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Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:Soraya
Last Name:Valles
Title:Assistant Profesor
Advanced Degrees:Ph D.
Affiliation:Faccultad de medicina
Department:Physiology
Street Address 1:Blasco Ibañez 17
City:Valencia
State/Province:Valencia
Zip/Postal Code:46010
Country/Territory:Spain
Phone:0034963983813
Fax:0034963864642
Email Address: 
Disclosure:
(view policy) 
Member reports no financial or other potential conflicts of interest. [Last Modified: 30 December 2011]
View all comments by Soraya Valles
Clinical Interests:
Alzheimer Disease, Polyglutamine Disorders (Huntington's, etc.), Aging Process, Parkinson Disease, Neurodevelopmental Disorders (Down syndrome, etc.), Neuromuscular Disorders (ALS, etc.)
Research Focus:
Neurobiology, Neuroimmunology, Animal Models, Neurotransmission, Genetics, Signal transduction, Tau/Cytoskeleton, Microscopy, DNA microarrays, Molecular and Cell biology, Neuropathology, Oxidative Stress, Stem cells, Apoptosis/Cell cycle, Drug screening, A-beta PP/A-beta, inflammation
Work Sector(s):
Medical hospital, University
Web Sites:
Personal: www.uv.es/lilian.valles/
Professional: www.uv.es
Lab: www.uv.es
Top Papers
1.-Vallés, S., Pitarch, J., Renau-Piqueras, J. and Guerri, C. Ethanol exposure affects GFAP gene expression and transcription during rat brain development. J. Neurochem. 69: 2484-2493 (1997).

2.-Vallés, S., Christina Tsoi, Franco Carlotti, Wen-Yan Huang, David Wyllie, Janet Askari, Martin J. Humphries, Steven K. Dower, and Eva E. Qwarnstrom. Recruitment of a heparan sulphate subunit to the IL-1 receptor complex: Regulation by fibronectin attachment. Journal Biological Chemistry 274: 20103-20109 (1999) .

3.-Huang WY, Valles S, Qwarnstrom EE. Translocation of the IL-1 receptor to focal adhesions is regulated through the c-terminal end of the cytoplasmic domain. Cell Biol Int. 25(4): 309-317 (2001).

4.-Soraya Valles, Christopher J. Caunt, Michelle H. Walker, and Eva E. Qwarnstrom. PDGF Enhancement of IL-1 Receptor levels in Smooth Muscle Cells involves induction of an Attachment-Regulated, Heparan Sulfate Binding Site (IL-1RIII). Lab Invest. 2002 82: 855-862.

5.-Guasch R, Tomás M, Miñambres R, Vallés S, Renau-Piqueras J, Guerri C. RhoA and lysophosphatidic acid are involved in the actin cytoskeleton reorganization of astrocytes exposed to ethanol. J. Neurosci. Res. 72: 487-502 (2003).

6.-Vallés SL, Blanco AM, Azorin I, Guasch R, Pascual M, Gomez-Lechón MJ, Renau-Piqueras J and Guerri C. Chronic ethanol consumption enhances IL-1-mediated signal transduction in rat liver and in cultured hepatocytes. Alcohol Clin Exp Res. 27: 1979-1986 (2003)

7.-Pascual M, Valles SL, Renau-Piqueras J and Guerri C. (2003) Ceramide pathways modulate ethanol-induced cell death in astrocytes. J. Neurochemistry. 87: 1535-1545.

8.-Blanco AM, Pascual M, Valles SL and Guerri C. Ethanol-induced iNOS and COX-2 expression in cultured astrocyte via NFkB. Neuroreport. 15: 681-685.2004

9.-Vallés SL, Blanco AM, Pascual M and Guerri C. Chronic ethanol treatment enhances inflammatory mediators and cell death in the brain and in astrocytes. Brain Pathology. 14: 365-371. 2004.

10.-Blanco AM, Vallés SL, Pascual M and Guerra C. Etanol treatment enhances inflammatory mediators and cell death in astrocytes in culture. Journal of Immunology. 2005.

11.- Valles SL, et al., Aging Cell 2008
12.- Valles SL. et al., Brain research. 2010
What is the greatest void to date in our knowledge of Alzheimer's Disease?
Inflammation and oxidative stress in neurodegeneration.
What are the top three papers (not yours) you have read recently?
-Oncogenic Ras, but not V600EB-RAF, protects from cholesterol depletion-induced
apoptosis through the PI3K/AKT pathway in colorectal cancer cells.Laura Calleros et al., 2009
- Xu et al., 2009
- Mantel and Broxmeyerm,2008
- Chung et al., 2010
- Lee and Wey., 2009 and 2011
If resources were not limited, what research projects would you pursue?
brain dissease
Parkinson's disease
CNS DISEASES
Astrocytes and neurons in culture
Stem cells and production of astrocytes or neurons from adult cells
What is your leading hypothesis?
Something (toxic, virus, oxigen privation, etc)affects the neuronal cells (including astrocytes, radial glia, neurons, microglia, oligodendroglia)and cells produce beta-amiloid as a defence and to try to kill affected cells. Cell inside brain death by oxidative stress and inflammation by apoptosis or necrosis. Perhaps apnea sleep or vascular dementia decrease oxigen in brain and it produce increase amyloid in brain and increase Alzheimer's disease.
What piece of missing evidence would help prove it?
Perhaps we need to look for a relationship between alzheimer people and oxigen deprivation in brain. Perhaps if we know what kind of things produce beta-amiloid plaques we can attack Alzheimer dissease.
What is your fallback position?
My possition in University of Valencia: Associate professor and chief laboratory.

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