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Most relevant scientific articles
Research Groups
esteras n, alquéZar c, Bartolomé F, de la encar- nación a, BermeJo-PareJa F, molina Ja, martín-reque- ro a. G1/S Cell cycle checkpoint dysfunction in lympho- blasts from sporadic Parkinson’s disease patients. Mol Neurobiol. 2015; 52 (1): 386-98.
de la encarnación a, alquéZar c, martín-requero á. Increased Wnt signaling and reduced viability in a neu- ronal model of progranulin-deficient frontotemporal lobar degeneration. Mol Neurobiol. 2015 Dec 17. [Epub ahead of
alquéZar c, de la encarnación a, moreno F, lóPeZ de munain a, martín-requero a. Progranulin deficiency in- duces overactivation of WNT5A expression via TNF-α/ NF-κB pathway in peripheral cells from frontotemporal dementia-linked granulin mutation carriers. J Psychiatry Neurosci. 2015; 41 (1): 150131.
alquéZar c, esteras n, de la encarnación a, moreno F, lóPeZ de munain a, martín-requero a. Increasing progranulin levels and blockade of the ERK1/2 pathway:
print] PMID: 26676574.
de la encarnación a, alquéZar c, esteras n, martín-re- quero a. Progranulin deficiency reduces CDK4/6/pRb ac- tivation and survival of human neuroblastoma SH-SY5Y cells. Mol Neurobiol. 2015; 52 (3): 1714-25.
Highlights
RESULTS
• We have completed the phenotypic characteriza- tion of a mouse model with ablation of podocali- cina (Podxl) in the vascular endothelium, which represents an excellent tool for studying diseases involving increased vascular permeability, including systemic vasculitis (ORPHA52759). We are investi- gating the possibility that Podxl is an essential com- ponent of the glycocalyx in maintaining the integrity of the endothelial barrier.
• We continued to study the mechanisms that cause cell death in Alzheimer’s disease, frontotemporal de- mentia (FTLD-TDP), and other neurodegenerative disorders. The work focuses on cell cycle dysfunc- tion, apoptosis, mitochondrial impairment, oxida- tive damage, and protein degradation using in vivo models of neurodegeneration and in vitro culture of cells, including peripheral cells from patients. In par- ticular, we have evaluated the pathogenic influence of mutations on the GRN gene, leading to haploin-
upstream and downstream strategies for the treatment of progranulin deficient frontotemporal dementia. Eur Neu- ropsychopharmacol. 2015; 25 (3): 386-403.
sufficiency of the protein, in neurodegeneration as- sociated to FTLD-TDP. Our work allowed us to unveil an important role of the Wnt5a/ERK1/2CDK6/pRb cascade in FTLD-TDP pathogenesis. In addition, we have used lymphoblatoid cell lines from FTLD or Parkinson (PD) patients as a platform to test the therapeutic potential of certain drugs impacting this signaling cascade and/or the cell cycle.
PATENTS
Patent Application Ref # ES 1641.1194
Title of the invention: A new family of indazol car- bonyl derivatives with properties of cannabinoids and/or cholinergic and/or regulator of peptide be- ta-amyloid.
Inventors: JA Paez Prosper, NE Campillo Martin, C Perez Martin, PJ González Naranjo, M Perez Macias, M López de Ceballos, A Martin Requero, C Alquézar Burillo, MI Martin Fontelles, MR Garcia Moreno, EM Sánchez Robles, J Romero Paredes.
Institution: Agencia Estatal Consejo Superior de Investigaciones Científicas
Contact: Centro de Investigaciones Biológicas. Ramiro de Maeztu, 9. 28040 Madrid
Tel.: 91 837 31 12 ext 4221 · E.mail: [email protected]
Webs: https://www.cib.csic.es/es/grupo.php?idgrupo=58 https://www.cib.csic.es/es/grupo.php?idgrupo=57
CIBERER I Annual report 2015 I 107