Evidence map›Paper›PMID 27696527›Full record

ArticleGlia2017

Differential Kv1.3, KCa3.1, and Kir2.1 expression in "classically" and "alternatively" activated microglia.

Hai M Nguyen, Eva M Grössinger, Makoto Horiuchi, Kyle W Davis, Lee-Way Jin, Izumi Maezawa, Heike Wulff

Open access · hybridAbstract read
In one paragraph

Article in Glia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 3% 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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 168 citations in OpenAlex.

  1. Pooled it
  2. KArchiv der Pharmazie · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
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  12. Article
  13. Article
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  15. Article
  16. Article
  17. Validation of HvFrontiers in cellular neuroscience · 2025
    Article
  18. Review
  19. Article
  20. Repurposing the KTranslational stroke research · 2024
    Article

36 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 2 institutions in 1 country.

Hai M NguyenDepartment of Pharmacology, University of California, Davis, California.
Eva M GrössingerDepartment of Pharmacology, University of California, Davis, California.
Makoto HoriuchiDepartment of Pathology and Laboratory Medicine, University of California Davis Medical Center, Sacramento, California.
Kyle W DavisDepartment of Pathology and Laboratory Medicine, University of California Davis Medical Center, Sacramento, California.
Lee-Way JinDepartment of Pathology and Laboratory Medicine, University of California Davis Medical Center, Sacramento, California.
Izumi MaezawaDepartment of Pathology and Laboratory Medicine, University of California Davis Medical Center, Sacramento, California.
Heike WulffDepartment of Pharmacology, University of California, Davis, California.
University of California Davis Medical Center · USUniversity of California, Davis · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Gina M Dayton · 2002 to 2026
$84.9M
The Role of KCa3.1 in Neuroinflammation in Alzheimer DiseaseR01AG043788 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI MAEZAWA, IZUMI · 2013 to 2017
$1.6M
Microglial K+ Channels in Ischemic StrokeR01NS100294 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI WULFF, HEIKE · 2017 to 2020
$1.3M
Microglial Potassium Channels in Ischemic StrokeR56NS098328 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI WULFF, HEIKE · 2016 to 2016
$393k
NCI NIH HHS P30 CA093373NIA NIH HHS R01 AG043788NINDS NIH HHS R01 NS100294NINDS NIH HHS R56 NS098328
6 · The paper itself

Abstract

Microglia are highly plastic cells that can assume different phenotypes in response to microenvironmental signals. Lipopolysaccharide (LPS) and interferon-γ (IFN-γ) promote differentiation into classically activated M1-like microglia, which produce high levels of pro-inflammatory cytokines and nitric oxide and are thought to contribute to neurological damage in ischemic stroke and Alzheimer's disease. IL-4 in contrast induces a phenotype associated with anti-inflammatory effects and tissue repair. We here investigated whether these microglia subsets vary in their K

Indexed as

AnimalsCells, CulturedInterferon-gammaIntermediate-Conductance Calcium-Activated Potassium ChannelsKv1.3 Potassium ChannelLipopolysaccharidesMacrophage ActivationMembrane PotentialsMice, Inbred C57BLMicrogliaPotassium Channels, Inwardly RectifyingInterferon-gammaIntermediate-Conductance Calcium-Activated Potassium ChannelsKcnn4 protein, mouseKir2.1 channelKv1.3 Potassium ChannelLipopolysaccharidesPotassium Channels, Inwardly RectifyingKCa3.1Kir2.1Kv1.3microgliaPAP-1potassium channelTRAM-34

Identifiers

PMID27696527
PMCPMC5113690
OpenAlexW2528530823

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.