Evidence map›Paper›PMID 15858067›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Involvement of a Rac activator,P-Rex1, in neurotrophin-derived signaling and neuronal migration.

Masato Yoshizawa, Takeshi Kawauchi, Masaki Sone, Yoshiaki V Nishimura, Mami Terao, Kaori Chihama, Yo-ichi Nabeshima, Mikio Hoshino

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

62 citing papers in PubMed, 110 citations in OpenAlex.

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  5. A genome-wide association study identified 10 novel genomic loci associated with intrinsic capacity.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025
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  6. F-BAR Proteins CIP4 and FBP17 Function in Cortical Neuron Radial Migration and Process Outgrowth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  11. AUTS2 Syndrome: Molecular Mechanisms and Model Systems.Frontiers in molecular neuroscience · 2022
    Review
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  16. PI 3-kinase delta enhances axonal PIPEMBO molecular medicine · 2020
    Article
  17. Review
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2 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

8 authors at 2 institutions in 1 country.

Masato YoshizawaDepartment of Pathology and Tumor Biology, Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan.
Takeshi Kawauchi
Masaki Sone
Yoshiaki V Nishimura
Mami Terao
Kaori Chihama
Yo-ichi Nabeshima
Mikio Hoshino
Kyoto University · JPJapan Science and Technology Agency · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rho-family GTPases play key roles in regulating cytoskeletal reorganization, contributing to many aspects of nervous system development. Their activities are known to be regulated by guanine nucleotide exchange factors (GEFs), in response to various extracellular cues. P-Rex1, a GEF for Rac, has been mainly investigated in neutrophils, in which this molecule contributes to reactive oxygen species formation. However, its role in the nervous system is essentially unknown. Here we describe the expression profile and a physiological function of P-Rex1 in nervous system development. In situ hybridization revealed that P-Rex1 is dynamically expressed in a variety of cells in the developing mouse brain, including some cortical and DRG neurons. In migrating neurons in the intermediate zone, P-Rex1 protein was found to localize in the leading process and adjacent cytoplasmic region. When transfected in pheochromocytoma PC12 cells, P-Rex1 can be activated by NGF, causing an increase in GTP-bound Rac1 and cell motility. Deletion analyses suggested roles for distinct domains of this molecule. Experiments using a P-Rex1 mutant lacking the Dbl-homology domain, a dominant-negative-like form, and small interfering RNA showed that endogenous P-Rex1 was involved in cell migration of PC12 cells and primary cultured neurons from the embryonic day 14 cerebral cortices, induced by extracellular stimuli (NGF, BDNF, and epidermal growth factor). Furthermore, in utero electroporation of the mutant protein into the embryonic cerebral cortex perturbed radial neuronal migration. These findings suggest that P-Rex1, which is expressed in a variety of cell types, is activated by extracellular cues such as neurotrophins and contributes to neuronal migration in the developing nervous system.

Indexed as

ActinsAnimalsBlotting, NorthernBrainCell MovementCells, CulturedEmbryo, MammalianFluorescent Antibody TechniqueGene DeletionGene Expression Regulation, DevelopmentalGreen Fluorescent ProteinsGuanine Nucleotide Exchange FactorsHumansIn Situ HybridizationMiceMice, Inbred ICRActinsGreen Fluorescent ProteinsGuanine Nucleotide Exchange FactorsNerve Growth FactorNerve Growth FactorsPhosphatidylinositol 3-KinasesPREX1 protein, humanrac GTP-Binding ProteinsReceptor, trkBrho GTP-Binding Proteins

Identifiers

PMID15858067
PMCPMC6725123
OpenAlexW2159381226

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.