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Dr Ines Pineda Torra
5 University St-The Rayne Building
British Heart Foundation Laboratories
London
WC1 EJJ
Tel: 020 7679 6535
Appointment
  • Senior Lecturer
  • Metabolism & Experi Therapeutics
  • Div of Medicine
  • Faculty of Medical Sciences
Biography
My research career to date has mainly focused on the knowledge of the different aspects of nuclear receptor function as transcriptional regulators involved in the control of lipid metabolism. As an undergraduate student with a EU ERASMUS Fellowship, I worked at the Center for Biomembranes and Lipid Enzymology at the University of Utrecht (The Netherlands) in the laboratory of Prof Van den Bosch to characterize the effect of aspirin on the regulation of IL-1ß-induced phospholipase A2.

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.
Research Summary

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.

Academic Background
2006 Cert. Certificate – Bioscience State University of New York at Stony Brook
2001 PhD Doctor of Philosophy – Pharmaceutical Sciences Institut Pasteur
1996 MAST Master – Biochemistry Universiteit Utrecht
1995 BSc Bachelor of Science – Chemistry and Biochemistry Universidad Complutense de Madrid
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