Evidence map›Paper›PMID 17101229›Full record

ArticleNeuroscience2007

Neurotrophin B receptor kinase increases Kv subfamily member 1.3 (Kv1.3) ion channel half-life and surface expression.

B S Colley, K C Biju, A Visegrady, S Campbell, D A Fadool

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

33 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
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  6. Article
  7. Article
  8. Cardiac T-Tubule Microanatomy and Function.Physiological reviews · 2017
    Review
  9. Article
  10. BIN1 regulates dynamic t-tubule membrane.Biochimica et biophysica acta · 2016
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
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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

5 authors at 1 institution in 1 country.

B S ColleyDepartment of Biological Science, Programs in Neuroscience and Molecular Biophysics, Florida State University, Tallahassee, FL 32306, USA.
K C Biju
A Visegrady
S Campbell
D A Fadool
Florida State University · US

Funding

Modulation of Olfactory Bulb Neuron Current PropertiesR01DC003387 · NIDCD · FLORIDA STATE UNIVERSITY · PI FADOOL, DEBRA ANN · 2003 to 2013
$2.7M
MODULATION OF OLFACTORY BULB NEURON CURRENT PROPERTIESR29DC003387 · NIDCD · FLORIDA STATE UNIVERSITY · PI FADOOL, DEBRA ANN · 1998 to 2002
$333k
NIDCD NIH HHS DC03387NIDCD NIH HHS R01 DC003387NIDCD NIH HHS R29 DC003387
6 · The paper itself

Abstract

Kv subfamily member 1.3 (Kv1.3), a member of the Shaker family of potassium channels, has been found to play diverse roles in immunity, metabolism, insulin resistance, sensory discrimination, and axonal targeting in addition to its traditional role in the stabilization of the resting potential. We demonstrate that the neurotrophin B receptor (TrkB) causes an upregulation of Kv1.3 ion channel protein expression in the absence of the preferred ligand for the receptor (brain-derived neurotrophic factor; BDNF) and oppositely downregulates levels of Kv subfamily member 1.5. Although the effect occurs in the absence of the ligand, Kv1.3 upregulation by TrkB is dependent upon the catalytic domain of the TrkB kinase as well as tyrosine (Y) residues in the N and C terminus of the Kv1.3 channel. Using pulse-chase experiments we find that TrkB alters the half-life residence of the channel by approximately 2x and allows it to sustain activity as reflected in an increased current magnitude without alteration of kinetic properties. TrkB and Kv1.3 co-immunoprecipitate from tissue preparations of the mouse olfactory bulb and olfactory cortex, and by immunocytochemical approaches, are found to be co-localized in the glomerular, mitral cell, and internal plexiform layers of the olfactory bulb. These data suggest that Kv1.3 is not only modulated by direct phosphorylation in the presence of BDNF-activated TrkB kinase, but also may be fine tuned via regulation of surface expression while in the proximity of neurotrophic factor receptors. Given the variability of TrkB expression during development, regeneration, or neuronal activation, modulation of surface expression and turnover of Kv channels could significantly impact neuronal excitability, distinct from that of tyrosine kinase phosphorylation.

Indexed as

Blotting, WesternBrain-Derived Neurotrophic FactorCell Line, TransformedDose-Response Relationship, RadiationElectric StimulationGene Expression RegulationHalf-LifeHumansImmunohistochemistryImmunoprecipitationInsulinKv1.3 Potassium ChannelMembrane PotentialsPatch-Clamp TechniquesReceptor, trkBTime FactorsBrain-Derived Neurotrophic FactorInsulinKv1.3 Potassium ChannelReceptor, trkB

Identifiers

PMID17101229
PMCPMC1884406
OpenAlexW1995705401

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.