Evidence map›Paper›PMID 27507934›Full record

ArticleFrontiers in cellular neuroscience2016

Neuronal Actin Dynamics, Spine Density and Neuronal Dendritic Complexity Are Regulated by CAP2.

Atul Kumar, Lars Paeger, Kosmas Kosmas, Peter Kloppenburg, Angelika A Noegel, Vivek S Peche

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  8. Cofilin Signaling in the CNS Physiology and Neurodegeneration.International journal of molecular sciences · 2021
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  15. CAP2 deficiency delays myofibril actin cytoskeleton differentiation and disturbs skeletal muscle architecture and function.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  16. Article
  17. Review
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

6 authors at 2 institutions in 1 country.

Atul KumarInstitute of Biochemistry I, Medical Faculty, University of Cologne, CologneGermany; Center for Molecular Medicine Cologne, University of Cologne, CologneGermany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, CologneGermany.
Lars PaegerCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, CologneGermany; Biocenter, Institute for Zoology, University of Cologne, CologneGermany.
Kosmas KosmasInstitute of Biochemistry I, Medical Faculty, University of Cologne, CologneGermany; Center for Molecular Medicine Cologne, University of Cologne, CologneGermany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, CologneGermany.
Peter KloppenburgCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, CologneGermany; Biocenter, Institute for Zoology, University of Cologne, CologneGermany.
Angelika A NoegelInstitute of Biochemistry I, Medical Faculty, University of Cologne, CologneGermany; Center for Molecular Medicine Cologne, University of Cologne, CologneGermany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, CologneGermany.
Vivek S PecheInstitute of Biochemistry I, Medical Faculty, University of Cologne, CologneGermany; Center for Molecular Medicine Cologne, University of Cologne, CologneGermany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, CologneGermany.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Actin remodeling is crucial for dendritic spine development, morphology and density. CAP2 is a regulator of actin dynamics through sequestering G-actin and severing F-actin. In a mouse model, ablation of CAP2 leads to cardiovascular defects and delayed wound healing. This report investigates the role of CAP2 in the brain using Cap2(gt/gt) mice. Dendritic complexity, the number and morphology of dendritic spines were altered in Cap2(gt/gt) with increased number of excitatory synapses. This was accompanied by increased F-actin content and F-actin accumulation in cultured Cap2(gt/gt) neurons. Moreover, reduced surface GluA1 was observed in mutant neurons under basal condition and after induction of chemical LTP. Additionally, we show an interaction between CAP2 and n-cofilin, presumably mediated through the C-terminal domain of CAP2 and dependent on cofilin Ser3 phosphorylation. In vivo, the consequences of this interaction were altered phosphorylated cofilin levels and formation of cofilin aggregates in the neurons. Thus, our studies identify a novel role of CAP2 in neuronal development and neuronal actin dynamics.

Indexed as

actinactin binding proteinsAMPACAP2cyclase associated proteindendritic spinen-cofilin

Identifiers

PMID27507934
PMCPMC4960234
OpenAlexW2481855664

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.