Signaling and New Therapeutic Targets (SINDIATER)

 

 

 

Group Coordinator: - Dr. Jose Miguel Lizcano


LABORATORIES:

- Dr. Carlos Barcia

- Dr. Jose Ramón Bayascas

- Dr. Enrique Claro

- Dr. Esther Dalfó

- Dr. Roser Masgrau

- Dr. Jose Miguel Lizcano

- Dr. Víctor Yuste

 

Our group is interested in understanding the mechanisms that control cellular signaling, in order to propose new therapeutic targets to tackle degenerative diseases caused by an imbalance in the homeostatic process that rules cell proliferation and cell death. Specifically, we are interested in signaling processes that are altered in cancer (excess of cell proliferation) and neurodegenerative diseases (excess of cell death), since defects in cellular signaling lead to pathological states.

During the last years our Group has gained experience, know-how and technology to decipher alterations in cell signaling. Also, we have established collaborations with many leading academic laboratories in the field, both at national and international level. Furthermore, we are involved in the preclinical and clinical development of new therapeutic agents with anticancer activity, and we have stablished strong bonds with few Companies interested in the translational application of our research.

 

Active projects

 

- RTC-2017-6261; Nuevas estrategias para incrementar efectividad de los tratamientos con ABTL0812 (convocatoria Retos-Colaboración. Financiado por: FEDER/Ministerio de Ciencia, Innovación y Universidades–Agencia Estatal de Investigación)

 

- SAF2015-64237-R; Desarrollo de nuevas herramientas farmacológicas antitumorales que dirijan su acción al silenciamiento o a la inhibición de la MAP kinasa ERK5

 

- SAF2014-52813-R; Participacion de PDK1 en las respuestas a PI3K durante el desarrollo neuronal definida mediante el analisis de ratones knock-in de PDK1: implicacion en patologia mental

 

- SAF2015-64123-P; PRIMING MICROGLIAL EN AMBIENTES NEUROINFLAMATORIOS: MANIPULACION DE LA DINAMICA DE INTERACCION GLIAPTICA PARA CONTROLAR LA "FAGOPTOSIS" DE CELULAS DIANA

 

- PI15/01255; Mecanismos convergentes entre autofagia y función axonal e influencia metabòlica en la regulación de las enfermedades neurodegenerativas (Cofunded by European Union and Instituto de Salud Carlos III)

 

 

 

 

Featured publications

 

- Erazo T, Lorente M, López-Plana A, Muñoz-Guardiola P, Fernandez-Nogueira P, Bragado P, Fuster G, Salazar M, Espadaler J, Hernandez-Losa J, Bayascas JR, Cortal M, Vidal L, Gascon P, Alfón J, Velasco G, Domenech C, Lizcano JM. The new antitumor drug ABTL0812 inhibits Akt/mTORC1 axis by upregulating Tribbles-3 pseudokinase. Clinical Cancer Research. 22: 2508-19 (2016).

 

- Hasel P, Dando O, Jiwaji Z, Baxter P, Todd AC, Heron S, Márkus NM, McQueen J, Hampton DW, Torvell M, Tiwari SS, McKay S, Eraso-Pichot A, Zorzano A, Masgrau R, Galea E, Chandran S, Wyllie DJA, Simpson TI, Hardingham GE. Neurons and neuronal activity control gene expression in astrocytes to regulate their development and metabolism. Nature Communications, 8, 15132 (2017)

 

- Sánchez-Osuna M, Martínez-Escardó L, Granados-Colomina C, Martínez-Soler F, Pascual-Guiral S, Iglesias-Guimarais V, Velasco R, Plans G, Vidal N, Tortosa A, Barcia C, Bruna J, Yuste VJ. An intrinsic DFF40/CAD endonuclease deficiency impairs oligonucleosomal DNA hydrolysis during caspase-dependent cell death: a common trait in human glioblastoma cells. Neuro Oncology, 18: 950-61 (2016)

 

- Cordón-Barris L, Pascual-Guiral S, Yang S, Giménez-Llort L, Lope-Piedrafita S; Niemeyer C, Claro E, Lizcano JM, Bayascas JR. Mutation of the 3-phosphoinositide-dependent protein kinase-1 (PDK1) substrate-docking site in the developing brain causes microcephaly with abnormal brain morphogenesis independently of Akt, leading to impaired cognition and disruptive behaviors. Molecular and Cellular Biology, 36: 2967-82 (2016)

 

- Mitxitorena I, Saavedra E, Barcia C. Kupfer-type immunological synapses in vivo: Raison D'être of SMAC. Immunology and Cell Biology, 93:51-6 (2015)

 

 

Funding

 

 

Ref: SGR 2017-1780