Ligne de temps

Amel Mettouchi
Chercheur(euse) Permanent(e)
01 déc. 2023
publication

Parvimonas micra, an oral pathobiont associated with colorectal cancer, epigenetically reprograms human colonocytes.

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13 oct. 2022
publication

Optineurin links Hace1-dependent Rac ubiquitylation to integrin-mediated mechanotransduction to control bacterial invasion and cell division.

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05 oct. 2022
publication

The cnf1 gene is associated with an expanding Escherichia coli ST131 H30Rx/C2 subclade and confers a competitive advantage for gut colonization.

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15 juil. 2022
publication

C910 chemical compound inhibits the traffiking of several bacterial AB toxins with cross-protection against influenza virus.

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20 janv. 2022
team

Interactions hôte-microbes et pathophysiologie

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08 déc. 2021
publication

DHA-phospholipids control membrane fusion and transcellular tunnel dynamics.

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13 sept. 2019
project

Chronic carriage of CNF1-producing bacteria in the gut and development of colorectal cancer

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13 sept. 2019
project

Landscape of protein ubiquitylation during infection by CNF1-producing uropathogenic E. coli

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23 juil. 2019
project

CNF1 and Rho GTPases ubiquitylation in cellular invasion by uropathogenic E. coli

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20 avr. 2019
publication

UBTD1 is a mechano-regulator controlling cancer aggressiveness

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03 janv. 2019
publication

Acto-myosin force organization modulates centriole separation and PLK4 recruitment to ensure centriole fidelity

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21 sept. 2018
publication

Cell polarity and adherens junction formation inhibit epithelial Fas cell death receptor signaling

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06 juil. 2017
team

Toxines Bactériennes

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01 oct. 2015
publication

Contractile actin cables induced by Bacillus anthracis lethal toxin depend on the histone acetylation machinery.

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25 févr. 2011
publication

Escherichia coli producing CNF1 toxin hijacks Tollip to trigger Rac1-dependent cell invasion

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20 mai 2010
publication

Transcriptome dysregulation by anthrax lethal toxin plays a key role in induction of human endothelial cell cytotoxicity

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05 juin 2006
publication

Induction of transient macroapertures in endothelial cells through RhoA inhibition by Staphylococcus aureus factors.

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