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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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Journal ArticleDOI

Reduced migration, altered matrix and enhanced TGFβ1 signaling are signatures of mouse keratinocytes lacking Sdc1

TL;DR: TGFβ1 signaling and SDC1 expression are identified as important factors regulating integrin surface expression, activity and migration in keratinocyte and provide new insight into the functions regulated by Sdc1.
Journal ArticleDOI

Role of G protein-coupled receptor kinases in cell migration

TL;DR: The overall effect of altering GRK levels or activity on chemotaxis would depend on how such different roles are integrated in a given cell type and physiological context, and may have relevant implications in inflammatory diseases or cancer progression.
Journal ArticleDOI

The role of sphingosine-1-phosphate in endothelial barrier function.

TL;DR: Evidence providing mechanistic insights into how S1P maintains endothelial barrier function is summarized, highlighting the recent findings that implicate the major S 1P carrier, HDL, in the maintenance of the persistent S1p-signaling needed to maintain endothelial Barrier function.
Journal ArticleDOI

Autocrine CCL2 promotes cell migration and invasion via PKC activation and tyrosine phosphorylation of paxillin in bladder cancer cells

TL;DR: High levels of CCL2 expressed in bladder cancer mediates tumor invasion and is involved with advanced tumorigenesis, and the findings suggest that this CCL 2/CCR2 pathway is a potential candidate for the attenuation of bladder cancer metastases.
Journal ArticleDOI

Modulation of cellular signaling by herpesvirus-encoded G protein-coupled receptors.

TL;DR: Knowing on the mechanisms by which herpesviruses reprogram cellular signaling might provide insight in the contribution of vGPCRs to viral survival and herpesvirus-associated pathologies is provided.
References
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Journal ArticleDOI

The hallmarks of cancer.

TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.
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Involvement of chemokine receptors in breast cancer metastasis.

TL;DR: It is reported that the chemokine receptors CXCR4 and CCR7 are highly expressed in human breast cancer cells, malignant breast tumours and metastases and their respective ligands CXCL12/SDF-1α and CCL21/6Ckine exhibit peak levels of expression in organs representing the first destinations of breast cancer metastasis.
Journal ArticleDOI

Rho GTPases in cell biology.

TL;DR: Rho GTPases are molecular switches that control a wide variety of signal transduction pathways in all eukaryotic cells and their ability to influence cell polarity, microtubule dynamics, membrane transport pathways and transcription factor activity is probably just as significant.
Journal ArticleDOI

Rho, Rac, and Cdc42 GTPases regulate the assembly of multimolecular focal complexes associated with actin stress fibers, lamellipodia, and filopodia

TL;DR: It is reported here that cdc42, another member of the rho family, triggers the formation of a third type of actin-based structure found at the cell periphery, filopodia, in addition to stress fibers, and rho controls the assembly of focal adhesion complexes.
Journal ArticleDOI

The small GTP-binding protein rac regulates growth factor-induced membrane ruffling.

TL;DR: It is proposed that rac and rho are essential components of signal transduction pathways linking growth factors to the organization of polymerized actin and that growth factors act through rac to stimulate this rho-dependent response.
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