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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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RanBPM Protein Acts as a Negative Regulator of BLT2 Receptor to Attenuate BLT2-mediated Cell Motility

TL;DR: It is proposed that Akt-induced BLT2 phosphorylation at residue Thr355, which occurs after the addition ofBLT2 ligands, is a potential mechanism by which BLT 2 dissociates from RanBPM, resulting in stimulation of BLT1 signaling.
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Aggresome Formation by the Adenoviral Protein E1B55K Is Not Conserved among Adenovirus Species and Is Not Required for Efficient Degradation of Nuclear Substrates

TL;DR: A comprehensive analysis of the localization of E1B55K products from representatives of six of the seven adenovirus species in the presence and the absence of the corresponding E4orf6 protein found that although in some species E1 B55K localized in aggresomes, such was not always the case, suggesting that these structures are not necessary for the efficient degradation of substrates.
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Long-Term Fluoride Release from Dental Resins Affects STRO-1+ Cell Behavior

TL;DR: The data demonstrate that long-term exposure of STRO-1+ cells to a continuous release of a low amount of fluoride by RK-F10 increases their migratory response to transforming growth factor β1 (TGF-β1) and stromal cell–derived factor 1 (SDF-1), both important promoters of pulp stem cell recruitment.
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RhoB controls the Rab11-mediated recycling and surface reappearance of LFA-1 in migrating T lymphocytes

TL;DR: It is proposed that vesicle-associated RhoB is a regulator of the Rab11-mediated recycling of LFA-1 to the cell surface, an event that is necessary for T lymphocyte motility.
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Genetic Deletion of β-Arrestin-2 and the Mitigation of Established Airway Hyperresponsiveness in a Murine Asthma Model.

TL;DR: The finding thatβarr2 participates in the perpetuation of AHR in an asthma model means that targeting βarr2 may provide immediate and potentially long-term relief from daily asthma symptoms due to AHR irrespective of inflammation.
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.
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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.
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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.
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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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