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Cyclin-dependent kinase 5, a node protein in diminished tauopathy: a systems biology approach.
Castro-Alvarez, John F; Uribe-Arias, S Alejandro; Mejía-Raigosa, Daniel; Cardona-Gómez, Gloria P.
Afiliação
  • Castro-Alvarez JF; Neuroscience Group of Antioquia, Cellular and Molecular Neurobiology Area, Faculty of Medicine, University of Antioquia, Sede de Investigación Universitaria Medellin, Colombia.
  • Uribe-Arias SA; Neuroscience Group of Antioquia, Cellular and Molecular Neurobiology Area, Faculty of Medicine, University of Antioquia, Sede de Investigación Universitaria Medellin, Colombia.
  • Mejía-Raigosa D; Group of Biophysics, Faculty of Exact and Natural Sciences, Institute of Physics, University of Antioquia Medellin, Colombia.
  • Cardona-Gómez GP; Neuroscience Group of Antioquia, Cellular and Molecular Neurobiology Area, Faculty of Medicine, University of Antioquia, Sede de Investigación Universitaria Medellin, Colombia.
Front Aging Neurosci ; 6: 232, 2014.
Article em En | MEDLINE | ID: mdl-25225483
Alzheimer's disease (AD) is the most common cause of dementia worldwide. One of the main pathological changes that occurs in AD is the intracellular accumulation of hyperphosphorylated Tau protein in neurons. Cyclin-dependent kinase 5 (CDK5) is one of the major kinases involved in Tau phosphorylation, directly phosphorylating various residues and simultaneously regulating various substrates such as kinases and phosphatases that influence Tau phosphorylation in a synergistic and antagonistic way. It remains unknown how the interaction between CDK5 and its substrates promotes Tau phosphorylation, and systemic approaches are needed that allow an analysis of all the proteins involved. In this review, the role of the CDK5 signaling pathway in Tau hyperphosphorylation is described, an in silico model of the CDK5 signaling pathway is presented. The relationship among these theoretical and computational models shows that the regulation of Tau phosphorylation by PP2A and glycogen synthase kinase 3ß (GSK3ß) is essential under basal conditions and also describes the leading role of CDK5 under excitotoxic conditions, where silencing of CDK5 can generate changes in these enzymes to reverse a pathological condition that simulates AD.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Front Aging Neurosci Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Colômbia País de publicação: Suíça
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Front Aging Neurosci Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Colômbia País de publicação: Suíça