Evidence map›Paper›PMID 10964960›Full record

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

Regulation of neurite outgrowth by integrin activation.

J K Ivins, P D Yurchenco, A D Lander

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 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

56 citing papers in PubMed, 147 citations in OpenAlex.

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  14. Integrins promote axonal regeneration after injury of the nervous system.Biological reviews of the Cambridge Philosophical Society · 2018
    Review
  15. Dendrite regeneration of adultGenes & development · 2018
    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

3 authors at 2 institutions in 1 country.

J K IvinsDepartment of Developmental and Cell Biology and the Developmental Biology Center, University of California at Irvine, Irvine, California 92697, USA. jkivins@uci.edu
P D Yurchenco
A D Lander
University of California, Irvine · USJohnson University · US

Funding

MECHANISMS OF NEURONAL GUIDANCER01NS036049 · NINDS · UNIVERSITY OF CALIFORNIA IRVINE · PI LANDER, ARTHUR D · 1997 to 2000
$186k
NINDS NIH HHS NS 36049
6 · The paper itself

Abstract

During late-embryonic development, retinal neurons lose the ability to attach and extend neurites on the extracellular matrix molecule laminin-1 (LN-1), despite the fact that they retain expression of integrin receptors for LN-1. Here we show that the developmental loss of responsiveness to LN-1 can be reversed by treatments that increase the activation state of integrins. Both extracellular application of Mn(2+) (at micromolar concentrations) and viral-mediated neuronal expression of a constitutively active form of the ras-related GTPase R-ras (R-ras(38V)) potently promoted late-embryonic retinal neurite outgrowth on LN-1 substrata. In both cases, outgrowth was mediated by integrin alpha6beta1 and not alpha3beta1, even though these neurons express alpha3beta1 and use it for outgrowth on other laminin isoforms, as well as on LN-1 that has been proteolytically or conformationally activated (Ivins et al., 1998). Mn(2+)-and to a much lesser extent R-ras(38V)-also reversed the developmental loss of retinal neuron responsiveness to type IV collagen, by promoting the function of integrin alpha1beta1. Interestingly, the responses of other late-embryonic CNS neurons to LN-1 were also enhanced by treatments that activate integrin function, but those of peripheral nervous system neurons (dorsal root ganglion neurons) were either not enhanced (embryonic neurons) or only modestly improved (adult neurons). These results suggest that a developmental decline occurs in the activation state of neuronal integrins, particularly among CNS neurons. Such a decline may underlie some of the intrinsic loss of regenerative ability sustained by CNS neurons during development and may be a valid target for therapeutic intervention.

Indexed as

AnimalsCells, CulturedCerebral CortexCollagenEmbryo, MammalianExtracellular MatrixGenetic VectorsHippocampusIntegrinsLamininManganeseNeuritesNeuronsras GTPase-Activating ProteinsRatsRecombinant Fusion ProteinsCollagenIntegrinsLamininlaminin 1Manganeseras GTPase-Activating ProteinsRecombinant Fusion Proteins

Identifiers

PMID10964960
PMCPMC6772972
OpenAlexW2121965026

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.