scholarly journals RETRACTED: Reversion of hepatic steatosis by exercise training in obese mice: The role of sterol regulatory element-binding protein-1c

Life Sciences ◽  
2012 ◽  
Vol 91 (11-12) ◽  
pp. 395-401 ◽  
Author(s):  
Dennys E. Cintra ◽  
Eduardo R. Ropelle ◽  
Marcelo F. Vitto ◽  
Thais F. Luciano ◽  
Daniela R. Souza ◽  
...  
Keyword(s):  
Exercise Training ◽  
Hepatic Steatosis ◽  
Binding Protein ◽  
Regulatory Element ◽  
Obese Mice ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

The Potential Role of Sterol Regulatory Element Binding Protein Transcription Factors in Renal Injury

2007 ◽  
Vol 17 (1) ◽  
pp. 62-65 ◽  
Author(s):  
Marek Szolkiewicz ◽  
Michal Chmielewski ◽  
Anna Nogalska ◽  
Ewa Stelmanska ◽  
Julian Swierczynski ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Renal Injury ◽  
Potential Role ◽  
Binding Protein ◽  
Regulatory Element ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Protein Transcription

Modulation of human Niemann-Pick C1-like 1 gene expression by sterol: role of sterol regulatory element binding protein 2

2007 ◽  
Vol 292 (1) ◽  
pp. G369-G376 ◽  
Author(s):  
Waddah A. Alrefai ◽  
Fadi Annaba ◽  
Zaheer Sarwar ◽  
Alka Dwivedi ◽  
Seema Saksena ◽  
...  
Keyword(s):  
Promoter Activity ◽  
Binding Protein ◽  
Regulatory Element ◽  
Cholesterol Absorption ◽  
Cholesterol Depletion ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Niemann Pick ◽  
Coa Reductase

Niemann-Pick C1-like 1 (NPC1L1) is an essential intestinal component of cholesterol absorption. However, little is known about the molecular regulation of intestinal NPC1L1 expression and promoter activity. We demonstrated that human NPC1L1 mRNA expression was significantly decreased by 25-hydroxycholesterol but increased in response to cellular cholesterol depletion achieved by incubation with Mevinolin (an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase) in human intestinal Caco-2 cells. We also showed that a −1741/+56 fragment of the NPC1L1 gene demonstrated high promoter activity in Caco-2 cells that was reduced by 25-hydroxycholesterol and stimulated by cholesterol depletion. Interestingly, we showed that the NPC1L1 promoter is remarkably transactivated by the overexpression of sterol regulatory element (SRE) binding protein (SREBP)-2, suggesting its involvement in the sterol-induced alteration in NPC1L1 promoter activity. Finally, we identified two putative SREs in the human NPC1L1 promoter and established their essential roles in mediating the effects of cholesterol on promoter activity. Our study demonstrated the modulation of human NPC1L1 expression and promoter activity by cholesterol in a SREBP-2-dependent mechanism.

Regulation of sterol regulatory-element binding protein 1 gene expression in liver: role of insulin and protein kinase B/cAkt

2000 ◽  
Vol 349 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Mark FLEISCHMANN ◽  
Patrick B. IYNEDJIAN
Keyword(s):  
Gene Expression ◽  
Protein Kinase ◽  
Recombinant Protein ◽  
Protein Kinase B ◽  
Binding Protein ◽  
Regulatory Element ◽  
Mutant Form ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

Insulin stimulates the transcription of the sterol regulatory- element binding protein (SREBP) 1/ADD1 gene in liver. Hepatocytes in primary culture were used to delineate the insulin signalling pathway for induction of SREBP1 gene expression. The inhibitors of phosphoinositide 3-kinase (PI 3-kinase), wortmannin and LY 294002, abolished the insulin-dependent increase in SREBP1 mRNA, whereas the inhibitor of the mitogen- activated protein kinase cascade, PD 98059, was without effect. To investigate the role of protein kinase B (PKB)/cAkt downstream of PI 3-kinase, hepatocytes were transduced with an adenovirus encoding a PKB-oestrogen receptor fusion protein. The PKB activity of this recombinant protein was rapidly activated in hepatocytes challenged with 4-hydroxytamoxifen (OHT), as was endogenous PKB in hepatocytes challenged with insulin. The addition of OHT to transduced hepatocytes resulted in accumulation of SREBP1 mRNA, with a time-course and magnitude similar to the effect of insulin in non-transduced cells. The level of SREBP1 mRNA was not increased by OHT in hepatocytes expressing a mutant form of the recombinant protein whose PKB activity was not activated by OHT. Thus acute activation of PKB is sufficient to induce SREBP1 mRNA accumulation in primary hepatocytes, and might be the major signalling event by which insulin induces SREBP1 gene expression in the liver.

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