Evidence map›Paper›PMID 35069252›Full record

ArticleFrontiers in physiology2021

LY294002 Inhibits Intermediate Conductance Calcium-Activated Potassium (KCa3.1) Current in Human Glioblastoma Cells.

Concetta Caglioti, Federico Palazzetti, Lorenzo Monarca, Raffaele Lobello, Maria Rachele Ceccarini, Rossana Giulietta Iannitti, Roberta Russo, Francesco Ragonese, Chiara Pennetta, Antonella De Luca and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. KCa3.1 mediates radioresistance of silver nanoparticles in human glioblastoma cells.Pflugers Archiv : European journal of physiology · 2026
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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

12 authors at 1 institution in 1 country.

Concetta CagliotiDepartment of Chemistry, Biology and Biotechnologies, University of Perugia, Perugia, Italy.
Federico PalazzettiDepartment of Chemistry, Biology and Biotechnologies, University of Perugia, Perugia, Italy.
Lorenzo MonarcaDepartment of Chemistry, Biology and Biotechnologies, University of Perugia, Perugia, Italy.
Raffaele LobelloRelab S.r.l., Genova, Italy.
Maria Rachele CeccariniDepartment of Pharmaceutical Sciences, University of Perugia, Perugia, Italy.
Rossana Giulietta IannittiS&R Farmaceutici S.p.A Bastia Umbra, Perugia, Italy.
Roberta RussoDepartment of Chemistry, Biology and Biotechnologies, University of Perugia, Perugia, Italy.
Francesco RagoneseDepartment of Chemistry, Biology and Biotechnologies, University of Perugia, Perugia, Italy.
Chiara PennettaDepartment of Chemistry, Biology and Biotechnologies, University of Perugia, Perugia, Italy.
Antonella De LucaDepartment of Chemistry, Biology and Biotechnologies, University of Perugia, Perugia, Italy.
Michela CodiniDepartment of Pharmaceutical Sciences, University of Perugia, Perugia, Italy.
Bernard FiorettiDepartment of Chemistry, Biology and Biotechnologies, University of Perugia, Perugia, Italy.
University of Perugia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastomas (GBs) are among the most common tumors with high malignancy and invasiveness of the central nervous system. Several alterations in protein kinase and ion channel activity are involved to maintain the malignancy. Among them, phosphatidylinositol 3-kinase (PI3K) activity and intermediate conductance calcium-activated potassium (KCa3.1) current are involved in several aspects of GB biology. By using the electrophysiological approach and noise analysis, we observed that KCa3.1 channel activity is LY294002-sensitive and Wortmannin-resistant in accordance with the involvement of PI3K class IIβ (PI3KC2β). This modulation was observed also during the endogenous activation of KCa3.1 current with histamine. The principal action of PI3KC2β regulation was the reduction of open probability in intracellular free calcium saturating concentration. An explanation based on the "three-gate" model of the KCa3.1 channel by PI3KC2β was proposed. Based on the roles of KCa3.1 and PI3KC2β in GB biology, a therapeutic implication was suggested to prevent chemo- and radioresistance mechanisms.

Indexed as

calcium homeostasischemio and radioresistanceglioblastomahistamine (H1) receptorKCa3.1 (intermediate-conductance Ca2+-activated K+ channel)LY294002 (PI3K inhibitor)

Identifiers

PMID35069252
PMCPMC8782274
OpenAlexW4206104434

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

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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.