scholarly journals Sterol regulation of human fatty acid synthase promoter I requires nuclear factor-Y- and Sp-1-binding sites

2000 ◽  
Vol 97 (8) ◽  
pp. 3948-3953 ◽  
Author(s):  
S. Xiong ◽  
S. S. Chirala ◽  
S. J. Wakil
Keyword(s):  
Fatty Acid ◽  
Binding Sites ◽  
Fatty Acid Synthase ◽  
Nuclear Factor ◽  
Nuclear Factor Y

scholarly journals A key role of nuclear factor Y in the refeeding response of fatty acid synthase in adipocytes

FEBS Letters ◽  
2017 ◽  
Vol 591 (7) ◽  
pp. 965-978 ◽  
Author(s):  
Makiko Nishi-Tatsumi ◽  
Naoya Yahagi ◽  
Yoshinori Takeuchi ◽  
Naoki Toya ◽  
Ayako Takarada ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthase ◽  
Nuclear Factor ◽  
Nuclear Factor Y

scholarly journals Nuclear Factor-κB (NF-κB) Mediates a Protective Response in Cancer Cells Treated with Inhibitors of Fatty Acid Synthase

2011 ◽  
Vol 286 (36) ◽  
pp. 31457-31465 ◽  
Author(s):  
Colleen R. M. Lemmon ◽  
Ju-Hyung Woo ◽  
Ellen Tully ◽  
Kathleen Wilsbach ◽  
Edward Gabrielson
Keyword(s):  
Fatty Acid ◽  
Cancer Cells ◽  
Fatty Acid Synthase ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Protective Response

scholarly journals Occupancy and Function of the −150 Sterol Regulatory Element and −65 E-Box in Nutritional Regulation of the Fatty Acid Synthase Gene in Living Animals

2003 ◽  
Vol 23 (16) ◽  
pp. 5896-5907 ◽  
Author(s):  
Maria-Jesus Latasa ◽  
Michael J. Griffin ◽  
Yang Soo Moon ◽  
Chulho Kang ◽  
Hei Sook Sul
Keyword(s):  
Fatty Acid ◽  
Binding Sites ◽  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Nutritional Regulation ◽  
Fed State ◽  
E Box ◽  
Sterol Regulatory Element ◽  
E Boxes

ABSTRACT Upstream regulatory factor (USF) and sterol regulatory element binding protein (SREBP) play key roles in the transcriptional regulation of the fatty acid synthase (FAS) gene by feeding and insulin. Due to the dual binding specificity of SREBP, as well as the presence of multiple consensus sites for these transcription factors in the FAS promoter, their physiologically relevant functional binding sites have been controversial. Here, in order to determine the occupancy of the putative USF and SREBP binding sites, we examined their protein-DNA interactions in living animals by using formaldehyde cross-linking and immunoprecipitation of chromatin and tested the function of these elements by employing mice transgenic for a reporter gene driven by various 5′ deletions as well as site-specific mutations of the FAS promoter. We show that the −332 and −65 E-boxes are bound by USF in both fasted and refed mice, while the −150 SRE is bound by SREBP-1 only in refed mice. We also found that mutation of either the −150 SRE or the −65 E-box abolishes the feeding-induced activation of the FAS promoter in transgenic mice. Furthermore, in vivo occupancy of the FAS promoter by SREBP in the fed state can be prevented by mutation not only of the −150 SRE but, unexpectedly, of the −65 E-box as well. We conclude that the FAS promoter is activated during refeeding via the induced binding of SREBP to the −150 SRE and that USF binding to the −65 E-box is also required for SREBP binding and activation of the FAS promoter.

Investigation of NADPH and acyl-binding sites on avian fatty acid synthase

Biochemistry ◽  
1982 ◽  
Vol 21 (12) ◽  
pp. 2863-2870 ◽  
Author(s):  
Jeffrey W. Cardon ◽  
Gordon G. Hammes
Keyword(s):  
Fatty Acid ◽  
Binding Sites ◽  
Fatty Acid Synthase

scholarly journals Transcriptional regulation of the human Sp1 gene promoter by the specificity protein (Sp) family members nuclear factor Y (NF-Y) and E2F

2003 ◽  
Vol 371 (2) ◽  
pp. 265-275 ◽  
Author(s):  
Marta NICOLÁS ◽  
Vèronique NOÉ ◽  
Carlos J. CIUDAD
Keyword(s):  
Binding Sites ◽  
Specific Binding ◽  
Gene Promoter ◽  
Minimal Promoter ◽  
Nuclear Factor ◽  
Nuclear Factor Y ◽  
Enhancer Binding Protein ◽  
Complex Regulation ◽  
E2f Transcription Factors ◽  
Specificity Protein

We analysed in detail the minimal promoter of transcription factor Sp1, which extends 217bp from the initiation of transcription. Within this sequence we identified putative binding sites for Sp1, nuclear factor Y (NF-Y), activator protein 2 ('AP-2'), CCAAT/enhancer-binding protein ('C/EBP') and E2F transcription factors. In one case, the boxes for Sp1 and NF-Y are overlapping. Gel-shift and supershift assays demonstrated specific binding of Sp1, Sp3 and NF-Y proteins. Transient transfections and luciferase assays revealed activation of the Sp1 minimal promoter upon overexpression of Sp1 itself, NF-Y and E2F. Whereas overexpression of NF-Y or E2F had an additive effect on Sp1 overexpression, the activation of Sp1 transcription due to Sp1 was counteracted by Sp3 overexpression. Mutagenesis analysis of the NFY/Sp1-overlapping box revealed that both factors compete for this box, and that when the NF-Y site of this overlapping box is specifically mutated there is an increase in Sp1 binding, thus increasing transcriptional activity. These results help to explain the complex regulation of the Sp1 gene, which depends on the relative amounts of Sp1, Sp3, E2F and NF-Y proteins in the cell.

scholarly journals Characterization of the human topoisomerase IIβ (TOP2B) promoter activity: essential roles of the nuclear factor-Y (NF-Y)- and specificity protein-1 (Sp1)-binding sites

2002 ◽  
Vol 368 (3) ◽  
pp. 741-751 ◽  
Author(s):  
Chun-Nam LOK ◽  
Alexander J. LANG ◽  
Shelagh E.L. MIRSKI ◽  
Susan P.C. COLE
Keyword(s):  
Binding Sites ◽  
Promoter Activity ◽  
Luciferase Reporter ◽  
Cancer Drug ◽  
Resting Cells ◽  
Nuclear Factor ◽  
Nuclear Factor Y ◽  
Specificity Protein 1 ◽  
Topo Ii ◽  
Specificity Protein

Eukaryotic topoisomerase II (topo II) catalyses topological genomic changes essential for chromosome segregation, chromatin reorganization, DNA replication and transcription. Mammalian topo II exists as two isoforms, designated α and β. Human topo IIα is an important cancer drug target, and an established determinant of drug sensitivity and resistance. Human topo IIβ is also the target of anticancer drugs but its role in drug resistance is less clear. The two human topo II proteins are encoded by the TOP2A and TOP2B genes, respectively, which despite their highly conserved structural organization, are subject to distinctly different modes of regulation. In the present study, we have cloned and characterized the human TOP2B promoter containing a 1.3kb fragment of the 5′-flanking and untranslated region (-1067 to +193). We found that the promoter activity of this TOP2B fragment was constant throughout the cell cycle, in contrast to the activity of the proximal promoter of TOP2A which was low in resting cells and enhanced during proliferation. Analyses of 5′-serially and internally deleted luciferase reporter constructs revealed that 80% of the TOP2B promoter activity could be attributed to the region between −533 and −481. Mutational analyses of putative regulatory elements indicated that two inverted CCAAT boxes (ICBs) within this region were essential for TOP2B promoter activity and gel mobility-shift assays indicated these sites bound the transcription factor nuclear factor-Y (NF-Y). Co-transfection experiments using a dominant-negative form of subunit A of NF-Y suggested that TOP2B promoter activity required direct interaction of NF-Y with the ICBs. In addition, a specificity protein-1 (Sp1)-binding GC box located just upstream of the ICBs was shown to contribute to TOP2B promoter activity in a synergistic manner with the ICBs. Our results suggest that the binding sites for NF-Y and Sp1 are critical for TOP2B transcription.

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