Evidence map›Paper›PMID 11809819›Full record

ArticleMolecular biology of the cell2002

Protein kinase Cepsilon actin-binding site is important for neurite outgrowth during neuronal differentiation.

Ruth Zeidman, Ulrika Trollér, Arathi Raghunath, Sven Påhlman, Christer Larsson

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 71 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Ruth ZeidmanDepartment of Laboratory Medicine, Molecular Medicine, Lund University, Malmö University Hospital, 205 02 Malmö, Sweden.
Ulrika Trollér
Arathi Raghunath
Sven Påhlman
Christer Larsson
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously shown that protein kinase Cepsilon (PKCepsilon) induces neurite outgrowth via its regulatory domain and independently of its kinase activity. This study aimed at identifying mechanisms regulating PKCepsilon-mediated neurite induction. We show an increased association of PKCepsilon to the cytoskeleton during neuronal differentiation. Furthermore, neurite induction by overexpression of full-length PKCepsilon is suppressed if serum is removed from the cultures or if an actin-binding site is deleted from the protein. A peptide corresponding to the PKCepsilon actin-binding site suppresses neurite outgrowth during neuronal differentiation and outgrowth elicited by PKCepsilon overexpression. Neither serum removal, deletion of the actin-binding site, nor introduction of the peptide affects neurite induction by the isolated regulatory domain. Membrane targeting by myristoylation renders full-length PKCepsilon independent of both serum and the actin-binding site, and PKCepsilon colocalized with F-actin at the cortical cytoskeleton during neurite outgrowth. These results demonstrate that the actin-binding site is of importance for signals acting on PKCepsilon in a pathway leading to neurite outgrowth. Localization of PKCepsilon to the plasma membrane and/or the cortical cytoskeleton is conceivably important for its effect on neurite outgrowth.

Indexed as

ActinsBinding SitesCell DifferentiationCytoskeletonHumansImage CytometryIsoenzymesMicroscopy, ConfocalMicroscopy, FluorescenceNeuritesNeuroblastomaProtein ConformationProtein Kinase CProtein Kinase C-epsilonRecombinant Fusion ProteinsSubstrate SpecificityActinsIsoenzymesPRKCE protein, humanProtein Kinase CProtein Kinase C-epsilonRecombinant Fusion Proteins

Identifiers

PMID11809819
PMCPMC65069
OpenAlexW1980335498

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.