TEAM LEADER

   
   
Deborah J. Burks
TEL: +34 963289681 Ext. 2206
FAX: +34 963289701

EQUIPO INVESTIGACIÓN
Estudiante
Sara Jorda Climent


Investigador
Mª Amparo Galan Albiñana

Luke Noon


Investigadores Postdoctorales
Carlos Acosta Umanzor


Investigadores Predoctorales
Fatima Manzano Nuñez


Técnico de laboratorio
Arantxa Leal Tassias

Neuroendocrinología Molecular


The incidence of diabetes and obesity is increasing at alarming rates throughout the world, creating a significant social and economic burden in industrialised countries. Defective expression or function of insulin signaling pathway components causes insulin resistance, which occurs with normal ageing but is also a hallmark of disease states such as diabetes. The overall aim of our research is to understand precisely how impaired insulin signaling contributes to metabolic diseases. Throughout the lifetime of an individual, stem cells represent a mechanism for the maintenance and regeneration of tissues. The ability of stem cells to contribute to these processes depends on both the generation of new stem cells (self-renewal) as well as specialized cell types (differentiation). However, the effects of insulin resistance and metabolic disease on stem function are not known at present. Thus, one specific goal of our laboratory is to identify the molecular mechanisms by which insulin signaling modulates the proliferation and differentiation of progenitor cells of the adipose, pancreatic/hepatic, and neuronal lineages.Another line of research is related with the role of cancer stem cells in the origin and progression of lung cancer. Thus, the results of the current project will impact both basic research related with stem cell biology and clinical investigation of metabolic disorders and cancer. Given that it seeks to identify the molecular basis of obesity and diabetes, the project has great potential for promoting the development of new and innovative strategies for the detection, treatment and prevention of metabolic disorders including lifestyle changes or drugs that promote IRS-2 expression or signaling.

Publicaciones Seleccionadas


IRS-2 Deficiency impairs NMDA receptor-dependent long-term potentiation.
Martín ED, Sánchez-Perez A, Trejo JL, Martin-Aldana JA, Cano Jaimez M, Pons S, Acosta Umanzor C, Menes L, White MF, Burks DJ
Cerebral cortex (New York, N.Y. : 1991) , 2012 Aug, vol. 22, pag. 1717-27, Impact Factor: 6.828
Development of a human extracellular matrix for applications related with stem cells and tissue engineering.
Escobedo-Lucea C, Ayuso-Sacido A, Xiong C, Prado-López S, del Pino MS, Melguizo D, Bellver-Estellés C, Gonzalez-Granero S, Valero ML, Moreno R, Burks DJ, Stojkovic M
Stem cell reviews , 2012 Mar, vol. 8, pag. 170-83, Impact Factor: 4.523
A central role for the ERK-signaling pathway in controlling Schwann cell plasticity and peripheral nerve regeneration in vivo.
Napoli I, Noon LA, Ribeiro S, Kerai AP, Parrinello S, Rosenberg LH, Collins MJ, Harrisingh MC, White IJ, Woodhoo A, Lloyd AC
Neuron , 2012 Feb 23, vol. 73, pag. 729-42, Impact Factor: 15.766
Differential sensitivity to adrenergic stimulation underlies the sexual dimorphism in the development of diabetes caused by Irs-2 deficiency.
Garcia-Barrado MJ, Iglesias-Osma MC, Moreno-Viedma V, Pastor Mansilla MF, Gonzalez SS, Carretero J, Moratinos J, Burks DJ
Biochemical pharmacology , 2011 Jan 15, vol. 81, pag. 279-88, Impact Factor: 4.705
IRS-2 pathways integrate female reproduction and energy homeostasis.
Burks DJ, Font de Mora J, Schubert M, Withers DJ, Myers MG, Towery HH, Altamuro SL, Flint CL, White MF
Nature , 2000 Sep 21, vol. 407, pag. 377-82

Factores de Crecimiento Metabólico y Medicina Regenerativa