Evidence map›Paper›PMID 12707308›Full record

ArticleThe Journal of cell biology2003

Control of axon elongation via an SDF-1alpha/Rho/mDia pathway in cultured cerebellar granule neurons.

Yoshiki Arakawa, Haruhiko Bito, Tomoyuki Furuyashiki, Takahiro Tsuji, Sayaka Takemoto-Kimura, Kazuhiro Kimura, Kazuhiko Nozaki, Nobuo Hashimoto, Shuh Narumiya

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
4.9field-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

76 citing papers in PubMed, 202 citations in OpenAlex.

  1. Article
  2. MTCL2 Is Essential for the Bipolar-to-Multipolar Transition in the Dendrite Extension of Cerebellar Granule Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  3. Review
  4. Review
  5. CXCL12 Engages Cortical Inhibitory Neurons to Enhance Dendritic Spine Plasticity and Structured Network Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  6. Article
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  9. Article
  10. Novel insights into the nervous system affected by prolonged hyperglycemia.Journal of molecular medicine (Berlin, Germany) · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Axonal spheroids in neurodegeneration.Molecular and cellular neurosciences · 2021
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

16 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

9 authors at 2 institutions in 1 country.

Yoshiki ArakawaDept. of Pharmacology, Kyoto University Faculty of Medicine, Yoshida, Sakyo-ku, Kyoto 606-8315, Japan.
Haruhiko Bito
Tomoyuki Furuyashiki
Takahiro Tsuji
Sayaka Takemoto-Kimura
Kazuhiro Kimura
Kazuhiko Nozaki
Nobuo Hashimoto
Shuh Narumiya
Kyoto University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rho-GTPase has been implicated in axon outgrowth. However, not all of the critical steps controlled by Rho have been well characterized. Using cultured cerebellar granule neurons, we show here that stromal cell-derived factor (SDF)-1alpha, a neural chemokine, is a physiological ligand that can turn on two distinct Rho-dependent pathways with opposite consequences. A low concentration of the ligand stimulated a Rho-dependent pathway that mediated facilitation of axon elongation. In contrast, Rho/ROCK activation achieved by a higher concentration of SDF-1alpha caused repression of axon formation and induced no more increase in axon length. However, even at this higher concentration a Rho-dependent axon elongating activity could be recovered upon removal of ROCK activity using Y-27632. SDF-1alpha-induced axon elongating activity under ROCK inhibition was replicated by the dominant-active form of the mammalian homologue of the Drosophila gene Diaphanous (mDia)1 and counteracted by its dominant-negative form. Furthermore, RNAi knockdown of mDia1 abolished SDF-1alpha-induced axon elongation. Together, our results support a critical role for an SDF-1alpha/Rho/mDia1 pathway in mediating axon elongation.

Indexed as

ActinsAnimalsCarrier ProteinsCell DifferentiationCells, CulturedCerebellar CortexChemokine CXCL12Chemokines, CXCDose-Response Relationship, DrugEnzyme InhibitorsForminsGene Expression Regulation, DevelopmentalGrowth ConesIntracellular Signaling Peptides and ProteinsMiceMutationActinsCarrier ProteinsChemokine CXCL12Chemokines, CXCCxcl12 protein, mouseDiap1 protein, mouseEnzyme InhibitorsForminsIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine Kinasesrac GTP-Binding Proteinsrho-Associated Kinasesrho GTP-Binding Proteins

Identifiers

PMID12707308
PMCPMC2172896
OpenAlexW2027840594

What OpenQuestion holds

Textmetadata
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.