Evidence map›Paper›PMID 20643936›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Role of calpain-mediated p53 truncation in semaphorin 3A-induced axonal growth regulation.

Qingyu Qin, Guanghong Liao, Michel Baudry, Xiaoning Bi

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Calpain Promotes LPS-induced Lung Endothelial Barrier Dysfunction via Cleavage of Talin.American journal of respiratory cell and molecular biology · 2023
    Article
  4. Article
  5. Article
  6. Calpain-Mediated Proteolysis of Talin and FAK Regulates Adhesion Dynamics Necessary for Axon Guidance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. p53 in cell invasion, podosomes, and invadopodia.Cell adhesion & migration · 2014
    Review
  12. Article
  13. Learning and memory: an emergent property of cell motility.Neurobiology of learning and memory · 2013
    Review
  14. Article
  15. Conditional disruption of calpain in the CNS alters dendrite morphology, impairs LTP, and promotes neuronal survival following injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  16. Calpain-2-mediated PTEN degradation contributes to BDNF-induced stimulation of dendritic protein synthesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  17. Article
  18. p53 Regulates the neuronal intrinsic and extrinsic responses affecting the recovery of motor function following spinal cord injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  19. Calpain cleaves and activates the TRPC5 channel to participate in semaphorin 3A-induced neuronal growth cone collapse.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  20. Article
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

4 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, CA 91766, USA.
Guanghong Liao
Michel Baudry
Xiaoning Bi
Western University of Health Sciences · USUniversity of Southern California · US

Funding

Potential use of a decoy peptide for hypoxia/ischemia treatmentR21NS062167 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BAUDRY, MICHEL · 2009 to 2010
$440k
NINDS NIH HHS NS062167NINDS NIH HHS R21 NS062167
6 · The paper itself

Abstract

Neurite outgrowth represents a critical stage in the correct development of neuronal circuitries, and is dependent on the complex regulation of actin filament and microtubule dynamics by intrinsic as well as extrinsic signals. Previous studies have implicated the tumor suppressor factor, p53, in the regulation of axonal outgrowth through a nontranscriptional effect involving local regulation of the Rho kinase signaling pathway that controls these dynamics. In the present study, we first showed that semaphorin 3A-induced growth cone collapse in cultured hippocampal neurons was associated with the partial truncation of phosphorylated p53, and that both effects were prevented by calpain inhibition with either m-calpain-specific siRNA or inhibitors. We further determined that semaphorin 3A-mediated calpain activation and growth cone collapse were associated with m-calpain phosphorylation and prevented by inhibition of MAPK, ERK, or p38. In vitro studies confirmed that p53 and especially phosphorylated p53 were partially truncated by calpain. Thus, our results indicate that semaphorin 3A-mediated growth cone collapse is mediated in part by m-calpain activation, possibly through MAPK-mediated phosphorylation, and the resulting truncation of phosphorylated p53, leading to Rho kinase activation and cytoskeletal reorganization. They provide a pathway by which extrinsic signals regulate axonal growth through activation of m-calpain and p53 truncation.

Indexed as

Gene DeletionAnimalsAxonsCalpainCells, CulturedEnzyme ActivationExtracellular Signal-Regulated MAP KinasesGrowth ConesMAP Kinase Signaling SystemMiceMice, Inbred BALB Cp38 Mitogen-Activated Protein KinasesPhosphorylationSemaphorin-3ATumor Suppressor Protein p53CalpainExtracellular Signal-Regulated MAP Kinasesm-calpainp38 Mitogen-Activated Protein KinasesSema3a protein, mouseSemaphorin-3ATumor Suppressor Protein p53

Identifiers

PMID20643936
PMCPMC2922263
OpenAlexW2031148024

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.