Evidence map›Paper›PMID 24206842›Full record

ArticleCurrent biology : CB2013

Tks5 and SHIP2 regulate invadopodium maturation, but not initiation, in breast carcinoma cells.

Ved P Sharma, Robert Eddy, David Entenberg, Masayuki Kai, Frank B Gertler, John Condeelis

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

96 citing papers in PubMed, 177 citations in OpenAlex.

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  19. Phosphoinositide Conversion Inactivates R-RAS and Drives Metastases in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  20. PIPFEBS letters · 2022
    Article

36 more citing papers are in PubMed but not listed here.

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 2 countries.

Ved P SharmaDepartment of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA; Gruss Lipper Biophotonics Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA. Electronic address: ved.sharma@einstein.yu.edu.
Robert Eddy
David Entenberg
Masayuki Kai
Frank B Gertler
John Condeelis
Albert Einstein College of Medicine · USMassachusetts Institute of Technology · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Tumor Cell Networks CenterU54CA112967 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAUFFENBURGER, DOUGLAS A · 2004 to 2015
$26.2M
Signal transduction regulating tumor cell disseminationR01CA150344 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CONDEELIS, JOHN S · 2010 to 2020
$3.7M
NCI NIH HHS CA150344NCI NIH HHS P30 CA014051NCI NIH HHS R01 CA150344NCI NIH HHS U54 CA112967NCI NIH HHS U54-CA112967
6 · The paper itself

Abstract

backgroundTks5 regulates invadopodium formation, but the precise timing during invadopodium lifetime (initiation, stabilization, maturation) when Tks5 plays a role is not known.

resultsWe report new findings based on high-resolution spatiotemporal live-cell imaging of invadopodium precursor assembly. Cortactin, N-WASP, cofilin, and actin arrive together to form the invadopodium precursor, followed by Tks5 recruitment. Tks5 is not required for precursor initiation but is needed for precursor stabilization, which requires the interaction of the phox homology (PX) domain of Tks5 with PI(3,4)P2. During precursor formation, PI(3,4)P2 is uniformly distributed but subsequently starts accumulating at the precursor core 3-4 min after core initiation, and conversely, PI(3,4,5)P3 gets enriched in a ring around the precursor core. SHIP2, a 5'-inositol phosphatase, localizes at the invadopodium core and regulates PI(3,4)P2 levels locally at the invadopodium. The timing of SHIP2 arrival at the invadopodium precursor coincides with the onset of PI(3,4)P2 accumulation. Consistent with its late arrival, we found that SHIP2 inhibition does not affect precursor formation but does cause decreases in mature invadopodia and matrix degradation, whereas SHIP2 overexpression increases matrix degradation.

conclusionsTogether, these findings lead us to propose a new sequential model that provides novel insights into molecular mechanisms underlying invadopodium precursor initiation, stabilization, and maturation into a functional invadopodium.

Indexed as

Cell MovementAdaptor Proteins, Vesicular TransportBiosensing TechniquesBreast NeoplasmsCell Surface ExtensionsFemaleHumansInositol Polyphosphate 5-PhosphatasesMicrofilament ProteinsNeoplasm MetastasisPhosphoric Monoester HydrolasesAdaptor Proteins, Vesicular TransportInositol Polyphosphate 5-PhosphatasesMicrofilament ProteinsPhosphoric Monoester HydrolasesSH3PXD2A protein, human

Identifiers

PMID24206842
PMCPMC3882144
OpenAlexW2069998843

What OpenQuestion holds

Textmetadata
LicenceTDM
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.