Evidence map›Paper›PMID 21976490›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Leukocyte common antigen-related phosphatase is a functional receptor for chondroitin sulfate proteoglycan axon growth inhibitors.

Daniel Fisher, Bin Xing, John Dill, Hui Li, Hai Hiep Hoang, Zhenze Zhao, Xiao-Li Yang, Robert Bachoo, Stephen Cannon, Frank M Longo and 3 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed, 1 pooled it
10.7field-weighted citation impact, top 1% 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

179 citing papers in PubMed, 1 synthesis or guideline pooled it, 304 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The role of type I collagen in white matter injury.Anatomical science international · 2026
    Review
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  5. Article
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  7. Article
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  9. Article
  10. Neuronal Axon Generation/Regeneration Regulated by Sulfated Glycans.Advances in experimental medicine and biology · 2026
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
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  20. Article

119 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

13 authors at 4 institutions in 1 country.

Daniel FisherDepartment of Neurology and Neuroscience Graduate Program, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8813, USA.
Bin Xing
John Dill
Hui Li
Hai Hiep Hoang
Zhenze Zhao
Xiao-Li Yang
Robert Bachoo
Stephen Cannon
Frank M Longo
Morgan Sheng
Jerry Silver
Shuxin Li
The University of Texas Southwestern Medical Center · USCase Western Reserve University · USHoward Hughes Medical Institute · USStanford University · US

Funding

FACTORS AFFECTING REGENERATION THRU THE GLIAL SCARR01NS025713 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI SILVER, JERRY · 1988 to 2016
$3.1M
Factors Affecting Regeneration Through the Glial ScarR37NS025713 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI SILVER, JERRY · 2005 to 2011
$2.7M
Overcoming glial scar inhibitions on axonal growthR21NS066114 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LI, SHUXIN · 2010 to 2011
$432k
NINDS NIH HHS 1R21 NS066114-01A1NINDS NIH HHS NS025713NINDS NIH HHS R01 NS025713NINDS NIH HHS R21 NS066114NINDS NIH HHS R37 NS025713
6 · The paper itself

Abstract

Chondroitin sulfate proteoglycans (CSPGs) are a family of extracellular matrix molecules with various functions in regulating tissue morphogenesis, cell division, and axon guidance. A number of CSPGs are highly upregulated by reactive glial scar tissues after injuries and form a strong barrier for axonal regeneration in the adult vertebrate CNS. Although CSPGs may negatively regulate axonal growth via binding and altering activity of other growth-regulating factors, the molecular mechanisms by which CSPGs restrict axonal elongation are not well understood. Here, we identified a novel receptor mechanism whereby CSPGs inhibit axonal growth via interactions with neuronal transmembrane leukocyte common antigen-related phosphatase (LAR). CSPGs bind LAR with high affinity in transfected COS-7 cells and coimmunoprecipitate with LAR expressed in various tissues including the brain and spinal cord. CSPG stimulation enhances activity of LAR phosphatase in vitro. Deletion of LAR in knock-out mice or blockade of LAR with sequence-selective peptides significantly overcomes neurite growth restrictions of CSPGs in neuronal cultures. Intracellularly, CSPG-LAR interaction mediates axonal growth inhibition of neurons partially via inactivating Akt and activating RhoA signals. Systemic treatments with LAR-targeting peptides in mice with thoracic spinal cord transection injuries induce significant axon growth of descending serotonergic fibers in the vicinity of the lesion and beyond in the caudal spinal cord and promote locomotor functional recovery. Identification of LAR as a novel CSPG functional receptor provides a therapeutic basis for enhancing axonal regeneration and functional recovery after CNS injuries in adult mammals.

Indexed as

AnimalsAxonsCells, CulturedChlorocebus aethiopsChondroitin Sulfate ProteoglycansCOS CellsFemaleGrowth InhibitorsHumansMiceMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsProtein BindingReceptor-Like Protein Tyrosine Phosphatases, Class 2Chondroitin Sulfate ProteoglycansGrowth InhibitorsReceptor-Like Protein Tyrosine Phosphatases, Class 2

Identifiers

PMID21976490
PMCPMC3220601
OpenAlexW2086085796

What OpenQuestion holds

Textmetadata
LicenceTDM
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.