Evidence map›Paper›PMID 27143109›Full record

ArticleScientific reports2016

Novel Coronin7 interactions with Cdc42 and N-WASP regulate actin organization and Golgi morphology.

Kurchi Bhattacharya, Karthic Swaminathan, Vivek S Peche, Christoph S Clemen, Philipp Knyphausen, Michael Lammers, Angelika A Noegel, Raphael H Rastetter

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  7. Actin filament debranching regulates cell polarity during cell migration and asymmetric cell division.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

8 authors at 2 institutions in 1 country.

Kurchi BhattacharyaCenter for Biochemistry, Medical Faculty, University of Cologne, 50931 Cologne, Germany.
Karthic SwaminathanCenter for Biochemistry, Medical Faculty, University of Cologne, 50931 Cologne, Germany.
Vivek S PecheCenter for Biochemistry, Medical Faculty, University of Cologne, 50931 Cologne, Germany.
Christoph S ClemenCenter for Biochemistry, Medical Faculty, University of Cologne, 50931 Cologne, Germany.
Philipp KnyphausenCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany.
Michael LammersCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany.
Angelika A NoegelCenter for Biochemistry, Medical Faculty, University of Cologne, 50931 Cologne, Germany.
Raphael H RastetterCenter for Biochemistry, Medical Faculty, University of Cologne, 50931 Cologne, Germany.
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

The contribution of the actin cytoskeleton to the unique architecture of the Golgi complex is manifold. An important player in this process is Coronin7 (CRN7), a Golgi-resident protein that stabilizes F-actin assembly at the trans-Golgi network (TGN) thereby facilitating anterograde trafficking. Here, we establish that CRN7-mediated association of F-actin with the Golgi apparatus is distinctly modulated via the small Rho GTPase Cdc42 and N-WASP. We identify N-WASP as a novel interaction partner of CRN7 and demonstrate that CRN7 restricts spurious F-actin reorganizations by repressing N-WASP 'hyperactivity' upon constitutive Cdc42 activation. Loss of CRN7 leads to increased cellular F-actin content and causes a concomitant disruption of the Golgi structure. CRN7 harbours a Cdc42- and Rac-interactive binding (CRIB) motif in its tandem β-propellers and binds selectively to GDP-bound Cdc42N17 mutant. We speculate that CRN7 can act as a cofactor for active Cdc42 generation. Mutation of CRIB motif residues that abrogate Cdc42 binding to CRN7 also fail to rescue the cellular defects in fibroblasts derived from CRN7 KO mice. Cdc42N17 overexpression partially rescued the KO phenotypes whereas N-WASP overexpression failed to do so. We conclude that CRN7 spatiotemporally influences F-actin organization and Golgi integrity in a Cdc42- and N-WASP-dependent manner.

Indexed as

ActinsAmino Acid MotifsAmino Acid SequenceAnimalscdc42 GTP-Binding ProteinCell LineCell MovementFibroblastsGene DeletionGene TargetingGenetic LociGolgi ApparatusGuanosine DiphosphateHumansMiceMice, KnockoutActinscdc42 GTP-Binding Proteincoronin proteinsGuanosine DiphosphateMicrofilament ProteinsWiskott-Aldrich Syndrome Protein

Identifiers

PMID27143109
PMCPMC4855144
OpenAlexW2346280548

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.