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Modulation of L-alpha-Lysophosphatidylinositol/GPR55 Mitogen-activated Protein Kinase (MAPK) Signaling by Cannabinoids

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Modulation of L-alpha-Lysophosphatidylinositol/GPR55 Mitogen-activated Protein Kinase (MAPK) Signaling by Cannabinoids. / Anavi-Goffer, Sharon; Baillie, Gemma; Irving, Andrew J.; Gertsch, Juerg; Greig, Iain R.; Pertwee, Roger G.; Ross, Ruth A.

In: Journal of Biological Chemistry, Vol. 287, No. 1, 02.01.2012, p. 91-104.

Research output: Contribution to journalArticle

Harvard

Anavi-Goffer, S, Baillie, G, Irving, AJ, Gertsch, J, Greig, IR, Pertwee, RG & Ross, RA 2012, 'Modulation of L-alpha-Lysophosphatidylinositol/GPR55 Mitogen-activated Protein Kinase (MAPK) Signaling by Cannabinoids' Journal of Biological Chemistry, vol 287, no. 1, pp. 91-104.

APA

Anavi-Goffer, S., Baillie, G., Irving, A. J., Gertsch, J., Greig, I. R., Pertwee, R. G., & Ross, R. A. (2012). Modulation of L-alpha-Lysophosphatidylinositol/GPR55 Mitogen-activated Protein Kinase (MAPK) Signaling by Cannabinoids. Journal of Biological Chemistry, 287(1), 91-104doi: 10.1074/jbc.M111.296020

Vancouver

Anavi-Goffer S, Baillie G, Irving AJ, Gertsch J, Greig IR, Pertwee RG et al. Modulation of L-alpha-Lysophosphatidylinositol/GPR55 Mitogen-activated Protein Kinase (MAPK) Signaling by Cannabinoids. Journal of Biological Chemistry. 2012 Jan 2;287(1):91-104.

Author

Anavi-Goffer, Sharon; Baillie, Gemma; Irving, Andrew J.; Gertsch, Juerg; Greig, Iain R.; Pertwee, Roger G.; Ross, Ruth A. / Modulation of L-alpha-Lysophosphatidylinositol/GPR55 Mitogen-activated Protein Kinase (MAPK) Signaling by Cannabinoids.

In: Journal of Biological Chemistry, Vol. 287, No. 1, 02.01.2012, p. 91-104.

Research output: Contribution to journalArticle

Bibtex - Download

@article{d3b85b2ccaca462bbc90e7c7cad1b45c,
title = "Modulation of L-alpha-Lysophosphatidylinositol/GPR55 Mitogen-activated Protein Kinase (MAPK) Signaling by Cannabinoids",
author = "Sharon Anavi-Goffer and Gemma Baillie and Irving, {Andrew J.} and Juerg Gertsch and Greig, {Iain R.} and Pertwee, {Roger G.} and Ross, {Ruth A.}",
year = "2012",
volume = "287",
number = "1",
pages = "91--104",
journal = "Journal of Biological Chemistry",
issn = "0021-9258",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - Modulation of L-alpha-Lysophosphatidylinositol/GPR55 Mitogen-activated Protein Kinase (MAPK) Signaling by Cannabinoids

A1 - Anavi-Goffer,Sharon

A1 - Baillie,Gemma

A1 - Irving,Andrew J.

A1 - Gertsch,Juerg

A1 - Greig,Iain R.

A1 - Pertwee,Roger G.

A1 - Ross,Ruth A.

AU - Anavi-Goffer,Sharon

AU - Baillie,Gemma

AU - Irving,Andrew J.

AU - Gertsch,Juerg

AU - Greig,Iain R.

AU - Pertwee,Roger G.

AU - Ross,Ruth A.

PY - 2012/1/2

Y1 - 2012/1/2

N2 - <p>GPR55 is activated by L-alpha-lysophosphatidylinositol (LPI) but also by certain cannabinoids. In this study, we investigated the GPR55 pharmacology of various cannabinoids, including analogues of the CB1 receptor antagonist Rimonabant (R), CB2 receptor agonists, and Cannabis sativa constituents. To test ERK1/2 phosphorylation, a primary downstream signaling pathway that conveys LPI-induced activation of GPR55, a high throughput system, was established using the AlphaScreen (R) SureFire (R) assay. Here, we show that CB1 receptor antagonists can act both as agonists alone and as inhibitors of LPI signaling under the same assay conditions. This study clarifies the controversy surrounding the GPR55-mediated actions of SR141716A; some reports indicate the compound to be an agonist and some report antagonism. In contrast, we report that the CB2 ligand GW405833 behaves as a partial agonist of GPR55 alone and enhances LPI signaling. GPR55 has been implicated in pain transmission, and thus our results suggest that this receptor may be responsible for some of the antinociceptive actions of certain CB2 receptor ligands. The phytocannabinoids Delta(9)-tetrahydrocannabivarin, cannabidivarin, and cannabigerovarin are also potent inhibitors of LPI. These Cannabis sativa constituents may represent novel therapeutics targeting GPR55.</p>

AB - <p>GPR55 is activated by L-alpha-lysophosphatidylinositol (LPI) but also by certain cannabinoids. In this study, we investigated the GPR55 pharmacology of various cannabinoids, including analogues of the CB1 receptor antagonist Rimonabant (R), CB2 receptor agonists, and Cannabis sativa constituents. To test ERK1/2 phosphorylation, a primary downstream signaling pathway that conveys LPI-induced activation of GPR55, a high throughput system, was established using the AlphaScreen (R) SureFire (R) assay. Here, we show that CB1 receptor antagonists can act both as agonists alone and as inhibitors of LPI signaling under the same assay conditions. This study clarifies the controversy surrounding the GPR55-mediated actions of SR141716A; some reports indicate the compound to be an agonist and some report antagonism. In contrast, we report that the CB2 ligand GW405833 behaves as a partial agonist of GPR55 alone and enhances LPI signaling. GPR55 has been implicated in pain transmission, and thus our results suggest that this receptor may be responsible for some of the antinociceptive actions of certain CB2 receptor ligands. The phytocannabinoids Delta(9)-tetrahydrocannabivarin, cannabidivarin, and cannabigerovarin are also potent inhibitors of LPI. These Cannabis sativa constituents may represent novel therapeutics targeting GPR55.</p>

KW - L-ALPHA-LYSOPHOSPHATIDYLINOSITOL

KW - CANCER-CELL PROLIFERATION

KW - CB1 RECEPTOR ANTAGONIST

KW - B-RAF INHIBITORS

KW - ALLOSTERIC MODULATION

KW - PLANT CANNABINOIDS

KW - ENDOTHELIAL-CELLS

KW - NEUROPATHIC PAIN

KW - GPR55

KW - IDENTIFICATION

U2 - 10.1074/jbc.M111.296020

DO - 10.1074/jbc.M111.296020

M1 - Article

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 1

VL - 287

SP - 91

EP - 104

ER -

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