Control presináptico por receptores acoplados a proteínas G, GPCRs, en un ratón modelo del síndrome X frágil

  1. Garcia Font, Nuria
Supervised by:
  1. José Sánchez-Prieto Borja Director
  2. María Jesús Oset Gasque Director

Defence university: Universidad Complutense de Madrid

Fecha de defensa: 21 November 2019

Committee:
  1. Miguel Díaz Hernández Chair
  2. Jesús Miguel Pradillo Justo Secretary
  3. José María Solís Torralba Committee member
  4. David Bartolomé Martín Committee member
  5. Gertrudis Perea Parrilla Committee member
Department:
  1. Bioquímica y Biología Molecular

Type: Thesis

Teseo: 151722 DIALNET lock_openDocta Complutense editor

Abstract

Fragile X syndrome (FXS) is the most common inherited intellectual disability and it is associated with multiple behavioral alterations, including cognitive deficits, hyperactivity, anxiety and deficits in social behavior. In FXS, the Fmr1 gene that encodes the fragile mental retardation protein (FMRP) is silenced. FMRP modulates gene expression through changes in the stability and transport of its mRNA targets. When FMRP is absent the expression of many postsynaptic proteins is altered as well as postsynaptic long-term forms of plasticity. FMRP is also found in axons and presynaptic nerve terminals and mRNA targets encoding for presynaptic proteins were identified...