Evidence map›Paper›PMID 23261316›Full record

ArticleCell calcium2013

Calcium entry via TRPC1 channels activates chloride currents in human glioma cells.

Vishnu Anand Cuddapah, Kathryn L Turner, Harald Sontheimer

Open access · greenAbstract read
In one paragraph

Article in Cell calcium, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Function of TRPC1 in modulating hepatocellular carcinoma progression.Medical oncology (Northwood, London, England) · 2023
    Article
  3. Review
  4. Article
  5. Review
  6. CaCancers · 2021
    Review
  7. Review
  8. Review
  9. Ion Channels in Glioma Malignancy.Reviews of physiology, biochemistry and pharmacology · 2021
    Review
  10. Review
  11. Review
  12. CaAdvances in cancer research · 2020
    Review
  13. Roles of TRP Channels in Neurological Diseases.Oxidative medicine and cellular longevity · 2020
    Review
  14. The Role of TRP Channels in the Metastatic Cascade.Pharmaceuticals (Basel, Switzerland) · 2018
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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.

Vishnu Anand CuddapahDepartment of Neurobiology and Center for Glial Biology in Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Kathryn L Turner
Harald Sontheimer
University of Alabama at Birmingham · US

Funding

The Role of Ion Transport in Glioma Migration, Proliferation, and ApoptosisR01NS036692 · NINDS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI SONTHEIMER, HARALD W · 1997 to 2024
$6.8M
PROPERTIES AND FUNCTION OF GLIA ION CHANNELSR01NS031234 · NINDS · YALE UNIVERSITY · PI SONTHEIMER, HARALD W · 1994 to 2011
$3.3M
Regulation of ClC-3 in Human Malignant GliomaF31NS073181 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CUDDAPAH, VISHNU ANAND · 2011 to 2012
$69k
NINDS NIH HHS F31 NS073181NINDS NIH HHS R01 NS031234NINDS NIH HHS R01 NS036692
6 · The paper itself

Abstract

Malignant gliomas are highly invasive brain cancers that carry a dismal prognosis. Recent studies indicate that Cl(-) channels facilitate glioma cell invasion by promoting hydrodynamic cell shape and volume changes. Here we asked how Cl(-) channels are regulated in the context of migration. Using patch-clamp recordings we show Cl(-) currents are activated by physiological increases of [Ca(2+)]i to 65 and 180nM. Cl(-) currents appear to be mediated by ClC-3, a voltage-gated, CaMKII-regulated Cl(-) channel highly expressed by glioma cells. ClC-3 channels colocalized with TRPC1 on caveolar lipid rafts on glioma cell processes. Using perforated-patch electrophysiological recordings, we demonstrate that inducible knockdown of TRPC1 expression with shRNA significantly inhibited glioma Cl(-) currents in a Ca(2+)-dependent fashion, placing Cl(-) channels under the regulation of Ca(2+) entry via TRPC1. In chemotaxis assays epidermal growth factor (EGF)-induced invasion was inhibition by TRPC1 knockdown to the same extent as pharmacological block of Cl(-) channels. Thus endogenous glioma Cl(-) channels are regulated by TRPC1. Cl(-) channels could be an important downstream target of TRPC1 in many other cells types, coupling elevations in [Ca(2+)]i to the shape and volume changes associated with migrating cells.

Indexed as

CalciumChloride ChannelsChloridesElectric ConductivityGliomaHumansTRPC Cation ChannelsCalciumChloride ChannelsChloridestransient receptor potential cation channel, subfamily C, member 1TRPC Cation Channels

Identifiers

PMID23261316
PMCPMC3594368
OpenAlexW2088189699

What OpenQuestion holds

Textmetadata
LicenceTDM
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.