José M. López obtained his PhD in Biological Sciences in1994 at Hospital Clinic i Provincial de Barcelona, Facultat de Medicina, Universitat de Barcelona. Then, he was a Postdoctoral Research Associate at University of California, Irvine, USA, in the laboratory of Dr. Timothy F. Osborne, working in the transcriptional control of cholesterol and fatty acid biosynthesis. Coming back to Spain he worked as Postdoctoral Research Associate at Departament de Ciències Fisiològiques Humanes i de la Nutrició, Universitat de Barcelona, in the laboratory of Dr. Diego Haro; as Associate Professor at Departament de Ciències Fisiològiques II, Universitat de Barcelona in the laboratory of Dr. Joan Gil investigating cell death mechanisms for the treatment of Chronic Lymphocytic Leukemia; and as Postdoctoral Researcher Associate at Centro de Regulación Genómica (CRG), in the laboratory of Raúl Mendez, where he studied the mechanisms of translational control mediated by cytoplasmic polyadenylation. In 2004, he obtained a “Ramón y Cajal” contract at Institut de Neurociències, Universitat Autònoma de Barcelona, as a Group Leader. From 2011 he is Assistant Professor at Departament de Bioquímica i Biología Molecular, Universitat Autònoma de Barcelona, where he is teaching in the Medicine and Physiotherapy Degrees.
RESEARCH INTERESTS
The overall objective of his group is to understand the mechanisms that regulate osmostress-induced apoptosis. They have reported that calpains and stress protein kinases regulate hyperosmotic shock-induced apoptosis, using Xenopus oocytes as a cell model. Now, they are investigating the role of different JNK and p38 isoforms in the regulation of osmostress-induced apoptosis. In addition, we have characterized Xenopus AMPK, a central regulator of cell metabolism, to study its role in apoptosis and meiosis.
MAIN RESEARCH LINES
1) To study the function of stress protein kinases in cell death and meiosis
The aim of this project is to determine the role of the stress protein kinases AMPK, JNK and p38 during oocyte death induced by osmotic shock and during meiotic progression induced by progesterone. They will study in detail the regulation of citochrome c release and caspase activation by these protein kinases. They will also investigate the role of AMPK and JNK in translational control during meiotic progression. We use as a model system Xenopus oocytes, which have great advantages for biochemical manipulation.
2) To study the role of ZMP accumulation and AMPK activation on the development of Lesch-Nyhan disease
Lesch-Nyhan disease is an illness with severe neurological effects as a consequence of a deficiency in the purine savage enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT). How a simple alteration in the purine metabolism produces dramatic effects in human behaviour is still a mystery. HPRT deficiency is associated with a relatively selective dysfunction of brain dopamine systems. Different hypotheses have been suggested, some of them claiming for the accumulation of a toxic metabolite in the brain. They propose that ZMP is the toxic agent, and acting by a pleiotropic effect would induce several changes in the cell, accounting for brain dysfunction. One of the initial changes would be the activation of the stress sensor AMP-activated protein kinase (AMPK).
PATENTS
López JM, Campas C, Gil J.Novel therapeutic use of riboside of 5-aminoimidazole-4-carboxamide (acadesine).ES03/00130, WO 03/080076 A1, Universidad de Barcelona.
Date: 21-3-2002.
