Evidence map›Paper›PMID 19561078›Full record

ArticleThe Journal of biological chemistry2009

Knockdown of ASIC1 and epithelial sodium channel subunits inhibits glioblastoma whole cell current and cell migration.

Niren Kapoor, Rafal Bartoszewski, Yawar J Qadri, Zsuzsanna Bebok, James K Bubien, Catherine M Fuller, Dale J Benos

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

89 citing papers in PubMed, 133 citations in OpenAlex.

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  16. Ion Channels in Gliomas-From Molecular Basis to Treatment.International journal of molecular sciences · 2023
    Review
  17. Article
  18. Review
  19. Article
  20. Article

29 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Niren KapoorDepartment of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
Rafal Bartoszewski
Yawar J Qadri
Zsuzsanna Bebok
James K Bubien
Catherine M Fuller
Dale J Benos
University of Alabama at Birmingham · US

Funding

SODIUM ENTRY INTO AMILORIDE-SENSITIVE EPITHELIAR01DK037206 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI FULLER, CATHERINE M · 1986 to 2014
$3.9M
Cell Biology of ASIC2 in GliomaR01CA101952 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENOS, DALE J · 2003 to 2005
$963k
Sodium Entry into Amiloride-Sensitive EpitheliaR56DK037206 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENOS, DALE J · 2009 to 2009
$363k
NCI NIH HHS CA101952NCI NIH HHS R01 CA101952NIDDK NIH HHS DK37206NIDDK NIH HHS R01 DK037206NIDDK NIH HHS R56 DK037206
6 · The paper itself

Abstract

High grade gliomas such as glioblastoma multiforme express multiple members of the epithelial sodium channel (ENaC)/Degenerin family, characteristically displaying a basally active amiloride-sensitive cation current not seen in normal human astrocytes or lower grade gliomas. Using quantitative real time PCR, we have shown higher expression of ASIC1, alphaENaC, and gammaENaC in D54-MG human glioblastoma multiforme cells compared with primary human astrocytes. We hypothesize that this glioma current is mediated by a hybrid channel composed of a mixture of ENaC and acid-sensing ion channel (ASIC) subunits. To test this hypothesis we made dominant negative cDNAs for ASIC1, alphaENaC, gammaENaC, and deltaENaC. D54-MG cells transfected with the dominant negative constructs for ASIC1, alphaENaC, or gammaENaC showed reduced protein expression and a significant reduction in the amiloride-sensitive whole cell current as compared with untransfected D54-MG cells. Knocking down alphaENaC or gammaENaC also abolished the high P(K)(+)/P(Na)(+) of D54-MG cells. Knocking down deltaENaC in D54-MG cells reduced deltaENaC protein expression but had no effect on either the whole cell current or K(+) permeability. Using co-immunoprecipitation we show interactions between ASIC1, alphaENaC, and gammaENaC, consistent with these subunits interacting with each other to form an ion channel in glioma cells. We also found a significant inhibition of D54-MG cell migration after ASIC1, alphaENaC, or gammaENaC knockdown, consistent with the hypothesis that ENaC/Degenerin subunits play an important role in glioma cell biology.

Indexed as

Cell MovementMembrane PotentialsAcid Sensing Ion ChannelsAnimalsAstrocytesCHO CellsCricetinaeCricetulusEpithelial Sodium ChannelsGene Knockdown TechniquesGlioblastomaHumansNerve Tissue ProteinsProtein BindingProtein SubunitsSodium ChannelsAcid Sensing Ion ChannelsASIC1 protein, humanEpithelial Sodium ChannelsNerve Tissue ProteinsProtein SubunitsSodium Channels

Identifiers

PMID19561078
PMCPMC2782044
OpenAlexW2009697157

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.