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Conditional expression of human PPARδ and a dominant negative variant of hPPARδ in vivo

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Conditional expression of human PPARδ and a dominant negative variant of hPPARδ in vivo. / Higgins, Larry G.; Garbacz, Wojciech G.; Gustafsson, Mattias C. U.; Sitheswaran, Nainamalai; Ashby, Peter R.; Wolf, C. Roland; Palmer, Colin N. A.

In: PPAR Research, 2012.

Research output: Contribution to journalArticle

Harvard

Higgins, LG, Garbacz, WG, Gustafsson, MCU, Sitheswaran, N, Ashby, PR, Wolf, CR & Palmer, CNA 2012, 'Conditional expression of human PPARδ and a dominant negative variant of hPPARδ in vivo' PPAR Research., 10.1155/2012/216817

APA

Higgins, L. G., Garbacz, W. G., Gustafsson, M. C. U., Sitheswaran, N., Ashby, P. R., Wolf, C. R., & Palmer, C. N. A. (2012). Conditional expression of human PPARδ and a dominant negative variant of hPPARδ in vivo. PPAR Research, [216817]. 10.1155/2012/216817

Vancouver

Higgins LG, Garbacz WG, Gustafsson MCU, Sitheswaran N, Ashby PR, Wolf CR et al. Conditional expression of human PPARδ and a dominant negative variant of hPPARδ in vivo. PPAR Research. 2012. 216817. Available from: 10.1155/2012/216817

Author

Higgins, Larry G.; Garbacz, Wojciech G.; Gustafsson, Mattias C. U.; Sitheswaran, Nainamalai; Ashby, Peter R.; Wolf, C. Roland; Palmer, Colin N. A. / Conditional expression of human PPARδ and a dominant negative variant of hPPARδ in vivo.

In: PPAR Research, 2012.

Research output: Contribution to journalArticle

Bibtex - Download

@article{09215408fd3041f8b1509f619a48eb7a,
title = "Conditional expression of human PPARδ and a dominant negative variant of hPPARδ in vivo",
author = "Higgins, {Larry G.} and Garbacz, {Wojciech G.} and Gustafsson, {Mattias C. U.} and Nainamalai Sitheswaran and Ashby, {Peter R.} and Wolf, {C. Roland} and Palmer, {Colin N. A.}",
year = "2012",
doi = "10.1155/2012/216817",
journal = "PPAR Research",
issn = "1687-4757",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - Conditional expression of human PPARδ and a dominant negative variant of hPPARδ in vivo

A1 - Higgins,Larry G.

A1 - Garbacz,Wojciech G.

A1 - Gustafsson,Mattias C. U.

A1 - Sitheswaran,Nainamalai

A1 - Ashby,Peter R.

A1 - Wolf,C. Roland

A1 - Palmer,Colin N. A.

AU - Higgins,Larry G.

AU - Garbacz,Wojciech G.

AU - Gustafsson,Mattias C. U.

AU - Sitheswaran,Nainamalai

AU - Ashby,Peter R.

AU - Wolf,C. Roland

AU - Palmer,Colin N. A.

PY - 2012

Y1 - 2012

N2 - <p>The nuclear receptor, NR1C2 or peroxisome proliferator-activated receptor (PPAR)-delta, is ubiquitously expressed and important for placental development, fatty acid metabolism, wound healing, inflammation, and tumour development. PPAR delta has been hypothesized to function as both a ligand activated transcription factor and a repressor of transcription in the absence of agonist. In this paper, treatment of mice conditionally expressing human PPAR delta with GW501516 resulted in a marked loss in body weight that was not evident in nontransgenic animals or animals expressing a dominant negative derivative of PPAR delta. Expression of either functional or dominant negative hPPAR delta blocked bezafibrate-induced PPAR alpha-dependent hepatomegaly and blocked the effect of bezafibrate on the transcription of PPAR alpha target genes. These data demonstrate, for the first time, that PPAR delta could inhibit the activation of PPAR alpha in vivo and provide novel models for the investigation of the role of PPAR delta in pathophysiology.</p>

AB - <p>The nuclear receptor, NR1C2 or peroxisome proliferator-activated receptor (PPAR)-delta, is ubiquitously expressed and important for placental development, fatty acid metabolism, wound healing, inflammation, and tumour development. PPAR delta has been hypothesized to function as both a ligand activated transcription factor and a repressor of transcription in the absence of agonist. In this paper, treatment of mice conditionally expressing human PPAR delta with GW501516 resulted in a marked loss in body weight that was not evident in nontransgenic animals or animals expressing a dominant negative derivative of PPAR delta. Expression of either functional or dominant negative hPPAR delta blocked bezafibrate-induced PPAR alpha-dependent hepatomegaly and blocked the effect of bezafibrate on the transcription of PPAR alpha target genes. These data demonstrate, for the first time, that PPAR delta could inhibit the activation of PPAR alpha in vivo and provide novel models for the investigation of the role of PPAR delta in pathophysiology.</p>

UR - http://www.scopus.com/inward/record.url?scp=84859776080&partnerID=8YFLogxK

U2 - 10.1155/2012/216817

DO - 10.1155/2012/216817

M1 - Article

JO - PPAR Research

JF - PPAR Research

SN - 1687-4757

ER -

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