José Manuel Lopez Blanco

José Manuel  Lopez Blanco

     

 

José Manuel Lopez Blanco

Academic Staff

Phone:
+34 935 814 278

Email:
josemanuel.lopez@uab.cat

Adress:

Department of Biochemistry and Molecular Biology
Institut de Neurociències
Faculty  of Medicine (room M2-117)
Universitat Autònoma de Barcelona (UAB)
Bellaterra Campus 08193-Cerdanyola del Vallés

Area

Thesis number in address


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.

Dr. López has his own laboratory, included in the  Laboratory of Molecular Neuropharmacology and Bioinformatics research group.
 
 
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.
  • Yue J, López JM. JNK does not regulate meiotic progression in Xenopus oocytes: The strange case of pJNK and pERK. Dev Biol. 416: 42-51, 2016.
  • Yue J, Ben Messaoud N, López JM. Hyperosmotic Shock Engages Two Positive Feedback Loops through Caspase-3-dependent Proteolysis of JNK1-2 and Bid. J Biol Chem. 290: 30375-89, 2015.
  • Ben Messaoud N, Katzarova I, López JM. Basic Properties of the p38 Signaling Pathway in Response to Hyperosmotic Shock. PLoS One. doi: 10.1371/journal.pone.0135249, 2015.
  • Ben Messaoud N, Yue J, Valent D, Katzarova I, López JM. Osmostress-induced apoptosis in Xenopus oocytes: role of stress protein kinases, calpains and Smac/DIABLO. PLoS One. doi: 10.1371/journal.pone.0124482, 2015.
  • López JM.Digital kinases: A cell model for sensing, integrating and making choices. Communicative & Integrative Biology. 3: 146-150, 2010.
  • Martiáñez T, Francès S, López JM. Generation of digital responses in stress sensors.  Journal of Biological Chemistry. 284: 23902-23911, 2009.
  • Piqué M, López JM, Sylvain F, Guigó R, Méndez R. A combinatorial code for CPE-mediated translational control. Cell. 132: 434-448, 2008.
  • Iglesias-Serret D, Piqué M, Gil J, Pons G, López JM.Transcriptional and translational control of Mcl-1 during apoptosis.Archives of Biochemistry and Biophysics. 417: 141-152, 2003.
  • López JM*, Campàs C*, Barragán M, Bellosillo B, Colomer D, Gil J.Acadesine activates AMPK and induces apoptosis in B-cell chronic lymphocytic leukemia cells but not in T lymphocytes.Blood. 101: 3674-3680, 2003.*Both should be considered as first author.
  • López JM, Santidrian AF, Campàs C, Gil J.5-Aminoimidazole-4-carboxamide riboside induces apoptosis in Jurkat cells, but the AMP-activated protein kinase is not involved.Biochemical Journal.370: 1027-1032, 2003.
  • López JM, Bombi JA, Valderrama R, Giménez A, Parés A, Caballería J, Imperial S, Navarro S. Effects of prolonged ethanol intake and malnutrition on rat pancreas.Gut. 38: 285-292, 1996.
  • López JM, Bennett MK, Sanchez HB, Rosenfeld JM, Osborne TF. Sterol regulation of acetyl CoA carboxylase provides a mechanism for coordinate control of cellular lipid. Proceedings of the National Academy of Sciences of the United States of America. 93: 1049-1053, 1996.
  • López JM*, Bennett MK*, Sanchez HB, Osborne TF. Sterol regulation of fatty acid synthase promoter: coordinate feedback regulation of two mayor lipid pathways. Journal of Biological Chemistry. 270: 25578-25583, 1995. *Both should be considered as first author.

 

See all Jose Manuel Lopez Blanco publications at PubMed.

Institut de Neurociències
Tel: 93 581 3861 / Fax: +34 93 581 3327

Facultat de Medicina. Edifici M-1
Avinguda de Can Domènech - Campus de la UAB · 08193
Bellaterra (Cerdanyola del Vallès) · Barcelona