Examinando por Autor "Urrutia, Daniela"

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  • Miniatura
    Ítem
    Aplicación de un programa de estimulación para la succión nutritiva en neonatos RNPT
    (Universidad Andrés Bello, 2010) Espinoza, Natalia; Guzmán, Francisca; Pérez, Pamela; Urrutia, Daniela; Vargas, Carolina; Vivanco, Zulema; López Bravo, Ilse; Facultad de Ciencias de la Rehabilitación; Escuela de Fonoaudiología
    El presente Seminario, que lleva por titulo "Aplicación de un programa de estimulación para la succión nutritiva en neonatos RNPT" pretende describir e indagar la factibilidad que, tras aplicar el programa de estimulación de la succión nutritiva, se producirían factores positivos los que serán determinantes para lograr un correcto proceso de succión por parte del bebé, ya que la estimulación de la succión nutritiva y no- nutritiva incidiría en la mejoría de la eficiencia de los procesos de succión-deglución-respiración.
  • Miniatura
    Ítem
    c-Abl Tyrosine Kinase Is Required for BDNF-Induced Dendritic Branching and Growth
    (2023-02) Chandía-Cristi, América; Stuardo, Nicolás; Trejos, Cristian; Leal, Nancy; Urrutia, Daniela; Bronfman, Francisca C.; Álvarez Rojas, Alejandra
    Brain-derived neurotrophic factor (BDNF) induces activation of the TrkB receptor and several downstream pathways (MAPK, PI3K, PLC-γ), leading to neuronal survival, growth, and plasticity. It has been well established that TrkB signaling regulation is required for neurite formation and dendritic arborization, but the specific mechanism is not fully understood. The non-receptor tyrosine kinase c-Abl is a possible candidate regulator of this process, as it has been implicated in tyrosine kinase receptors’ signaling and trafficking, as well as regulation of neuronal morphogenesis. To assess the role of c-Abl in BDNF-induced dendritic arborization, wild-type and c-Abl-KO neurons were stimulated with BDNF, and diverse strategies were employed to probe the function of c-Abl, including the use of pharmacological inhibitors, an allosteric c-Abl activator, and shRNA to downregulates c-Abl expression. Surprisingly, BDNF promoted c-Abl activation and interaction with TrkB receptors. Furthermore, pharmacological c-Abl inhibition and genetic ablation abolished BDNF-induced dendritic arborization and increased the availability of TrkB in the cell membrane. Interestingly, inhibition or genetic ablation of c-Abl had no effect on the classic TrkB downstream pathways. Together, our results suggest that BDNF/TrkB-dependent c-Abl activation is a novel and essential mechanism in TrkB signaling.