Evidence map›Paper›PMID 24840388›Full record

ArticleCell adhesion & migration2014

Cdc42 and Tks5: a minimal and universal molecular signature for functional invadosomes.

Julie Di Martino, Lisa Paysan, Caroline Gest, Valérie Lagrée, Amélie Juin, Frédéric Saltel, Violaine Moreau

Open access · goldAbstract read
In one paragraph

Article 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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

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  11. Actin dynamics during tumor cell dissemination.International review of cell and molecular biology · 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

7 authors at 2 institutions in 1 country.

Julie Di MartinoINSERM; Physiopathologie du cancer du foie; U1053; Bordeaux, France; Univ. Bordeaux; Physiopathologie du cancer du foie; U1053; Bordeaux, France.
Lisa PaysanINSERM; Physiopathologie du cancer du foie; U1053; Bordeaux, France; Univ. Bordeaux; Physiopathologie du cancer du foie; U1053; Bordeaux, France.
Caroline GestINSERM; Physiopathologie du cancer du foie; U1053; Bordeaux, France; Univ. Bordeaux; Physiopathologie du cancer du foie; U1053; Bordeaux, France.
Valérie LagréeINSERM; Physiopathologie du cancer du foie; U1053; Bordeaux, France; Univ. Bordeaux; Physiopathologie du cancer du foie; U1053; Bordeaux, France.
Amélie JuinINSERM; Physiopathologie du cancer du foie; U1053; Bordeaux, France; Univ. Bordeaux; Physiopathologie du cancer du foie; U1053; Bordeaux, France.
Frédéric SaltelINSERM; Physiopathologie du cancer du foie; U1053; Bordeaux, France; Univ. Bordeaux; Physiopathologie du cancer du foie; U1053; Bordeaux, France.
Violaine MoreauINSERM; Physiopathologie du cancer du foie; U1053; Bordeaux, France; Univ. Bordeaux; Physiopathologie du cancer du foie; U1053; Bordeaux, France.
Inserm · FRUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Invadosomes are actin-based structures involved in extracellular-matrix degradation. Invadosomes, either known as podosomes or invadopodia, are found in an increasing number of cell types. Moreover, their overall organization and molecular composition may vary from one cell type to the other. Some are constitutive such as podosomes in hematopoietic cells whereas others are inducible. However, they share the same feature, their ability to interact and to degrade the extracellular matrix. Based on the literature and our own experiments, the aim of this study was to establish a minimal molecular definition of active invadosomes. We first highlighted that Cdc42 is the key RhoGTPase involved in invadosome formation in all described models. Using different cellular models, such as NIH-3T3, HeLa, and endothelial cells, we demonstrated that overexpression of an active form of Cdc42 is sufficient to form invadosome actin cores. Therefore, active Cdc42 must be considered not only as an inducer of filopodia, but also as an inducer of invadosomes. Depending on the expression level of Tks5, these Cdc42-dependent actin cores were endowed or not with a proteolytic activity. In fact, Tks5 overexpression rescued this activity in Tks5 low expressing cells. We thus described the adaptor protein Tks5 as a major actor of the invadosome degradation function. Surprisingly, we found that Src kinases are not always required for invadosome formation and function. These data suggest that even if Src family members are the principal kinases involved in the majority of invadosomes, it cannot be considered as a common element for all invadosome structures. We thus define a minimal and universal molecular signature of invadosome that includes Cdc42 activity and Tks5 presence in order to drive the actin machinery and the proteolytic activity of these invasive structures.

Indexed as

Actin CytoskeletonAdaptor Proteins, Vesicular TransportAnimalscdc42 GTP-Binding ProteinCell MovementExtracellular MatrixHumansMiceMicroscopy, FluorescenceNIH 3T3 CellsPhosphate-Binding ProteinsPhosphoproteinsAdaptor Proteins, Vesicular Transportcdc42 GTP-Binding ProteinFish protein, mousePhosphate-Binding ProteinsPhosphoproteinsSH3PXD2A protein, humanactin cytoskeletonCdc42invadosomesinvasionSrcTks5

Identifiers

PMID24840388
PMCPMC4198353
OpenAlexW1597477883

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.