Protease-dependent versus -independent cancer cell invasion programs: three-dimensional amoeboid movement revisited - Wikidata - awgldk - TriplyDB

Protease-dependent versus -independent cancer cell invasion programs: three-dimensional amoeboid movement revisited

Protease-dependent versus -independent cancer cell invasion programs: three-dimensional amoeboid movement revisited

http://www.wikidata.org/entity/Q34971595

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FGF receptor-4 (FGFR4) polymorphism acts as an activity switch of a membrane type 1 matrix metalloproteinase-FGFR4 complex Endosomal WASH and exocyst complexes control exocytosis of MT1-MMP at invadopodia.CDC42 switches IRSp53 from inhibition of actin growth to elongation by clustering of VASP Gelatinase B/MMP-9 in Tumour Pathogenesis and Progression Bioengineering Models for Breast Cancer Research Utilization of Glycosaminoglycans/Proteoglycans as Carriers for Targeted Therapy Delivery The role of endocytic Rab GTPases in regulation of growth factor signaling and the migration and invasion of tumor cells Physical view on migration modes Exploiting nanotechnology to overcome tumor drug resistance: Challenges and opportunities Cell-cell and cell-matrix dynamics in intraperitoneal cancer metastasis Molecular mechanisms controlling vascular lumen formation in three-dimensional extracellular matrices The emerging molecular machinery and therapeutic targets of metastasis Tumor-derived microvesicles: shedding light on novel microenvironment modulators and prospective cancer biomarkers Tumor cell migration in complex microenvironments Proteolytic and non-proteolytic regulation of collective cell invasion: tuning by ECM density and organization.A quantitative comparison of human HT-1080 fibrosarcoma cells and primary human dermal fibroblasts identifies a 3D migration mechanism with properties unique to the transformed phenotype A synthetic modular approach for modeling the role of the 3D microenvironment in tumor progression Matrix-bound PAI-1 supports cell blebbing via RhoA/ROCK1 signaling Multiparametric classification links tumor microenvironments with tumor cell phenotype A membrane-type-1 matrix metalloproteinase (MT1-MMP)-discoidin domain receptor 1 axis regulates collagen-induced apoptosis in breast cancer cells A new method to address unmet needs for extracting individual cell migration features from a large number of cells embedded in 3D volumes Loss of myoferlin redirects breast cancer cell motility towards collective migration Quantitative FRET imaging to visualize the invasiveness of live breast cancer cells A novel 3D fibril force assay implicates src in tumor cell force generation in collagen networks Breast Cancer Cell Invasion into a Three Dimensional Tumor-Stroma Microenvironment.The Dimer Interface of the Membrane Type 1 Matrix Metalloproteinase Hemopexin Domain: CRYSTAL STRUCTURE AND BIOLOGICAL FUNCTIONS Initial steps of metastasis: cell invasion and endothelial transmigration Metastasis suppressor genes at the interface between the environment and tumor cell growth Bidirectional functions of arsenic as a carcinogen and an anti-cancer agent in human squamous cell carcinoma Bi-directional signaling: extracellular matrix and integrin regulation of breast tumor progression Highlighting the impact of aging on type I collagen: label-free investigation using confocal reflectance microscopy and diffuse reflectance spectroscopy in 3D matrix model Phosphoinositide 3-kinase p85beta regulates invadopodium formation.Matrix metalloproteinases: regulators of the tumor microenvironment Plasticity of cell migration: a multiscale tuning model Control of Entamoeba histolytica adherence involves metallosurface protease 1, an M8 family surface metalloprotease with homology to leishmanolysin.MT1-MMP- and Cdc42-dependent signaling co-regulate cell invasion and tunnel formation in 3D collagen matrices.Endothelial lumen signaling complexes control 3D matrix-specific tubulogenesis through interdependent Cdc42- and MT1-MMP-mediated events.Contractility of the cell rear drives invasion of breast tumor cells in 3D Matrigel.Corneal stromal cells use both high- and low-contractility migration mechanisms in 3-D collagen matrices.Regulation of the basement membrane by epithelia generated forces.

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P2860

Protease-dependent versus -independent cancer cell invasion programs: three-dimensional amoeboid movement revisited

http://www.wikidata.org/entity/Q34971595

description

2009 nî lūn-bûn

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2009 թուականի Մարտին հրատարակուած գիտական յօդուած

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2009 թվականի մարտին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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Protease-dependent versus -ind ...... al amoeboid movement revisited

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Protease-dependent versus -ind ...... al amoeboid movement revisited

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Protease-dependent versus -ind ...... al amoeboid movement revisited

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Protease-dependent versus -ind ...... al amoeboid movement revisited

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Protease-dependent versus -ind ...... al amoeboid movement revisited

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Protease-dependent versus -ind ...... al amoeboid movement revisited

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Protease-dependent versus -ind ...... al amoeboid movement revisited

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Protease-dependent versus -ind ...... al amoeboid movement revisited

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Protease-dependent versus -ind ...... al amoeboid movement revisited

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Journal of Cell Biology

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Protease-dependent versus -ind ...... al amoeboid movement revisited

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P2093

Farideh Sabeh

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Ryoko Shimizu-Hirota

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Stephen J Weiss

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P2860

Tumor cell invasion of collagen matrices requires coordinate lipid agonist-induced G-protein and membrane-type matrix metalloproteinase-1-dependent signaling

DOCK10-mediated Cdc42 activation is necessary for amoeboid invasion of melanoma cells

Cancer cell death enhances the penetration and efficacy of oncolytic herpes simplex virus in tumors

Cell motility through plasma membrane blebbing

A cancer cell metalloprotease triad regulates the basement membrane transmigration program

Regulation of cell polarity and protrusion formation by targeting RhoA for degradation

Cdc42-MRCK and Rho-ROCK signalling cooperate in myosin phosphorylation and cell invasion

Randomized phase III trial of marimastat versus placebo in patients with metastatic breast cancer who have responding or stable disease after first-line chemotherapy: Eastern Cooperative Oncology Group trial E2196

Rac activation and inactivation control plasticity of tumor cell movement

Tumour-cell invasion and migration: diversity and escape mechanisms

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10.1083/JCB.200807195

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1

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185

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2009-03-30T00:00:00Z

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24245204

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19332889

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2700505

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