Evidence map›Paper›PMID 19386914›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

A novel function for p53: regulation of growth cone motility through interaction with Rho kinase.

Qingyu Qin, Michel Baudry, Guanghong Liao, Albert Noniyev, James Galeano, Xiaoning Bi

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  6. Telomerase Reverse Transcriptase and p53 Regulate Mammalian Peripheral Nervous System and CNS Axon Regeneration Downstream of c-Myc.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  7. Article
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  9. Article
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  11. p53 on the crossroad between regeneration and cancer.Cell death and differentiation · 2017
    Review
  12. Article
  13. Bridged Analogues for p53-Dependent Cancer Therapy Obtained by S-Alkylation.International journal of peptide research and therapeutics · 2016
    Article
  14. Article
  15. Article
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  17. Article
  18. p53 protects against LPS-induced lung endothelial barrier dysfunction.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  19. Imbalanced mechanistic target of rapamycin C1 and C2 activity in the cerebellum of Angelman syndrome mice impairs motor function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  20. p53 in cell invasion, podosomes, and invadopodia.Cell adhesion & migration · 2014
    Review
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

6 authors at 2 institutions in 1 country.

Qingyu QinDepartment of Basic Medical Sciences, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, California 91766-1854, USA.
Michel Baudry
Guanghong Liao
Albert Noniyev
James Galeano
Xiaoning Bi
Western University of Health Sciences · USUniversity of Southern California · US

Funding

The Spine Cytoskeleton and Memory DisordersP01NS045260 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI GALL, CHRISTINE M · 2003 to 2015
$14.4M
Neurodegeneration in Niemann-Pick Type C DiseaseR01NS048423 · NINDS · WESTERN UNIVERSITY OF HEALTH SCIENCES · PI BI, XIAONING · 2005 to 2009
$860k
NINDS NIH HHS NS048423NINDS NIH HHS P01 NS045260NINDS NIH HHS R01 NS048423
6 · The paper itself

Abstract

The transcription factor p53 suppresses tumorgenesis by regulating cell proliferation and migration. We investigated whether p53 could also control cell motility in postmitotic neurons. p53 isoforms recognized by phospho-p53-specific (at Ser-15) or "mutant" conformation-specific antibodies were highly and specifically expressed in axons and axonal growth cones in primary hippocampal neurons. Inhibition of p53 function by inhibitors, small interfering RNAs, or by dominant-negative forms, induced axonal growth cone collapse, whereas p53 overexpression led to larger growth cones. Furthermore, deletion of the p53 nuclear export signal blocked its axonal distribution and induced growth cone collapse. p53 inhibition-induced axonal growth cone collapse was significantly reduced by the Rho kinase (ROCK) inhibitor, Y27632 [(R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide]. Our results reveal a new function for p53 as a critical regulator of axonal growth cone behavior by suppressing ROCK activity.

Indexed as

AnimalsCell MovementCells, CulturedGrowth ConesMiceMice, Inbred BALB CNeurogenesisProtein Bindingrho-Associated KinasesTumor Suppressor Protein p53rho-Associated KinasesTumor Suppressor Protein p53

Identifiers

PMID19386914
PMCPMC2696279
OpenAlexW2000753484

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.