Evidence map›Paper›PMID 11238458›Full record

ArticleThe Journal of cell biology2001

Protein kinase C activation promotes microtubule advance in neuronal growth cones by increasing average microtubule growth lifetimes.

N Kabir, A W Schaefer, A Nakhost, W S Sossin, P Forscher

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
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  12. Cytoskeletal dynamics in growth-cone steering.Journal of cell science · 2009
    Review
  13. Review
  14. Article
  15. Article
  16. PKC-induced intracellular trafficking of Ca(V)2 precedes its rapid recruitment to the plasma membrane.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008
    Article
  17. Disorganized microtubules underlie the formation of retraction bulbs and the failure of axonal regeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  18. Cytoplasmic dynein and LIS1 are required for microtubule advance during growth cone remodeling and fast axonal outgrowth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  19. 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

5 authors at 2 institutions in 2 countries.

N KabirYale University, New Haven, Connecticut 06520-8103, USA.
A W Schaefer
A Nakhost
W S Sossin
P Forscher
Yale University · USMcGill University · CA

Funding

Regulation of Neuronal Motility: the role of actin filament turnoverR01NS028695 · NINDS · YALE UNIVERSITY · PI FORSCHER, PAUL · 1990 to 2024
$7.8M
ANALYSIS OF MICROTUBULE DYNAMICS IN GROWTH CONESF32NS011122 · NINDS · YALE UNIVERSITY · PI SCHAEFER, ANDREW W · 2000 to 2002
$119k
NINDS NIH HHS 1F32NS11122NINDS NIH HHS F32 NS011122NINDS NIH HHS R01 NS028695NINDS NIH HHS R01-NS28695
6 · The paper itself

Abstract

We describe a novel mechanism for protein kinase C regulation of axonal microtubule invasion of growth cones. Activation of PKC by phorbol esters resulted in a rapid, robust advance of distal microtubules (MTs) into the F-actin rich peripheral domain of growth cones, where they are normally excluded. In contrast, inhibition of PKC activity by bisindolylmaleimide and related compounds had no perceptible effect on growth cone motility, but completely blocked phorbol ester effects. Significantly, MT advance occurred despite continued retrograde F-actin flow-a process that normally inhibits MT advance. Polymer assembly was necessary for PKC-mediated MT advance since it was highly sensitive to a range of antagonists at concentrations that specifically interfere with microtubule dynamics. Biochemical evidence is presented that PKC activation promotes formation of a highly dynamic MT pool. Direct assessment of microtubule dynamics and translocation using the fluorescent speckle microscopy microtubule marking technique indicates PKC activation results in a nearly twofold increase in the typical lifetime of a MT growth episode, accompanied by a 1.7-fold increase and twofold decrease in rescue and catastrophe frequencies, respectively. No significant effects on instantaneous microtubule growth, shortening, or sliding rates (in either anterograde or retrograde directions) were observed. MTs also spent a greater percentage of time undergoing retrograde transport after PKC activation, despite overall MT advance. These results suggest that regulation of MT assembly by PKC may be an important factor in determining neurite outgrowth and regrowth rates and may play a role in other cellular processes dependent on directed MT advance.

Indexed as

ActinsAnimalsAplysiaAxonal TransportAxonsBiopolymersCells, CulturedCytoskeletonEnzyme ActivationGrowth ConesIndolesKineticsMaleimidesMicrotubulesNeuronsNocodazoleActinsBiopolymersbisindolylmaleimideIndolesMaleimidesNocodazoleOctoxynolPhorbol 12,13-DibutyrateProtein Kinase CTubulin

Identifiers

PMID11238458
PMCPMC2198821
OpenAlexW2053978255

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.