Cecilio Giménez Martín
Catedrático. Facultad de Ciencias
Universidad Autónoma de Madrid
María del Carmen Aragón Rueda
Catedrática. Facultad de Ciencias
Universidad Autónoma de Madrid
Esther Arribas González
Investigadora Predoctoral
Universidad Autónoma de Madrid
Ignacio Ibáñez Sainz-Pardo
Investigador Predoctoral
Universidad Autónoma de Madrid
Beatriz Fuensanta López Corcuera
Profesora Titular. Facultad de Ciencias
Universidad Autónoma de Madrid
Enrique Núñez Balbuena
Investigador Postdoctoral
Universidad Autónoma de Madrid
Eva María Porlan Alonso
Investigador Postdoctoral 
Universidad Autónoma de Madrid
Francisco Zafra Gómez
Catedrático. Facultad de Ciencias
Universidad Autónoma de Madrid
Strategic Objective
The group studies the physiological and pathological aspects of the glycine transporters (GlyTs) in the central nervous system as emerging drug targets in transmission mediated glycine dysfunctions as hyperekplexia or pain.
A) Identification, analysis and classification of mutations in the gene of GlyT2 (SLC6A5) in human patients with hyperekplexia.
B) Effects of mutations of hyperekplexia on the molecular structure, biogenesis and intracellular trafficking of GlyT2. Study of the interaction of inhibitors with GlyT2 (dockings on 3D models) for selecting regions that facilitate folding or activity of hyperekplexia mutants.
C) Study of the interactome of GlyT2 with proteins already known or new mutants of human hyperekplexia.
D) Development of alternative cellular models for the study of hyperekplexia mutants such as infection of primary neurons with lentiviral particles or the generation of induced pluripotent stem cells (iPSC) from patient samples.
• Regulation of GlyTs by receptors involved in pain signal processing in nociceptive pathways of the spinal cord.
Research Lines
• Regulatory mechanisms of neurotransmitters flow between neurons and glia in the nervous system under physiological conditions and in ischemia.
a) Regulation of intracellular trafficking of neurotransmitter transporter systems.
b) Regulation of the expression of transporters, channels and receptors in the CNS by micro RNAs.
• Molecular mechanisms of Dravet syndrome. Study of the intracellular trafficking and regulation of Nav1.1 sodium channel.
• Molecular mechanisms underlying neurogenesis and its regulation by diverse kinases.