Results 1 - 10
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13
Resonant waveguide grating biosensor for living cell sensing
- Biophys.J
, 2006
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BMP4 induces EMT and Rho GTPase activation in human ovarian cancer cells
, 2007
"... We identified previously an autocrine bone morphogenetic protein-4 (BMP4) signalling pathway in primary human normal ovarian surface epithelial (OSE) and epithelial ovarian cancer (OvCa) cells. Herein we show that treatment of OvCa cells with BMP4 produced morphological alterations and increased cel ..."
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Cited by 6 (1 self)
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We identified previously an autocrine bone morphogenetic protein-4 (BMP4) signalling pathway in primary human normal ovarian surface epithelial (OSE) and epithelial ovarian cancer (OvCa) cells. Herein we show that treatment of OvCa cells with BMP4 produced morphological alterations and increased cellular adhesion, motility and invasion. The BMP4 inhibitor noggin blocked the BMP4-induced phenotype, and decreased autocrine BMP4-mediated OvCa cell motility and adherence. In response to exogenous BMP4, the epithelial–mesenchymal transition (EMT) markers Snail and Slug mRNA and protein were up-regulated, E-cadherin mRNA and protein were down-regulated and the net-work of alpha smooth muscle actin changed to resemble a mesen-chymal cell. We also observed changes in the level of activated Rho GTPases in OvCa cells treated with BMP4, strongly suggest-ing that the changes in morphology, adhesion, motility and inva-sion are probably mediated through the activation of these molecules. Strikingly, treatment of normal OSE cells with BMP4 or noggin failed to alter cell motility, providing evidence that OSE and OvCa cells possess a distinct capability to respond to BMP4. Overall, our studies suggest a link between autocrine BMP signalling mediated through the Rho GTPase family and Snail- and Slug-induced EMT that may collectively contribute to aggressive OvCa behaviour.
Initial dynamics of cell spreading are governed by dissipation in the actin cortex
- Biophys J
, 2011
"... Abstract. The initial stages of spreading of a suspended cell onto a substrate under the effect of (specific or nonspecific) adhesion exhibit a universal behaviour, which is cell-type independent. We show that this behaviour is governed by cell-scale phenomena only. This can be understood if the mai ..."
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Cited by 3 (2 self)
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Abstract. The initial stages of spreading of a suspended cell onto a substrate under the effect of (specific or nonspecific) adhesion exhibit a universal behaviour, which is cell-type independent. We show that this behaviour is governed by cell-scale phenomena only. This can be understood if the main retarding force that opposes cell adhesion is of mechanical origin, that is, dissipation occuring during the spreading. By comparing several naive models that generate different patterns of dissipation, we show by numerical simulation that only dissipation due to the deformation of the actin cortex is compatible with the experimental observations. This viscous-like dissipation corresponds to the energetic cost of rearranging the cytoskeleton, and is the trace of all dissipative events occuring in the cell cortex during the early spreading, such as the binding and unbinding of cross-linkers and molecular friction.
unknown title
"... Pathogen engulfment by host phagocytic cells and their subsequent killing in the phagocytic vacuole are major events for bacterial clearance and contribute to a robust innate immunity in most multicellular organisms (Beutler, 2004). In mammals, phagocytosis ..."
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Pathogen engulfment by host phagocytic cells and their subsequent killing in the phagocytic vacuole are major events for bacterial clearance and contribute to a robust innate immunity in most multicellular organisms (Beutler, 2004). In mammals, phagocytosis
unknown title
"... Pathogen engulfment by host phagocytic cells and their subsequent killing in the phagocytic vacuole are major events for bacterial clearance and contribute to a robust innate immunity in most multicellular organisms (Beutler, 2004). In mammals, phagocytosis ..."
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Pathogen engulfment by host phagocytic cells and their subsequent killing in the phagocytic vacuole are major events for bacterial clearance and contribute to a robust innate immunity in most multicellular organisms (Beutler, 2004). In mammals, phagocytosis
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"... Initial dynamics of cell spreading are governed by dissipation in the actin cortex ..."
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Initial dynamics of cell spreading are governed by dissipation in the actin cortex
A new method for rapid detection of T
, 2010
"... A new method for rapid detection of T lymphocyte decision to proliferate after encountering activating surfaces Article in Journal of immunological methods · October 2010 ..."
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A new method for rapid detection of T lymphocyte decision to proliferate after encountering activating surfaces Article in Journal of immunological methods · October 2010
Identification des « Ubiquitin Specific Proteases » impliquées dans
, 2009
"... la régulation des voies de l’immunité chez la drosophile ..."
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Cellular Morphogenesis and Tumor Progression
"... Cell adhesion and motility depend strongly on the interactions between cells and extracellular matrix (ECM) substrates. When plated onto artificial adhesive surfaces, cells first flatten and deform extensively as they spread. At the molecular level, the interaction of membrane-based integrins with t ..."
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Cell adhesion and motility depend strongly on the interactions between cells and extracellular matrix (ECM) substrates. When plated onto artificial adhesive surfaces, cells first flatten and deform extensively as they spread. At the molecular level, the interaction of membrane-based integrins with the ECM has been shown to initiate a complex cascade of signaling events [1], which subsequently triggers cellular morphological changes and results in the generation of contractile forces [2]. Here, we focus on the early stages of cell spreading and probe their dynamics by quantitative visualization and biochemical manipulation with a variety of cell types and adhesive surfaces, adhesion receptors, and cytoskeleton-altering drugs. We find that the dynamics of adhesion follows a universal power-law behavior. This is in sharp contrast with the common belief that spreading is regulated by either the diffusion of adhesion receptors toward the growing adhesive patch [3–5] or by actin polymerization [6–8]. To explain this, we propose a simple quantitative and predictive theory that models cells as viscous adhesive cortical shells enclosing a less viscous interior. Thus, although cell spreading is driven by well-identified biomolecular interactions, it is dynamically limited by its mesoscopic structure and material properties.
