Reference : PPARγ population shift produces disease-related changes in molecular networks associa... |
Scientific journals : Article | |||
Life sciences : Biochemistry, biophysics & molecular biology Human health sciences : Endocrinology, metabolism & nutrition Human health sciences : Cardiovascular & respiratory systems | |||
http://hdl.handle.net/10993/4559 | |||
PPARγ population shift produces disease-related changes in molecular networks associated with metabolic syndrome | |
English | |
Jurkowski, Wiktor [University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > >] | |
Roomp, Kirsten ![]() | |
Crespo, Isaac ![]() | |
Schneider, Jochen ![]() | |
del Sol Mesa, Antonio ![]() | |
2011 | |
Cell Death and Disease | |
Nature Publishing Group | |
2 | |
8 | |
e192 | |
Yes (verified by ORBilu) | |
International | |
2041-4889 | |
London | |
UK | |
[en] metabolic syndrome ; PPARγ ; protein population shift ; bi-stable switches ; disease-related networks | |
[en] Peroxisome proliferator-activated receptor gamma (PPARγ) is a key regulator of adipocyte differentiation and has an important role in metabolic syndrome. Phosphorylation of the receptor's ligand-binding domain at serine 273 has been shown to change the expression of a large number of genes implicated in obesity. The difference in gene expression seen when comparing wild-type phosphorylated with mutant non-phosphorylated PPARγ may have important consequences for the cellular molecular network, the state of which can be shifted from the healthy to a stable diseased state. We found that a group of differentially expressed genes are involved in bi-stable switches and form a core network, the state of which changes with disease progression. These findings support the idea that bi-stable switches may be a mechanism for locking the core gene network into a diseased state and for efficiently propagating perturbations to more distant regions of the network. A structural analysis of the PPARγ-RXRα dimer complex supports the hypothesis of a major structural change between the two states, and this may represent an important mechanism leading to the differential expression observed in the core network. | |
Luxembourg Centre for Systems Biomedicine (LCSB): Bioinformatics Core (R. Schneider Group) ; Luxembourg Centre for Systems Biomedicine (LCSB): Computational Biology (Del Sol Group) ; Luxembourg Centre for Systems Biomedicine (LCSB): Medical Translational Research (J. Schneider Group) | |
http://hdl.handle.net/10993/4559 | |
10.1038/cddis.2011.74 | |
e192 |
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