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Isabelle Gerin

Researcher at Université catholique de Louvain

Publications -  38
Citations -  5484

Isabelle Gerin is an academic researcher from Université catholique de Louvain. The author has contributed to research in topics: Adipogenesis & Wnt signaling pathway. The author has an hindex of 30, co-authored 37 publications receiving 5105 citations. Previous affiliations of Isabelle Gerin include Catholic University of Leuven & University of Michigan.

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p53-Mediated Activation of miRNA34 Candidate Tumor-Suppressor Genes

TL;DR: The data suggest the miRNA34s might be key effectors of p53 tumor-suppressor function, and their inactivation might contribute to certain cancers.
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The glucose-6-phosphatase system.

TL;DR: Findings support the model initially proposed by Arion, according to which G6Pase was thought to be a rather unspecific phosphatase, with its catalytic site oriented towards the lumen of the endoplasmic reticulum, and substrate provided by a translocase specific for glucose 6-phosphate.
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Wnt Signaling Stimulates Osteoblastogenesis of Mesenchymal Precursors by Suppressing CCAAT/Enhancer-binding Protein α and Peroxisome Proliferator-activated Receptor γ

TL;DR: It is demonstrated that transient activation of Wnt/β-catenin signaling rapidly suppresses C/EBPα and PPARγ, followed by activation of osteoblastogenic transcription factors, suggesting that Wnt signaling alters the fate of mesenchymal precursor cells primarily by suppressing C/Wntα andPPARγ.
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Wnt10b inhibits development of white and brown adipose tissues.

TL;DR: Inhibition by Wnt10b of white and brown adipose tissue development results in lean mice without lipodystrophic diabetes.
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Expression of miR-33 from an SREBP2 Intron Inhibits Cholesterol Export and Fatty Acid Oxidation,

TL;DR: Evidence is provided that the primary transcript of SREBP2 contains an intronic miRNA that reduces cellular cholesterol export via inhibition of translation of the cholesterol export pump ABCA1 and also inhibits translation of several transcripts involved in fatty acid β-oxidation, thereby reducing fatty acid degradation.