Evidence map›Paper›PMID 10884308›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000

Modulation of Kv1.5 currents by Src tyrosine phosphorylation: potential role in the differentiation of astrocytes.

S N MacFarlane, H Sontheimer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 75 citations in OpenAlex.

  1. Trial
  2. Article
  3. Eosinophilic esophagitis: Immune mechanisms and therapeutic targets.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2022
    Review
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  18. Association/dissociation of a channel-kinase complex underlies state-dependent modulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
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  20. 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

2 authors at 1 institution in 1 country.

S N MacFarlaneDepartment of Neurobiology, University of Alabama, Birmingham, Birmingham, Alabama 35294-0021, USA.
H Sontheimer
University of Alabama at Birmingham · US

Funding

PROPERTIES AND FUNCTION OF GLIA ION CHANNELSR01NS031234 · NINDS · YALE UNIVERSITY · PI SONTHEIMER, HARALD W · 1994 to 2011
$3.3M
ZINC AND FOLATE EFFECTS ON POSTNATAL CNS DEVELOPMENTP50HD032901 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RAMEY, SHARON L. · 1994 to 1998
–
NICHD NIH HHS P50HD32901NINDS NIH HHS R01 NS031234NINDS NIH HHS R01NS31234
6 · The paper itself

Abstract

Using biophysical techniques, we previously have implicated outwardly rectifying potassium currents in the proliferation of cultured spinal cord astrocytes and have demonstrated that delayed rectifier potassium currents (I(Kd)), in particular, are upregulated on entry into the cell cycle and downregulated with cell cycle exit and differentiation. In the present study, using specific antibodies and antisense oligodeoxynucleotides, we show that this proliferation-dependent potassium current is mediated by the Shaker potassium channel Kv1.5. Downregulation of Kv1.5 protein by antisense oligodeoxynucleotides reduces astrocyte proliferation by approximately 50%, although no observed changes occur in Kv1.5 protein expression during spontaneous differentiation in culture. Tyrosine phosphorylation of Kv1.5, however, is downregulated markedly in differentiated cells but unaltered on cell cycle arrest. Using immunoprecipitation, we show that Kv1.5 is associated with Src family protein tyrosine kinases and that this association does not change with cell differentiation. Inhibition of kinase activity with the Src-specific inhibitor PP2 decreases Kv1.5 phosphorylation, reduces I(Kd), and inhibits astrocyte proliferation, specifically in the G(0)/G(1) phase of cell cycle. Conversely, I(Kd) are potentiated when active Src is present in the pipette. Transfection of quiescent astrocytes with constitutively active Src (Src Y529F) causes marked upregulation of astrocyte proliferation. These data suggest that Kv1. 5 is phosphorylated constitutively by Src kinases during growth and that downregulation of Src activity may underlie both astrocyte differentiation and the accompanying changes in delayed rectifier potassium channel activity.

Indexed as

Potassium Channels, Voltage-GatedAnimalsAstrocytesCell DifferentiationCell DivisionCells, CulturedDelayed Rectifier Potassium ChannelsDown-RegulationEnzyme InhibitorsIon TransportKv1.5 Potassium ChannelPatch-Clamp TechniquesPhosphorylationPotassiumPotassium ChannelsPrecipitin TestsDelayed Rectifier Potassium ChannelsEnzyme InhibitorsKcna5 protein, ratKv1.5 Potassium ChannelPotassiumPotassium ChannelsPotassium Channels, Voltage-GatedPyrimidinessrc-Family KinasesTyrosine

Identifiers

PMID10884308
PMCPMC6772320
OpenAlexW1674100775

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.