Evidence map›Paper›PMID 1533397›Full record

ArticleThe Journal of cell biology1992

Suppression of kinesin expression in cultured hippocampal neurons using antisense oligonucleotides.

A Ferreira, J Niclas, R D Vale, G Banker, K S Kosik

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
6.2field-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

73 citing papers in PubMed, 189 citations in OpenAlex.

  1. Article
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  13. Role of kinesin-1-based microtubule sliding in Drosophila nervous system development.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  14. Kif1B Interacts with KBP to Promote Axon Elongation by Localizing a Microtubule Regulator to Growth Cones.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  15. Article
  16. Article
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  19. Review
  20. Article

13 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

5 authors at 1 institution in 1 country.

A FerreiraDepartment of Neuroscience, University of Virginia School of Medicine, Charlottesville 22908.
J Niclas
R D Vale
G Banker
K S Kosik
University of Virginia · US

Funding

Microtubule Complexes Involved in Intracelluar TransportR37GM038499 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VALE, RONALD D · 2006 to 2015
$3.2M
THE DEVELOPMENT OF HIPPOCAMPAL NEURONS IN CULTURER01NS017112 · NINDS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI BANKER, GARY A · 1985 to 2008
$2.6M
MICROTUBULE-BASED ORGANELLE TRANSPORTR01GM038499 · NIGMS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI VALE, RONALD D · 1988 to 2005
$1.2M
NEURONAL POLARITY--DISRUPTION IN AGING AND ALZHEIMERSR01NS029031 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI KOSIK, KENNETH S · 1991 to 2000
$297k
NIGMS NIH HHS GM38499NIGMS NIH HHS R01 GM038499NINDS NIH HHS NS17112NINDS NIH HHS NS29031
6 · The paper itself

Abstract

Kinesin, a microtubule-based force-generating molecule, is thought to translocate organelles along microtubules. To examine the function of kinesin in neurons, we sought to suppress kinesin heavy chain (KHC) expression in cultured hippocampal neurons using antisense oligonucleotides and study the phenotype of these KHC "null" cells. Two different antisense oligonucleotides complementary to the KHC sequence reduced the protein levels of the heavy chain by greater than 95% within 24 h after application and produced identical phenotypes. After inhibition of KHC expression for 24 or 48 h, neurons extended an array of neurites often with one neurite longer than the others; however, the length of all these neurites was significantly reduced. Inhibition of KHC expression also altered the distribution of GAP-43 and synapsin I, two proteins thought to be transported in association with membranous organelles. These proteins, which are normally localized at the tips of growing neurites, were confined to the cell body in antisense-treated cells. Treatment of the cells with the corresponding sense oligonucleotides affected neither the distribution of GAP-43 and synapsin I, nor the length of neurites. A full recovery of neurite length occurred after removal of the antisense oligonucleotides from the medium. These data indicate that KHC plays a role in the anterograde translocation of vesicles containing GAP-43 and synapsin I. A deficiency in vesicle delivery may also explain the inhibition of neurite outgrowth. Despite the inhibition of KHC and the failure of GAP-43 and synapsin I to move out of the cell body, hippocampal neurons can extend processes and acquire as asymmetric morphology.

Indexed as

AnimalsBase SequenceBiological Transport, ActiveCell PolarityCells, CulturedGAP-43 ProteinHippocampusImmunohistochemistryKinesinsMembrane GlycoproteinsMolecular Sequence DataMorphogenesisNerve Tissue ProteinsNeuritesNeurofilament ProteinsNeuronsGAP-43 ProteinKinesinsMembrane GlycoproteinsNerve Tissue ProteinsNeurofilament ProteinsOligonucleotides, AntisenseSynapsins

Identifiers

PMID1533397
PMCPMC2289440
OpenAlexW2043706080

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.