Evidence map›Paper›PMID 19570918›Full record

ArticleMolecular biology of the cell2009

Rac1 modulates stimulus-evoked Ca(2+) release in neuronal growth cones via parallel effects on microtubule/endoplasmic reticulum dynamics and reactive oxygen species production.

Xiao-Feng Zhang, Paul Forscher

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. STIM1 Is Required for Remodeling of the Endoplasmic Reticulum and Microtubule Cytoskeleton in Steering Growth Cones.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  6. Hydrogen Peroxide and Redox Regulation of Developments.Antioxidants (Basel, Switzerland) · 2018
    Review
  7. IPCellular and molecular life sciences : CMLS · 2017
    Review
  8. A Feed-Forward Mechanism Involving the NOX Complex and RyR-Mediated Ca2+ Release During Axonal Specification.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
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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

2 authors at 1 institution in 1 country.

Xiao-Feng ZhangDepartment of Molecular, Cellular, and Developmental Biology, Yale University, New Haven CT 06520, USA.
Paul Forscher
Yale University · US

Funding

Regulation of Neuronal Motility: the role of actin filament turnoverR01NS028695 · NINDS · YALE UNIVERSITY · PI FORSCHER, PAUL · 1990 to 2024
$7.8M
Ca and Rho GTPase Control of the Neuronal CytoskeletonR01NS051786 · NINDS · YALE UNIVERSITY · PI FORSCHER, PAUL · 2006 to 2009
$1.4M
NINDS NIH HHS R01 NS028695NINDS NIH HHS R01 NS051786NINDS NIH HHS R01-NS051786NINDS NIH HHS R01-NS28695
6 · The paper itself

Abstract

The small G protein Rac regulates cytoskeletal protein dynamics in neuronal growth cones and has been implicated in axon growth, guidance, and branching. Intracellular Ca(2+) is another well known regulator of growth cone function; however, effects of Rac activity on intracellular Ca(2+) metabolism have not been well characterized. Here, we investigate how Rac1 activity affects release of Ca(2+) from intracellular endoplasmic reticulum (ER) stores stimulated by application of serotonin (5-hydroxytriptamine). We also address how Rac1 effects on microtubule assembly dynamics affect distribution of Ca(2+) release sites. Multimode fluorescent microscopy was used to correlate microtubule and ER behavior, and ratiometric imaging was used to assess intracellular Ca(2+) dynamics. We report that Rac1 activity both promotes Ca(2+) release and affects its spatial distribution in neuronal growth cones. The underlying mechanism involves synergistic Rac1 effects on microtubule assembly and reactive oxygen species (ROS) production. Rac1 activity modulates Ca(2+) by 1) enhancing microtubule assembly which in turn promotes spread of the ER-based Ca(2+) release machinery into the growth cone periphery, and 2) by increasing ROS production which facilitated inositol 1,4,5-trisphosphate-dependent Ca(2+) release. These results cast Rac1 as a key modulator of intracellular Ca(2+) function in the neuronal growth cone.

Indexed as

NeuronsAnimalsAplysiaCalciumCells, CulturedEndoplasmic ReticulumGrowth ConesInositol 1,4,5-TrisphosphateMicroscopy, FluorescenceMicrotubulesrac1 GTP-Binding ProteinReactive Oxygen SpeciesSerotoninSignal TransductionType C PhospholipasesCalciumInositol 1,4,5-Trisphosphaterac1 GTP-Binding ProteinReactive Oxygen SpeciesSerotoninType C Phospholipases

Identifiers

PMID19570918
PMCPMC2777930
OpenAlexW1970243020

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.