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Molecular mechanisms mediating the G protein-coupled receptor regulation of cell cycle progression

G protein-coupled receptors are key regulators of cellular communication, mediating the efficient coordination of a cell's responses to extracellular stimuli. When stimulated these receptors modulate the activity of a wide range of intracellular signalling pathways that facilitate the ordered d...

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Detalles Bibliográficos
Autores principales: New, David C, Wong, Yung H
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808056/
https://www.ncbi.nlm.nih.gov/pubmed/17319972
http://dx.doi.org/10.1186/1750-2187-2-2
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author New, David C
Wong, Yung H
author_facet New, David C
Wong, Yung H
author_sort New, David C
collection PubMed
description G protein-coupled receptors are key regulators of cellular communication, mediating the efficient coordination of a cell's responses to extracellular stimuli. When stimulated these receptors modulate the activity of a wide range of intracellular signalling pathways that facilitate the ordered development, growth and reproduction of the organism. There is now a growing body of evidence examining the mechanisms by which G protein-coupled receptors are able to regulate the expression, activity, localization and stability of cell cycle regulatory proteins that either promote or inhibit the initiation of DNA synthesis. In this review, we will detail the intracellular pathways that mediate the G protein-coupled receptor regulation of cellular proliferation, specifically the progression from the G1 phase to the S phase of the cell cycle.
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spelling pubmed-18080562007-03-02 Molecular mechanisms mediating the G protein-coupled receptor regulation of cell cycle progression New, David C Wong, Yung H J Mol Signal Review G protein-coupled receptors are key regulators of cellular communication, mediating the efficient coordination of a cell's responses to extracellular stimuli. When stimulated these receptors modulate the activity of a wide range of intracellular signalling pathways that facilitate the ordered development, growth and reproduction of the organism. There is now a growing body of evidence examining the mechanisms by which G protein-coupled receptors are able to regulate the expression, activity, localization and stability of cell cycle regulatory proteins that either promote or inhibit the initiation of DNA synthesis. In this review, we will detail the intracellular pathways that mediate the G protein-coupled receptor regulation of cellular proliferation, specifically the progression from the G1 phase to the S phase of the cell cycle. BioMed Central 2007-02-26 /pmc/articles/PMC1808056/ /pubmed/17319972 http://dx.doi.org/10.1186/1750-2187-2-2 Text en Copyright © 2007 New and Wong; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
New, David C
Wong, Yung H
Molecular mechanisms mediating the G protein-coupled receptor regulation of cell cycle progression
title Molecular mechanisms mediating the G protein-coupled receptor regulation of cell cycle progression
title_full Molecular mechanisms mediating the G protein-coupled receptor regulation of cell cycle progression
title_fullStr Molecular mechanisms mediating the G protein-coupled receptor regulation of cell cycle progression
title_full_unstemmed Molecular mechanisms mediating the G protein-coupled receptor regulation of cell cycle progression
title_short Molecular mechanisms mediating the G protein-coupled receptor regulation of cell cycle progression
title_sort molecular mechanisms mediating the g protein-coupled receptor regulation of cell cycle progression
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808056/
https://www.ncbi.nlm.nih.gov/pubmed/17319972
http://dx.doi.org/10.1186/1750-2187-2-2
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