Evidence map›Paper›PMID 24727371›Full record

ReviewCell adhesion & migration2014

Coupling between acto-adhesive machinery and ECM degradation in invadosomes.

Olivier Destaing, Christos Petropoulos, Corinne Albiges-Rizo

Open access · goldAbstract readReview
In one paragraph

Review in Cell adhesion & migration, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Dynamics of the sealing zone in cultured osteoclasts.Cytoskeleton (Hoboken, N.J.) · 2017
    Article
  11. Article
  12. Article
  13. Invadosomes in real life.Cell adhesion & migration · 2014
    Article
  14. 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

3 authors at 2 institutions in 1 country.

Olivier DestaingInstitut Albert Bonniot; Université Joseph Fourier; Grenoble, France.
Christos PetropoulosInstitut Albert Bonniot; Université Joseph Fourier; Grenoble, France.
Corinne Albiges-RizoInstitut Albert Bonniot; Université Joseph Fourier; Grenoble, France.
Université Joseph Fourier · FRInstitut pour l'avancée des biosciences · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Invadosomes have two main functions represented by their actin-rich and adhesive components and their polarized secretory pathways controlling the delivery of metalloproteases necessary to degrade extracellular matrix (ECM). Invadosomes include invadopodia and podosomes, which have subtle differences in molecular composition, dynamics, and structure. These differences could reflect different stages of invadosome maturation. This review will outline current knowledge on the coupling between the acto-adhesive machinery and the ECM degradation activity in invadosome diversity. Multiple works support that these two functions are not automatically linked but seem to be finely regulated to allow different functions of invadosomes. We will explore the paradigmatic aspect of invadosomes, which are able to interact with ECM to degrade it so as to better control their own dynamics. Understanding the fine-tuning between these two functions could serve to understand the link between the different types of invadosomes from invadopodia to podosomes.

Indexed as

Actin CytoskeletonAnimalsCell MovementExtracellular MatrixHumansdynamicsinvadopodiainvadosomeinvasionpodosomes

Identifiers

PMID24727371
PMCPMC4198349
OpenAlexW2054076584

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.