Evidence map›Paper›PMID 9698307›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

Modulation of olfactory bulb neuron potassium current by tyrosine phosphorylation.

D A Fadool, I B Levitan

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

60 citing papers in PubMed, 117 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Modulating the Excitability of Olfactory Output Neurons Affects Whole-Body Metabolism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
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  13. Unconventional EGF-induced ERK1/2-mediated Kv1.3 endocytosis.Cellular and molecular life sciences : CMLS · 2016
    Article
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  15. Article
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  19. Common themes in PrP signaling: the Src remains the same.Frontiers in cell and developmental biology · 2014
    Article
  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.

D A FadoolBiochemistry Department and Volen Center for Complex Systems, Brandeis University, Waltham, Massachusetts 02254, USA.
I B Levitan
Brandeis University · US

Funding

MODULATION OF OLFACTORY BULB NEURON CURRENT PROPERTIESR29DC003387 · NIDCD · FLORIDA STATE UNIVERSITY · PI FADOOL, DEBRA ANN · 1998 to 2002
$333k
NIDCD NIH HHS R29 DC003387
6 · The paper itself

Abstract

Insulin causes a suppression of whole-cell voltage-dependent outward current in cultured neurons from the rat olfactory bulb. This suppression is time-dependent; it is mimicked by application of Src tyrosine kinase inside the cell via the whole-cell patch electrode or by treatment of the olfactory bulb neurons with the tyrosine phosphatase inhibitor pervanadate. The C-type inactivation properties of the outward current in olfactory bulb neurons resemble those of the cloned Kv1.3 potassium channel. In addition, at picomolar concentrations at which it is specific for Kv1.3, the scorpion toxin margatoxin blocks most of the olfactory bulb neuron outward current. Immunocytochemical analysis demonstrates that Kv1.3 is prominent in the cultured olfactory bulb neurons. To identify specific amino acid residues that might be important for potassium current modulation, we examined the effects of pervanadate and insulin on wild-type and mutant Kv1.3 channels expressed in human embryonic kidney (HEK 293) cells. As shown previously, treatment with either pervanadate or insulin suppresses Kv1.3 current in these cells. Mutational analysis demonstrates that at least two distinct tyrosine residues are required for current suppression by pervanadate. Insulin treatment stimulates the tyrosine phosphorylation of Kv1.3 in HEK 293 cells, and a different combination of tyrosine residues is required for the current suppression by insulin. The results suggest that complex patterns of phosphorylation may be involved in the modulation of neuronal potassium current by receptor and nonreceptor tyrosine kinases.

Indexed as

Potassium Channels, Voltage-GatedAnimalsCell LineCells, CulturedCSK Tyrosine-Protein KinaseDNA Mutational AnalysisElectric ConductivityHumansInsulinNeuronsOlfactory BulbPhosphorylationPotassiumPotassium ChannelsProtein-Tyrosine KinasesRatsCSK protein, humanCSK Tyrosine-Protein KinaseInsulinKcnc1 protein, ratpervanadatePotassiumPotassium ChannelsPotassium Channels, Voltage-GatedProtein-Tyrosine KinasesShaw Potassium Channelssrc-Family KinasesTyrosineVanadates

Identifiers

PMID9698307
PMCPMC6793192
OpenAlexW1492144011

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.