Evidence map›Paper›PMID 19530170›Full record

ArticleJournal of neuroscience research2009

Lipid raft-targeted Akt promotes axonal branching and growth cone expansion via mTOR and Rac1, respectively.

M H Grider, D Park, D M Spencer, H D Shine

Open access · greenAbstract read
In one paragraph

Article in Journal of neuroscience research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

38 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Inhibition of the Akt/PKB Kinase Increases NaInternational journal of molecular sciences · 2022
    Article
  3. Article
  4. Upregulating Lin28a Promotes Axon Regeneration in Adult Mice with Optic Nerve and Spinal Cord Injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
  5. Article
  6. Article
  7. Review
  8. Chronic cannabis promotes pro-hallucinogenic signaling of 5-HT2A receptors through Akt/mTOR pathway.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Article
  9. Article
  10. mTOR-Dependent Cell Proliferation in the Brain.BioMed research international · 2017
    Review
  11. Neuritin Mediates Activity-Dependent Axonal Branch Formation in Part via FGF Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Neu3 sialidase-mediated ganglioside conversion is necessary for axon regeneration and is blocked in CNS axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    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 1 institution in 1 country.

M H GriderDepartment of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.
D Park
D M Spencer
H D Shine
Baylor College of Medicine · US

Funding

Training In Cell and Gene TherapyT32HL092332 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI MALCOLM K. BRENNER, Bruno Di Stefano · 2008 to 2026
$6.9M
GENE DELIVERY FOR SPIRAL CORD INJURY REPAIRR01NS039198 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI SHINE, HAROLD DAVID · 1999 to 2004
$519k
NHLBI NIH HHS T32 HL092332NINDS NIH HHS NS39198NINDS NIH HHS R01 NS039198
6 · The paper itself

Abstract

The molecular mechanisms by which extracellular guidance cues regulate axonal morphology are not fully understood. Recent findings suggest that increased activity of the protein kinase Akt promotes dendritic branching and elongation in hippocampal neurons. We tested whether expression of constitutively active Akt (CA-Akt) in primary sensory neurons would promote axonal branching and whether targeting CA-Akt to lipid rafts, common sites of Akt function, would differentially regulate axonal morphology. Biolistic transduction of sensory neurons induced a rapid expression of CA-Akt, resulting in increased axonal branching, cell hypertrophy, and growth cone expansion. Additionally, we found that targeting of CA-Akt to lipid rafts significantly potentiated growth cone expansion compared with expression of CA-Akt throughout the neuron. Because lipid rafts are concentrated within the growth cone, this finding suggests that signaling of expansion is likely regulated locally. We found that CA-Akt-mediated growth cone expansion, but not axonal branching, was attenuated by coexpression of dominant-negative Rac1. In contrast, blockade of mammalian target of rapamycin (mTOR) prevented axonal branching and hypertrophy in response to CA-Akt, but not growth cone expansion. These data indicate that Akt activity can regulate growth cone expansion via localized Rac1 signaling and regulate axonal branching and soma size via activation of mTOR.

Indexed as

AnimalsAxonsBlotting, WesternChick EmbryoGrowth ConesImmunohistochemistryMembrane MicrodomainsMicroscopy, ConfocalNerve RegenerationProtein KinasesProto-Oncogene Proteins c-aktrac1 GTP-Binding ProteinTOR Serine-Threonine KinasesTransduction, GeneticProtein KinasesProto-Oncogene Proteins c-aktrac1 GTP-Binding ProteinTOR Serine-Threonine Kinases

Identifiers

PMID19530170
PMCPMC6561343
OpenAlexW2066046582

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.