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Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:Carlos
Last Name:Villalobos
Title:Associate Professor
Advanced Degrees:PhD
Affiliation:IBGM, University of Valladolid and Spanish Research Council (CSIC)
Department:Cell and Molecular Physiology
Street Address 1:IBGM, c/ Sanz y Forés s/n
City:Valladolid
Zip/Postal Code:47003
Country/Territory:Spain
Phone:+34 983 184821
Fax:+34 983 184800
Email Address: 
Disclosure:
(view policy) 
Member reports no financial or other potential conflicts of interest. [Last Modified: 6 August 2008]
View all comments by Carlos Villalobos
Research Focus:
Microscopy, Apoptosis/Cell cycle, Electrophysiology, A-beta PP/A-beta, Molecular and Cell biology, Oxidative Stress, calcium signalling
Work Sector(s):
Research institute
Web Sites:
Professional: http://www.ibgm.med.uva.es
Lab: http://www.ucan-ibgm.com
Researcher Bio
Carlos Villalobos got his PhD in Cell Physiology in 1994 by the Valladolid University School of Medicine. He did postdoctoral training at the Medical University of South Carolina, in Charleston, SC from 1996 to 1999. After obtaining a Ramon y Cajal position in 2001, Dr. Villalobos obtained a permanent position in 2005 as Associate Professor at the Instituto de Biología y Genética Molecular (IBGM) in Valladolid, Spain, a joint research institute by the University of Valladolid and the Spanish Research Council (CSIC).

Carlos Villalobos research interests are calcium signaling in excitable and non-excitable cells and is now interested in subcellular calcium homeostasis and the role of mitochondria in cancer cell proliferation and neuron cell death in Alzheimer disease.
Top Papers
Valero RA, Senovilla L, Núñez L, Villalobos C (2008) The role of mitochondrial potential in control of calcium signals involved in cell proliferation. Cell Calcium (en prensa; PMID: 18241916).

Sanz-Blasco S, Valero RA, Rodríguez-Crespo I, Villalobos C*, Núñez L (2008) Mitochondrial Ca2+ overload underlies Aβ oligomers neurotoxicity providing an unexpected mechanism of neuroprotection by NSAIDs. PLoS ONE 3(7): e2718 doi:10.1371/journal.pone.0002718. *corresponding author.

Núñez L, Valero RA, Senovilla L, Sanz-Blasco S, García-Sancho J, Villalobos C (2006) Cell proliferation depends on mitochondrial Ca2+ uptake: inhibition by salicylate. J Physiol 571, 57-73.

Senovilla L, García-Sancho J, Villalobos C (2005) Changes in expression of hypothalamic releasing hormone receptors in individual rat anterior pituitary cells during maturation, puberty and senescence. Endocrinology 146, 4627-4634.

Senovilla L, Núñez L, de Campos JM, de Luis DA, Romero E, Sánchez A, García-Sancho J, Villalobos C (2004) Multifunctional cells in human pituitary adenomas: implications for paradoxical secretion and tumorigenesis. J Clin Endocrinol Metab 89, 4545-4552.

Villalobos C, Núñez L, Senovilla L, García-Sancho J. (2003) Multifunctional cells of mouse anterior pituitary reveal a striking sexual dimorphism. J Physiol 549, 835-843.

Villalobos C, Núñez L, Montero M, García AG, Alonso MT, Chamero P, Alvarez J, García-Sancho J (2002) Redistribution of Ca2+ among cytosol and organella during stimulation of bovine chromaffin cells. FASEB J 16, 343-353.

Villalobos C, Núñez L, Chamero P, Alonso MT, García-Sancho J (2001) Mitochondrial [Ca2+] oscillations driven by local high-[Ca2+] domains generated by spontaneous electric activity. J Biol Chem 276, 40293-40297.

Villalobos C, Faught WJ, Frawley LS (1999) Dynamics of stimulus-expression coupling as revealed by monitoring of PRL-promoter-driven reporter activity in individual, living mammotropes. Mol Endocrinol 13, 1718-1727.

Villalobos C, Núñez L, Frawley LS, García-Sancho J, Sánchez A (1997) Multi-responsiveness of single anterior pituitary cells to hypothalamic releasing hormones: a cellular basis for paradoxical secretion. Proc Natl Acad Sci USA 94, 14132-14137.
What is the greatest void to date in our knowledge of Alzheimer's Disease?
Probably how to quantify dementia properly in clinical trials

When and how exactly disease starts

the physiological roles of APP and amyloid beta proteins

What are the top three papers (not yours) you have read recently?
Cheung KH, Shineman D, Müller M, Cárdenas C, Mei L,
Mechanism of Ca2+ disruption in Alzheimer's disease by presenilin regulation of InsP3 receptor channel gating.Neuron. 2008 Jun 26;58(6):871-83.


Nelson O, Tu H, Lei T, Bentahir M, de Strooper B, Bezprozvanny I. Familial Alzheimer disease-linked mutations specifically disrupt Ca2+ leak function of presenilin 1. J Clin Invest. 2007 May;117(5):1230-9. Epub 2007 Apr 12.

De Felice FG, Velasco PT, Lambert MP, Viola K, Fernandez SJ, Ferreira ST, Klein WL. Abeta oligomers induce neuronal oxidative stress through an N-methyl-D-aspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine. J Biol Chem. 2007 Apr 13;282(15):11590-601. Epub 2007 Feb 16.
If resources were not limited, what research projects would you pursue?
In vivo subcellular calcium homeostasis in Alzheimer´s disease

Cloning of the mitochondrial calcium uniporter as candidate target for preventing neurodegeneration
What is your leading hypothesis?
Mitochondrial calcium plays a pivotal role in neuron cell death in alzheimer´s disease. NSAIDs might protect against amyloid beta and Alzheimer acting as mitochondrial calcium antagonists (Sanz-Blasco et al Plos One 2008).
What piece of missing evidence would help prove it?
In vivo experiments.

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