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The making and breaking of ubiquitin chains in cholesterol metabolism

"Elevated levels of circulating LDL-cholesterol are a major determinant contributing to atherogenesis and coronary artery disease. Therefore, many studies address the central transcriptional pathways that regulate cholesterol meta... ver más

30/04/2019

Academisch Medisch...

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

Academisch Medisch Centrum AMC No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2019-04-30 No tenemos la información de la convocatoria

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1 Participantes

Academisch Medisch Centrum A...

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Líder del proyecto

Academisch Medisch Centrum AMC No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 2M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto "Elevated levels of circulating LDL-cholesterol are a major determinant contributing to atherogenesis and coronary artery disease. Therefore, many studies address the central transcriptional pathways that regulate cholesterol metabolism. However, transcriptional regulation does not allow cells to quickly adapt to the cholesterol fluxes that they encounter. For this, rapid and reversible post-transcriptional modifications are used, in conjunction with transcriptional control. Ubiquitylation - the post-transcriptional conjugation of ubiquitin to proteins – is studied in relation to many cellular processes. Much less is known about the contribution of the ubiquitin-proteasomal-system (UPS) to regulation of lipid metabolism and development of cardiovascular disease. I recently identified the E3-ubiquitin ligase IDOL as a novel post-transcriptional regulator of the LDLR pathway. My lab also recently identified two genes, the E3-ubiquitin ligase MARCH6 and the de-ubiquitylase USP2, for which no role in sterol metabolism was known, as important regulators of cellular cholesterol metabolism. With IDOL, these genes control key nodes of cholesterol synthesis and uptake and represent previously unrecognized mechanisms to control cholesterol homeostasis. To study the contribution of these genes to cholesterol metabolism, we will use state-of-the-art mutant mouse models, in vitro assays, and a unique collection of dyslipidemic patient material. Our goal is to characterize the contribution of these genes to cholesterol homeostasis and to examine their involvement in the development of dyslipidemia and atherosclerosis. Investigating these novel regulatory systems will provide important mechanistic insight into the contribution of the UPS to cholesterol metabolism in health and disease. As components of the UPS are amenable to pharmacological manipulation these studies could potentially lead to novel targets for treatment of hypercholesterolemia and coronary artery disease."

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