Evidence map›Paper›PMID 17854350›Full record

ArticleJournal of neurochemistry2007

Post-synaptic density perturbs insulin-induced Kv1.3 channel modulation via a clustering mechanism involving the SH3 domain.

D R Marks, D A Fadool

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of neurochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

39 citing papers in PubMed, 55 citations in OpenAlex.

  1. Identification of Novel Kv1.3 Channel-Interacting Proteins Using Proximity Labelling in T-Cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2025
    Article
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  4. Review
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  8. A Meta-Analysis Study to Infer Voltage-Gated KAntioxidants (Basel, Switzerland) · 2023
    Article
  9. Modulating the Excitability of Olfactory Output Neurons Affects Whole-Body Metabolism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  10. Article
  11. Hyperexcitability and Hyperplasticity Disrupt Cerebellar Signal Transfer in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  12. Article
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  15. Article
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  17. Unconventional EGF-induced ERK1/2-mediated Kv1.3 endocytosis.Cellular and molecular life sciences : CMLS · 2016
    Article
  18. Review
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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.

D R MarksDepartment of Biological Science, Program in Neuroscience, Biomedical Research Facility, The Florida State University, Tallahassee, Florida, USA.
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
Insulin as a Neuromodulator in the Olfactory BulbF31DC008045 · NIDCD · FLORIDA STATE UNIVERSITY · PI MARKS, DAVID R. · 2007 to 2007
$29k
NIDCD NIH HHS DC03387NIDCD NIH HHS F31 DC008045NIDCD NIH HHS F31DC008045NIDCD NIH HHS R01 DC003387NIDCD NIH HHS R29 DC003387
6 · The paper itself

Abstract

The olfactory bulb (OB) contains the highest concentration of the insulin receptor (IR) kinase in the central nervous system; however, its functional role and modulation in this region remains poorly understood. IR kinase contains a number of proline-rich motifs, making it an excellent candidate for modulation by SH(3) domain-containing adaptor proteins. Kv1.3, a voltage-gated Shaker potassium channel and tyrosine phosphorylation substrate of IR kinase, contains several proline-rich sequences and a canonical post-synaptic density 95 (PSD-95)/discs large/zO-1 domain (PDZ) recognition motif common to most Shaker family members. We sought to determine if a functional relationship existed between Kv1.3, IR kinase, and the SH(3)/PDZ adaptor protein PSD-95. Through patch-clamp electrophysiology, immunochemistry, and co-immunoprecipitation, we found that while Kv1.3 and PSD-95 alone interact via the canonical C-terminal PDZ recognition motif of the channel, this molecular site of interaction acts to cluster the channels but the PSD-95 SH(3)-guanylate kinase domain functionally modulates Kv1.3 activity via two proline-rich domains in its N- and C-terminal. Therefore, these data suggest that adaptor domains responsible for ion-channel clustering and functional modulation are not necessarily coupled. Moreover, IR kinase and Kv1.3 can only be co-immunoprecipitated in the presence of PSD-95 as the adapting linker. Functionally, insulin-dependent Kv1.3 phosphorylation that causes channel current suppression is blocked via interaction with the PSD-95 SH(3)-guanylate kinase domain. Because all the three proteins co-localize in multiple lamina of the OB that are known to be rich in synaptic connections, membrane excitability and synaptic transmission at critical locations in the OB have the capacity to be finely regulated.

Indexed as

Amino Acid MotifsCell LineDisks Large Homolog 4 ProteinHumansInsulinIntracellular Signaling Peptides and ProteinsKv1.3 Potassium ChannelMembrane ProteinsNerve Tissue ProteinsProtein Serine-Threonine KinasesReceptor, Insulinsrc Homology DomainsDisks Large Homolog 4 ProteinDLG4 protein, humanInsulininsulin receptor serine kinaseIntracellular Signaling Peptides and ProteinsKv1.3 Potassium ChannelMembrane ProteinsNerve Tissue Proteinspostsynaptic density proteinsProtein Serine-Threonine KinasesReceptor, Insulin

Identifiers

PMID17854350
PMCPMC2667938
OpenAlexW2110410730

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.