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- Senior Lecturer
- Metabolism & Experimental Therapeutics
- Div of Medicine
- Faculty of Medical Sciences
My work on the transcriptional regulation of gene expression by nuclear receptors started in the laboratory of Prof Bart Staels at the Pasteur Institute of Lille (France) as a recipient of a predoctoral Marie Curie grant. The primary goal of my research was to determine the molecular mechanisms governing the expression of the nuclear receptor peroxisome proliferator-activated receptor (PPAR) PPARalpha.
Subsequently, as a postdoctoral fellow in the laboratory of Dr Freedman at the Memorial Sloan-Kettering Cancer Center (USA), I determined the impact of the recruitment of the DRIP coactivator complex (identified in Dr. Freedman’s group) on the activity of the bile acid receptor FXR. In Dr Garabedian´s laboratory at the New York University School of Medicine (USA) I initiated and developed a novel research line aimed to uncover the role of phosphorylation on the lipid-activated nuclear receptor LXR alpha function in macrophages.
In 2008 I joined the Division of Medicine at UCl as a non-clinical Lecturer in the Centre for Clinical Pharmacology.
Nuclear receptors are ligand activated transcription factors with crucial and diverse roles in regulating developmental, reproductive, homeostatic, inflammatory, immune and metabolic processes. LXRs are nuclear receptors that act as metabolic sensors for cellular cholesterol, control the expression of key proteins in cholesterol and glucose homeostasis and possess anti-microbial and anti-inflammatory properties. Activation of LXRs increases circulating HDL levels, promotes cholesterol efflux and decreases progression of atherosclerosis in experimental models, which is why LXRs are considered promising drug development targets for the management of atherosclerosis. In light of the pivotal role of LXR in atherogenesis, elucidating the signaling pathways that regulate its activity is critical to our understanding of LXR function.
My group aims to better understand how genes are modulated by LXR in the context of atherosclerosis to help develop improved LXR ligands for the treatment of atherosclerosis and other vascular and inflammatory diseases. We are particularly interested in pathways regulated by LXR in a non-canonical fashion, e.g. by modulating post-translational modifications of the receptor or by triggering other signaling pathways. We are generating unique tools and experimental models to investigate whether changes observed in cultured cells are translated in vivo in a pathological context.
|2006||Cert.||Certificate||State University of New York at Stony Brook|
|2001||PhD||Doctor of Philosophy||Institut Pasteur|
|1995||BSc||Bachelor of Science||Universidad Complutense de Madrid|