Evidence map›Paper›PMID 28893863›Full record

ArticleEMBO reports2017

Bin1 directly remodels actin dynamics through its BAR domain.

Nina M Dräger, Eliana Nachman, Moritz Winterhoff, Stefan Brühmann, Pranav Shah, Taxiarchis Katsinelos, Steeve Boulant, Aurelio A Teleman, Jan Faix, Thomas R Jahn

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EMBO reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. BIN1 in cancer: biomarker and therapeutic target.Journal of cancer research and clinical oncology · 2023
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Synaptic tau: A pathological or physiological phenomenon?Acta neuropathologica communications · 2021
    Review
  16. Article
  17. Mechanisms and Regulation of Cardiac CaInternational journal of molecular sciences · 2021
    Review
  18. 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

10 authors at 3 institutions in 1 country.

Nina M DrägerProteostasis in Neurodegenerative Disease (B180), Schaller Research Group at the University of Heidelberg and DKFZ, Heidelberg, Germany.
Eliana NachmanProteostasis in Neurodegenerative Disease (B180), Schaller Research Group at the University of Heidelberg and DKFZ, Heidelberg, Germany.
Moritz WinterhoffInstitute for Biophysical Chemistry, Hannover Medical School, Hannover, Germany.
Stefan BrühmannInstitute for Biophysical Chemistry, Hannover Medical School, Hannover, Germany.
Pranav ShahSchaller Research Group at CellNetworks, Department of Infectious Diseases, Virology, Heidelberg University, Heidelberg, Germany.
Taxiarchis KatsinelosProteostasis in Neurodegenerative Disease (B180), Schaller Research Group at the University of Heidelberg and DKFZ, Heidelberg, Germany.
Steeve BoulantSchaller Research Group at CellNetworks, Department of Infectious Diseases, Virology, Heidelberg University, Heidelberg, Germany.
Aurelio A TelemanSignal Transduction in Cancer and Metabolism (B140), German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0002-4237-9368
Jan FaixInstitute for Biophysical Chemistry, Hannover Medical School, Hannover, Germany.ORCID 0000-0003-1803-9192
Thomas R JahnProteostasis in Neurodegenerative Disease (B180), Schaller Research Group at the University of Heidelberg and DKFZ, Heidelberg, Germany thomas.r.jahn@abbvie.com.ORCID 0000-0002-9266-6736
German Cancer Research Center · DEHeidelberg University · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endocytic processes are facilitated by both curvature-generating BAR-domain proteins and the coordinated polymerization of actin filaments. Under physiological conditions, the N-BAR protein Bin1 has been shown to sense and curve membranes in a variety of cellular processes. Recent studies have identified Bin1 as a risk factor for Alzheimer's disease, although its possible pathological function in neurodegeneration is currently unknown. Here, we report that Bin1 not only shapes membranes, but is also directly involved in actin binding through its BAR domain. We observed a moderate actin bundling activity by human Bin1 and describe its ability to stabilize actin filaments against depolymerization. Moreover, Bin1 is also involved in stabilizing tau-induced actin bundles, which are neuropathological hallmarks of Alzheimer's disease. We also provide evidence for this effect

Indexed as

Actin CytoskeletonActinsAdaptor Proteins, Signal TransducingAnimalsBinding SitesCarrier ProteinsCloning, MolecularDisease Models, AnimalDrosophila melanogasterDrosophila ProteinsEscherichia coliGene ExpressionGene Expression RegulationGenetic VectorsHumansNuclear ProteinsActinsAdaptor Proteins, Signal Transducingbicoid interacting protein 1, DrosophilaBIN1 protein, humanCarrier ProteinsDrosophila ProteinsMAPT protein, humanNuclear ProteinsProtein IsoformsRecombinant Proteinstau ProteinsTranscription FactorsTumor Suppressor Proteinsactin bindingAlzheimer's diseasegenetic risk factorN‐BAR protein Bin1tau

Identifiers

PMID28893863
PMCPMC5666605
OpenAlexW2751660345

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.