scholarly journals Food Components Modulate Obesity and Energy Metabolism via the Transcriptional Regulation of Lipid-Sensing Nuclear Receptors

2015 ◽  
Vol 61 (Supplement) ◽  
pp. S128-S130 ◽  
Author(s):  
Tsuyoshi GOTO ◽  
Nobuyuki TAKAHASHI ◽  
Teruo KAWADA
Keyword(s):  
Transcriptional Regulation ◽  
Energy Metabolism ◽  
Nuclear Receptors ◽  
Food Components ◽  
Lipid Sensing

scholarly journals Nuclear Receptor Cofactors in PPARγ-Mediated Adipogenesis and Adipocyte Energy Metabolism

PPAR Research ◽  
2007 ◽  
Vol 2007 ◽  
pp. 1-11 ◽  
Author(s):  
Emily Powell ◽  
Peter Kuhn ◽  
Wei Xu
Keyword(s):  
Transcriptional Regulation ◽  
Energy Metabolism ◽  
Nuclear Receptors ◽  
Nuclear Receptor ◽  
Proper Function ◽  
Peroxisome Proliferator ◽  
Clear Understanding ◽  
Receptor Function ◽  
Peroxisome Proliferator Activated Receptor ◽  
Transcriptional Cofactors

Transcriptional cofactors are integral to the proper function and regulation of nuclear receptors. Members of the peroxisome proliferator-activated receptor (PPAR) family of nuclear receptors are involved in the regulation of lipid and carbohydrate metabolism. They modulate gene transcription in response to a wide variety of ligands, a process that is mediated by transcriptional coactivators and corepressors. The mechanisms by which these cofactors mediate transcriptional regulation of nuclear receptor function are still being elucidated. The rapidly increasing array of cofactors has brought into focus the need for a clear understanding of how these cofactors interact in ligand- and cell-specific manners. This review highlights the differential effects of the assorted cofactors regulating the transcriptional action of PPARγand summarizes the recent advances in understanding the physiological functions of corepressors and coactivators.

scholarly journals Transcriptional Regulation of Central Carbon and Energy Metabolism in Bacteria by Redox-Responsive Repressor Rex

2011 ◽  
Vol 194 (5) ◽  
pp. 1145-1157 ◽  
Author(s):  
D. A. Ravcheev ◽  
X. Li ◽  
H. Latif ◽  
K. Zengler ◽  
S. A. Leyn ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Energy Metabolism ◽  
Redox Responsive ◽  
Central Carbon

scholarly journals Identification of a Liver-Specific Uridine Phosphorylase that Is Regulated by Multiple Lipid-Sensing Nuclear Receptors

2004 ◽  
Vol 18 (4) ◽  
pp. 851-862 ◽  
Author(s):  
Yuan Zhang ◽  
Joyce J. Repa ◽  
Yusuke Inoue ◽  
Graham P. Hayhurst ◽  
Frank J. Gonzalez ◽  
...  
Keyword(s):  
Nuclear Receptors ◽  
Uridine Phosphorylase ◽  
Lipid Sensing

scholarly journals Cancer Promoted by the Oncoprotein v-ErbA May Be Due to Subcellular Mislocalization of Nuclear Receptors

2005 ◽  
Vol 19 (5) ◽  
pp. 1213-1230 ◽  
Author(s):  
Ghislain M. C. Bonamy ◽  
Anne Guiochon-Mantel ◽  
Lizabeth A. Allison
Keyword(s):  
Transcriptional Regulation ◽  
Nuclear Receptors ◽  
Thyroid Hormone Receptor ◽  
Trichostatin A ◽  
Dominant Negative ◽  
Histone Deacetylase Inhibitor Trichostatin ◽  
Dna Elements ◽  
Dominant Negative Activity ◽  
Thyroid Hormone Receptor Α ◽  
Cellular Compartmentalization

Abstract The retroviral v-ErbA oncoprotein is a highly mutated variant of the thyroid hormone receptor α (TRα), which is unable to bind T3 and interferes with the action of TRα in mammalian and avian cancer cells. v-ErbA dominant-negative activity is attributed to competition with TRα for T3-responsive DNA elements and/or auxiliary factors involved in the transcriptional regulation of T3-responsive genes. However, competition models do not address the altered subcellular localization of v-ErbA and its possible implications in oncogenesis. Here, we report that v-ErbA dimerizes with TRα and the retinoid X receptor and sequesters a significant fraction of the two nuclear receptors in the cytoplasm. Recruitment of TRα to the cytoplasm by v-ErbA can be partially reversed in the presence of ligand and when chromatin is disrupted by the histone deacetylase inhibitor trichostatin A. These results define a new mode of action of v-ErbA and illustrate the importance of cellular compartmentalization in transcriptional regulation and oncogenesis.

scholarly journals PPARs in Calorie Restricted and Genetically Long-Lived Mice

PPAR Research ◽  
2007 ◽  
Vol 2007 ◽  
pp. 1-7 ◽  
Author(s):  
Michal M. Masternak ◽  
Andrzej Bartke
Keyword(s):  
Transcription Factors ◽  
Energy Metabolism ◽  
Nuclear Receptors ◽  
Calorie Restriction ◽  
Insulin Action ◽  
Peroxisome Proliferator ◽  
Physiological Functions ◽  
Multiple Organs ◽  
Longevity Genes ◽  
Peroxisome Proliferator Activated Receptors

Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptors superfamily. The three subtypes, PPARα, PPARγ, and PPARβ/δ, are expressed in multiple organs. These transcription factors regulate different physiological functions such as energy metabolism (including lipid and carbohydrate metabolism), insulin action, and immunity and inflammation, and apparently also act as important mediators of longevity and aging. Calorie restriction (CR) is the most effective intervention known to delay aging and increase lifespan. Calorie restriction affects the same physiological functions as PPARs. This review summarizes recent findings on the effects of CR and aging on the expression of PPARγ,α, andβ/δin mice and discusses possible involvement of PPARs in mediating the effects of murine longevity genes. The levels of PPARs change with age and CR appears to prevent these alterations which make “PPARs-CR-AGING” dependence of considerable interest.

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