUM ENTRY INTO AMILORIDE-SENSITIVE EPITHELIAR01DK037206 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI FULLER, CATHERINE M · 1986 to 2014
$3.9M
CATION SELECTIVITY, CONDUCTION, AND CA++ BLOCK OF ENACR01DK056095 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENOS, DALE J · 1999 to 2002
$593k
Sodium Entry into Amiloride-Sensitive EpitheliaR56DK037206 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENOS, DALE J · 2009 to 2009
$363k
NIDDK NIH HHS DK37206NIDDK NIH HHS DK56095
6 · The paper itself

Abstract

The mechanism by which the cytoskeletal protein actin affects the conductance of amiloride-sensitive epithelial sodium channels (ENaC) was studied in planar lipid bilayers. In the presence of monomeric actin, we found a decrease in the single-channel conductance of alpha-ENaC that did not occur when the internal [Ca2+]free was buffered to <10 nM. An analysis of single-channel kinetics demonstrated that Ca2+ induced the appearance of long-lived closed intervals separating bursts of channel activity, both in the presence and in the absence of actin. In the absence of actin, the duration of these bursts and the time spent by the channel in its open, but not in its short-lived closed state, were inversely proportional to [Ca2+]. This, together with a lengthening of the interburst intervals, translated into a dose-dependent decrease in the single-channel open probability. In contrast, a [Ca2+]-dependent decrease in alpha-ENaC conductance in the presence of actin was accompanied by lengthening of the burst intervals with no significant changes in the open or closed (both short- and long-lived) times. We conclude that Ca2+ acts as a "fast-to-intermediate" blocker when monomeric actin is present, producing a subsequent attenuation of the apparent unitary conductance of the channel.

Indexed as

ActinsAnimalsBiophysical PhenomenaBiophysicsCalciumDose-Response Relationship, DrugEpithelial Sodium ChannelsKineticsLipid BilayersModels, ChemicalMusclesProtein ConformationProteolipidsRabbitsSodium ChannelsActinsCalciumEpithelial Sodium ChannelsLipid BilayersProteolipidsproteoliposomesSodium Channels

Identifiers

PMID11325720
PMCPMC1301409
OpenAlexW2084714359

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.