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Journal ArticleDOI

G protein-coupled receptors stimulation and the control of cell migration.

Mathieu Cotton, +1 more
- 01 Jul 2009 - 
- Vol. 21, Iss: 7, pp 1045-1053
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TLDR
The role of GPCR mediated signal transduction and their importance in the regulation of actin remodeling leading to cell migration are reviewed.
About
This article is published in Cellular Signalling.The article was published on 2009-07-01. It has received 238 citations till now. The article focuses on the topics: Actin remodeling & Actin cytoskeleton.

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Citations
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Linking actin dynamics and gene transcription to drive cellular motile functions.

TL;DR: The discovery that globular actin polymerization liberates myocardin-related transcription factor (MRTF) cofactors induces the nuclear transcription factor serum response factor (SRF) to modulate the expression of genes encoding structural and regulatory effectors of actin dynamics stimulated research to better understand the actin–MRTF–SRF circuit.
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Endocytic trafficking of Rac is required for the spatial restriction of signaling in cell migration.

TL;DR: It is demonstrated that a Rab5-to-Rac circuitry controls the morphology of motile mammalian tumor cells and primordial germinal cells during zebrafish development, suggesting that this circuitry is relevant for the regulation of migratory programs in various cells, in both in vitro settings and whole organisms.
Journal ArticleDOI

The chemistry, physiology and pathology of pH in cancer

TL;DR: Elevated metabolism, weakened cell-to-capillary diffusive coupling, and adaptations involving H+/H+-equivalent transporters and extracellular-facing CAs give cancer cells the means to manipulate micro-environmental acidity, a cancer hallmark.
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The novel lipid raft adaptor p18 controls endosome dynamics by anchoring the MEK-ERK pathway to late endosomes.

TL;DR: Results indicate that the lipid raft adaptor p18 is essential for anchoring the MEK–ERK pathway to late endosomes, and shed new light on a role of endosomal MEK- ERK pathway in controlling endosome dynamics.
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Three-dimensional context regulation of metastasis

TL;DR: Synergistic interactions between matrix remodeling and tumor hypoxia influence common mechanisms that maximize tumor progression and cooperate to drive metastasis, which should identify novel therapeutic targets.
References
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Journal ArticleDOI

The G protein-coupled receptor kinase (GRK) interactome: Role of GRKs in GPCR regulation and signaling

TL;DR: The ever increasing map of functional interactions for GRK proteins is described as a basis to better understand its contribution to cellular processes.
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Functional specialization of β-arrestin interactions revealed by proteomic analysis

TL;DR: A global proteomics analysis of β-arrestin-interacting proteins (interactome) as modulated by a model seven-transmembrane receptor, the angiotensin II type 1a receptor, helps assess the full range of functions of these versatile molecules and underscores their potentially broad regulatory roles in mammalian cellular physiology.
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Angiotensin II Signaling in Vascular Smooth Muscle: New Concepts

TL;DR: The cellular events responsible for this unique series of events may involve receptor movement and the creation of a signaling domain and are important to the understanding of AT1 receptor function as a final effector of the renin-angiotensin system.
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Activation of ARF6 by ARNO stimulates epithelial cell migration through downstream activation of both Rac1 and phospholipase D

TL;DR: It is suggested that ARF6 activation stimulates two distinct signaling pathways, one leading to Rac activation, the other to changes in membrane phospholipid composition, and that both pathways are required for cell motility.
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β-Arrestin2 Is Critically Involved in CXCR4-mediated Chemotaxis, and This Is Mediated by Its Enhancement of p38 MAPK Activation

TL;DR: The results of this study suggest that β-arrestin2 can function not only as a regulator of CXCR4 signaling but also as a mediator of stromal cell-derived factor 1α-induced chemotaxis and that this activity probably occurs via the ASK1/p38 MAPK pathway.
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