scholarly journals Short communication: Identification of the bovine sterol regulatory element binding protein-1c promoter and its activation by liver X receptor

2010 ◽  
Vol 93 (12) ◽  
pp. 5831-5836 ◽  
Author(s):  
A.J. Lengi ◽  
B.A. Corl
Keyword(s):  
Short Communication ◽  
Binding Protein ◽  
Regulatory Element ◽  
Liver X Receptor ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

scholarly journals Sterol Regulatory Element-binding Protein-2- and Liver X Receptor-driven Dual Promoter Regulation of Hepatic ABC Transporter A1 Gene Expression

2007 ◽  
Vol 282 (29) ◽  
pp. 21090-21099 ◽  
Author(s):  
Norimasa Tamehiro ◽  
Yukari Shigemoto-Mogami ◽  
Tomoshi Kakeya ◽  
Kei-ichiro Okuhira ◽  
Kazuhiro Suzuki ◽  
...  
Keyword(s):  
Gene Expression ◽  
Abc Transporter ◽  
Binding Protein ◽  
Regulatory Element ◽  
Liver X Receptor ◽  
Promoter Regulation ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Dual Promoter

scholarly journals Insulin induction of glucokinase and fatty acid synthase in hepatocytes: analysis of the roles of sterol-regulatory-element-binding protein-1c and liver X receptor

2006 ◽  
Vol 399 (2) ◽  
pp. 275-283 ◽  
Author(s):  
Franck Hansmannel ◽  
Sylvie Mordier ◽  
Patrick B. Iynedjian
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthase ◽  
Glycogen Synthase ◽  
Binding Protein ◽  
Regulatory Element ◽  
Positive Control ◽  
Liver X Receptor ◽  
Transcription Activator ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

The transcription activator SREBP-1c (sterol-regulatory-element-binding protein-1c) is induced by insulin in the liver and is considered a master regulator of lipogenic genes such as FASN (fatty acid synthase). The question of whether SREBP-1c is also a mediator of insulin action on the regulatory enzyme of glucose metabolism GCK (glucokinase) is controversial. In the present paper, we induced SREBP-1c to various levels with insulin or the liver X receptor ligand T0901317 in primary hepatocytes and asked if these levels correlated with those of GCK or FASN mRNA expression, using the latter as positive control. Insulin and T0901317 triggered the accumulation of precursor and processed forms of SREBP-1c to similar levels and with comparable kinetics, and both effectors together caused synergistic increases in SREBP-1c protein levels. These effects were accompanied by commensurate elevation of FASN mRNA, notably by a synergistic response to both effectors. By contrast, GCK mRNA was unresponsive to T0901317 and was induced only by insulin. Treatment of hepatocytes with insulin and/or T0901317 resulted in the recruitment of SREBP-1c to the FASN promoter as shown by chromatin immunoprecipitation, whereas SREBP-1c did not bind to the GCK promoter. Lastly, we observed that the glycogen synthase kinase-3 inhibitor SB216763 produced a small increase in SREBP-1c protein level, which was further augmented in the presence of T0901317. The level of FASN mRNA varied in parallel with SREBP-1c, while GCK mRNA was unaffected. Collectively, these results showed that increases in SREBP-1c were neither necessary nor sufficient for GCK induction in hepatocytes, while at the same time they underscored the role of SREBP-1c as a key regulator of FASN.

scholarly journals Effects of fatty acids on gene expression: role of peroxisome proliferator-activated receptor α, liver X receptor α and sterol regulatory element-binding protein-1c

2002 ◽  
Vol 61 (3) ◽  
pp. 371-374 ◽  
Author(s):  
Sander Kersten
Keyword(s):  
Fatty Acids ◽  
Binding Protein ◽  
Regulatory Element ◽  
Liver X Receptor ◽  
Dietary Fatty Acids ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Liver X Receptor Α ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

Dietary fatty acids have numerous effects on cellular function, many of which are achieved by altering the expression of genes. The present paper reviews recent data on the mechanisms by which fatty acids influence DNA transcription, and focus specifically on the importance of three transcription factors: peroxisome proliferator-activated receptor α; liver X receptor α; sterol regulatory element-binding protein 1c. These data indicate that fatty acids induce or inhibit the mRNA expression of a variety of different genes by acting both as agonists and as antagonists for nuclear hormone receptors.

scholarly journals Protein Kinase A Suppresses Sterol Regulatory Element-binding Protein-1C Expression via Phosphorylation of Liver X Receptor in the Liver

2007 ◽  
Vol 282 (16) ◽  
pp. 11687-11695 ◽  
Author(s):  
Takashi Yamamoto ◽  
Hitoshi Shimano ◽  
Noriyuki Inoue ◽  
Yoshimi Nakagawa ◽  
Takashi Matsuzaka ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Binding Protein ◽  
Regulatory Element ◽  
Liver X Receptor ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Kinase A

scholarly journals Identification of Liver X Receptor-Retinoid X Receptor as an Activator of the Sterol Regulatory Element-Binding Protein 1c Gene Promoter

2001 ◽  
Vol 21 (9) ◽  
pp. 2991-3000 ◽  
Author(s):  
Tomohiro Yoshikawa ◽  
Hitoshi Shimano ◽  
Michiyo Amemiya-Kudo ◽  
Naoya Yahagi ◽  
Alyssa H. Hasty ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Fatty Acid ◽  
Binding Protein ◽  
Regulatory Element ◽  
Gene Promoter ◽  
Liver X Receptor ◽  
Retinoid X Receptor ◽  
Response Element ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

ABSTRACT In an attempt to identify transcription factors which activate sterol-regulatory element-binding protein 1c (SREBP-1c) transcription, we screened an expression cDNA library from adipose tissue of SREBP-1 knockout mice using a reporter gene containing the 2.6-kb mouse SREBP-1 gene promoter. We cloned and identified the oxysterol receptors liver X receptor (LXRα) and LXRβ as strong activators of the mouse SREBP-1c promoter. In the transfection studies, expression of either LXRα or -β activated the SREBP-1c promoter-luciferase gene in a dose-dependent manner. Deletion and mutation studies, as well as gel mobility shift assays, located an LXR response element complex consisting of two new LXR-binding motifs which showed high similarity to an LXR response element recently found in the ABC1 gene promoter, a reverse cholesterol transporter. Addition of an LXR ligand, 22(R)-hydroxycholesterol, increased the promoter activity. Coexpression of retinoid X receptor (RXR), a heterodimeric partner, and its ligand 9-cis-retinoic acid also synergistically activated the SREBP-1c promoter. In HepG2 cells, SREBP-1c mRNA and precursor protein levels were induced by treatment with 22(R)-hydroxycholesterol and 9-cis-retinoic acid, confirming that endogenous LXR-RXR activation can induce endogenous SREBP-1c expression. The activation of SREBP-1c by LXR is associated with a slight increase in nuclear SREBP-1c, resulting in activation of the gene for fatty acid synthase, one of its downstream genes, as measured by the luciferase assay. These data demonstrate that LXR-RXR can modify the expression of genes for lipogenic enzymes by regulating SREBP-1c expression, providing a novel link between fatty acid and cholesterol metabolism.

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