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

New DC, Wong YH - J Mol Signal (2007)

Bottom Line: 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biochemistry, the Molecular Neuroscience Center, and the Biotechnology Research Institute, Hong Kong University of Science and Technology, Clearwater Bay, Hong Kong, China. dnew@ust.hk

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

Further PKC-dependent cell cycle regulation. Gi/o-, Gs- and Gq-family coupled GPCRs can activate PLCβ and PKC activity via Gα or Gβγ subunits. Activated PKC can phosphorylate and activate PKD, leading to the activity of ERK-dependent proliferative pathways. PKC is also able to initiate a series of events that promotes the transcriptional activity of NF-κB. NF-κB activates the promoter regions of cyclin D1 as well as those of p21Cip1 and p27Kip1, causing S phase entry or delay. Dashed indicators identify the probable involvement of multiple, unidentified intermediates.
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Figure 4: Further PKC-dependent cell cycle regulation. Gi/o-, Gs- and Gq-family coupled GPCRs can activate PLCβ and PKC activity via Gα or Gβγ subunits. Activated PKC can phosphorylate and activate PKD, leading to the activity of ERK-dependent proliferative pathways. PKC is also able to initiate a series of events that promotes the transcriptional activity of NF-κB. NF-κB activates the promoter regions of cyclin D1 as well as those of p21Cip1 and p27Kip1, causing S phase entry or delay. Dashed indicators identify the probable involvement of multiple, unidentified intermediates.

Mentions: As well as its documented role in activating Raf-1 (see above), PKC also acts as a key mediator of a number of other GPCR-induced proliferative pathways. PKC isoforms, as well as DAG, are able to activate the protein kinase D (PKD) family of serine/threonine kinases [57]. Indeed, the proliferation of Swiss 3T3 cells in response to the activation of Gq-coupled bombesin or vasopressin receptors is greatly potentiated by the overexpression of PKD [58]. The pathways connecting GPCR activation to the control of cell cycle progression have not yet been outlined but it is known that PKD can activate ERK pathways and phosphorylate c-Jun (Fig. 4 and [57]).


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

New DC, Wong YH - J Mol Signal (2007)

Further PKC-dependent cell cycle regulation. Gi/o-, Gs- and Gq-family coupled GPCRs can activate PLCβ and PKC activity via Gα or Gβγ subunits. Activated PKC can phosphorylate and activate PKD, leading to the activity of ERK-dependent proliferative pathways. PKC is also able to initiate a series of events that promotes the transcriptional activity of NF-κB. NF-κB activates the promoter regions of cyclin D1 as well as those of p21Cip1 and p27Kip1, causing S phase entry or delay. Dashed indicators identify the probable involvement of multiple, unidentified intermediates.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC1808056&req=5

Figure 4: Further PKC-dependent cell cycle regulation. Gi/o-, Gs- and Gq-family coupled GPCRs can activate PLCβ and PKC activity via Gα or Gβγ subunits. Activated PKC can phosphorylate and activate PKD, leading to the activity of ERK-dependent proliferative pathways. PKC is also able to initiate a series of events that promotes the transcriptional activity of NF-κB. NF-κB activates the promoter regions of cyclin D1 as well as those of p21Cip1 and p27Kip1, causing S phase entry or delay. Dashed indicators identify the probable involvement of multiple, unidentified intermediates.
Mentions: As well as its documented role in activating Raf-1 (see above), PKC also acts as a key mediator of a number of other GPCR-induced proliferative pathways. PKC isoforms, as well as DAG, are able to activate the protein kinase D (PKD) family of serine/threonine kinases [57]. Indeed, the proliferation of Swiss 3T3 cells in response to the activation of Gq-coupled bombesin or vasopressin receptors is greatly potentiated by the overexpression of PKD [58]. The pathways connecting GPCR activation to the control of cell cycle progression have not yet been outlined but it is known that PKD can activate ERK pathways and phosphorylate c-Jun (Fig. 4 and [57]).

Bottom Line: 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biochemistry, the Molecular Neuroscience Center, and the Biotechnology Research Institute, Hong Kong University of Science and Technology, Clearwater Bay, Hong Kong, China. dnew@ust.hk

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus