Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

    We have a manual that explains all the features 

Record number 530930
Title Profiling of promoter occupancy by PPARα in human hepatoma cells via ChIP-chip analysis
Author(s) Meer, D.L.M. van der; Degenhardt, Tatjana; Väisänen, Sami; Groot, Philip de; Heinäniemi, Merja; Vries, Sacco de; Muller, Michael; Carlberg, Carsten; Kersten, Sander
Department(s) Biochemistry
Human Nutrition (HNE)
Publication type Dataset
Publication year 2010
Keyword(s) GSE25547 - Homo sapiens - PRJNA134025
Abstract The transcription factor Peroxisome Proliferator-Activated Receptor α (PPARα) is an important regulator of hepatic lipid metabolism. While PPARα is known to activate transcription of numerous genes, no comprehensive picture of PPARα binding to endogenous genes has yet been reported. To fill this gap, we performed ChIP-chip in combination with transcriptional profiling on HepG2 human hepatoma cells treated with the PPARα agonist GW7647. We found that GW7647 increased PPARα binding to 4220 binding regions. GW7647-induced binding regions showed a bias around the transcription start site and most contained a predicted PPAR binding motif. Several genes known to be regulated by PPARα, such as ACOX1, SULT2A1, ACADL, CD36, IGFBP1 and G0S2, showed GW7647-induced PPARα binding to their promoter. A GW7647-induced PPARα-binding region was also assigned to SREBP-targets HMGCS1, HMGCR, FDFT1, SC4MOL, and LPIN1, expression of which was induced by GW7647, suggesting cross-talk between PPARα and SREBP signaling. Our data furthermore demonstrate interaction between PPARα and STAT transcription factors in PPARα-mediated transcriptional repression, and suggest interaction between PPARα and TBP and C/EBPα in PPARα-mediated transcriptional activation. Overall, our analysis leads to important new insights into the mechanisms and impact of transcriptional regulation by PPARα in human liver and highlight the importance of cross-talk with other transcription factors.
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