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Glycolysis upregulation is neuroprotective as a compensatory mechanism in ALS.
Manzo, Ernesto; Lorenzini, Ileana; Barrameda, Dianne; O'Conner, Abigail G; Barrows, Jordan M; Starr, Alexander; Kovalik, Tina; Rabichow, Benjamin E; Lehmkuhl, Erik M; Shreiner, Dakotah D; Joardar, Archi; Liévens, Jean-Charles; Bowser, Robert; Sattler, Rita; Zarnescu, Daniela C.
Afiliación
  • Manzo E; Department of Molecular and Cellular Biology, University of Arizona, Tucson, United States.
  • Lorenzini I; Department of Neurology, Barrow Neurological Institute, Phoenix, United States.
  • Barrameda D; Department of Molecular and Cellular Biology, University of Arizona, Tucson, United States.
  • O'Conner AG; Department of Molecular and Cellular Biology, University of Arizona, Tucson, United States.
  • Barrows JM; Department of Molecular and Cellular Biology, University of Arizona, Tucson, United States.
  • Starr A; Department of Neurology, Barrow Neurological Institute, Phoenix, United States.
  • Kovalik T; Department of Neurology, Barrow Neurological Institute, Phoenix, United States.
  • Rabichow BE; Department of Neurology, Barrow Neurological Institute, Phoenix, United States.
  • Lehmkuhl EM; Department of Molecular and Cellular Biology, University of Arizona, Tucson, United States.
  • Shreiner DD; Department of Molecular and Cellular Biology, University of Arizona, Tucson, United States.
  • Joardar A; Department of Molecular and Cellular Biology, University of Arizona, Tucson, United States.
  • Liévens JC; Université de Montpellier, MMDN U1198, CC105, Montpellier, France.
  • Bowser R; Department of Neurology, Barrow Neurological Institute, Phoenix, United States.
  • Sattler R; Department of Neurology, Barrow Neurological Institute, Phoenix, United States.
  • Zarnescu DC; Department of Molecular and Cellular Biology, University of Arizona, Tucson, United States.
Elife ; 82019 06 10.
Article en En | MEDLINE | ID: mdl-31180318

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación hacia Arriba / Modelos Animales de Enfermedad / Glucosa / Glucólisis / Esclerosis Amiotrófica Lateral / Neuronas Motoras Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Elife Año: 2019 Tipo del documento: Article País de afiliación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación hacia Arriba / Modelos Animales de Enfermedad / Glucosa / Glucólisis / Esclerosis Amiotrófica Lateral / Neuronas Motoras Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Elife Año: 2019 Tipo del documento: Article País de afiliación: Estados Unidos
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