MolPharm

Home Help [Feedback] [For Subscribers] [Archive] [Search] --
 QUICK SEARCH:   [advanced]


     


Molecular Pharmacology Fast Forward
First published on July 14, 2005; DOI: 10.1124/mol.105.012260


This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
mol.105.012260v1
68/4/933    most recent
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gardner, O. S.
Right arrow Articles by Graves, L. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gardner, O. S.
Right arrow Articles by Graves, L. M.


Received for publication March 8, 2005.
Revised July 14, 2005.
Accepted for publication July 14, 2005.

Activation of mitogen-activated protein kinases by peroxisome proliferator-activated receptor ligands: an example of non-genomic signaling

Olivia S. Gardner 1, Brian J. Dewar 1, Lee M. Graves 1*

1 University of North Carolina

* Address correspondence to: E-mail: lmg{at}med.unc.edu

Abstract

Peroxisome proliferator-activated receptors (PPARs) are a subfamily of nuclear hormone receptors that function as ligand-activated transcription factors to regulate lipid metabolism and homeostasis. In addition to their ability to promote gene transcription in a PPAR-dependent manner, ligands for this receptor family have recently been shown to induce mitogen-activated protein kinase (MAPK) phosphorylation. Interestingly, the transcriptional changes induced by PPAR ligands can be separated into distinct PPAR- and MAPK-dependent signaling pathways, suggesting that MAPKs alone mediate some of the effects of PPAR agonists in a non-genomic manner. This review will highlight recent studies that elucidate the non-genomic mechanisms of PPAR ligand-induced MAPK phosphorylation. The potential relevance of MAPK signaling in PPAR biology is also discussed.


Key words: PPARs, MAP Kinase, Jun Kinase, P38 MAP Kinase


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
N. J. Smith, L. A. Stoddart, N. M. Devine, L. Jenkins, and G. Milligan
The Action and Mode of Binding of Thiazolidinedione Ligands at Free Fatty Acid Receptor 1
J. Biol. Chem., June 26, 2009; 284(26): 17527 - 17539.
[Abstract] [Full Text] [PDF]


Home page
J EndocrinolHome page
A. B Ropero, P. Juan-Pico, A. Rafacho, E. Fuentes, F J. Bermudez-Silva, E. Roche, I. Quesada, F. R. de Fonseca, and A. Nadal
Rapid non-genomic regulation of Ca2+ signals and insulin secretion by PPAR{alpha} ligands in mouse pancreatic islets of Langerhans
J. Endocrinol., February 1, 2009; 200(2): 127 - 138.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
L. Matthews, A. Berry, M. Tersigni, F. D'Acquisto, A. Ianaro, and D. Ray
Thiazolidinediones Are Partial Agonists for the Glucocorticoid Receptor
Endocrinology, January 1, 2009; 150(1): 75 - 86.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
M. Melis, G. Pillolla, A. Luchicchi, A. L. Muntoni, S. Yasar, S. R. Goldberg, and M. Pistis
Endogenous Fatty Acid Ethanolamides Suppress Nicotine-Induced Activation of Mesolimbic Dopamine Neurons through Nuclear Receptors
J. Neurosci., December 17, 2008; 28(51): 13985 - 13994.
[Abstract] [Full Text] [PDF]


Home page
Mol. Pharmacol.Home page
B. J. Dewar, O. S. Gardner, C.-S. Chen, H. S. Earp, J. M. Samet, and L. M. Graves
Capacitative Calcium Entry Contributes to the Differential Transactivation of the Epidermal Growth Factor Receptor in Response to Thiazolidinediones
Mol. Pharmacol., November 1, 2007; 72(5): 1146 - 1156.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
K. M. Hong, J. A. Belperio, M. P. Keane, M. D. Burdick, and R. M. Strieter
Differentiation of Human Circulating Fibrocytes as Mediated by Transforming Growth Factor-beta and Peroxisome Proliferator-activated Receptor {gamma}
J. Biol. Chem., August 3, 2007; 282(31): 22910 - 22920.
[Abstract] [Full Text] [PDF]


Home page
Mol. Pharmacol.Home page
L. A. Stoddart, A. J. Brown, and G. Milligan
Uncovering the Pharmacology of the G Protein-Coupled Receptor GPR40: High Apparent Constitutive Activity in Guanosine 5'-O-(3-[35S]thio)triphosphate Binding Studies Reflects Binding of an Endogenous Agonist
Mol. Pharmacol., April 1, 2007; 71(4): 994 - 1005.
[Abstract] [Full Text] [PDF]


Home page
Toxicol SciHome page
M. A. Peraza, A. D. Burdick, H. E. Marin, F. J. Gonzalez, and J. M. Peters
The Toxicology of Ligands for Peroxisome Proliferator-Activated Receptors (PPAR)
Toxicol. Sci., April 1, 2006; 90(2): 269 - 295.
[Abstract] [Full Text] [PDF]




Home Help [Feedback] [For Subscribers] [Archive] [Search] --
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
 Molecular Interventions Drug Metabolism and Disposition

Copyright © 2005 by the American Society for Pharmacology and Experimental Therapeutics