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Enhancing WNT Signaling Restores Cortical Neuronal Spine Maturation and Synaptogenesis in Tbr1 Mutants.
Fazel Darbandi, Siavash; Robinson Schwartz, Sarah E; Pai, Emily Ling-Lin; Everitt, Amanda; Turner, Marc L; Cheyette, Benjamin N R; Willsey, A Jeremy; State, Matthew W; Sohal, Vikaas S; Rubenstein, John L R.
Afiliación
  • Fazel Darbandi S; Department of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA.
  • Robinson Schwartz SE; Department of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA.
  • Pai EL; Department of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA.
  • Everitt A; Institute for Neurodegenerative Diseases, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA.
  • Turner ML; Department of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA.
  • Cheyette BNR; Department of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA.
  • Willsey AJ; Department of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA; Institute for Neurodegenerative Diseases, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA; Quantit
  • State MW; Department of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA; Quantitative Biosciences Institute (QBI), University of California, San Francisco, San Francisco, CA 94143, USA.
  • Sohal VS; Department of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA; Kavli Institute for Fundamental Neuroscience and Sloan-Swartz Center for Theoretical Neurobiology, University of California, San Francisco, San Francisco, CA 94
  • Rubenstein JLR; Department of Psychiatry and UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143, USA. Electronic address: john.rubenstein@ucsf.edu.
Cell Rep ; 31(2): 107495, 2020 04 14.
Article en En | MEDLINE | ID: mdl-32294447
Tbr1 is a high-confidence autism spectrum disorder (ASD) gene encoding a transcription factor with distinct pre- and postnatal functions. Postnatally, Tbr1 conditional knockout (CKO) mutants and constitutive heterozygotes have immature dendritic spines and reduced synaptic density. Tbr1 regulates expression of several genes that underlie synaptic defects, including a kinesin (Kif1a) and a WNT-signaling ligand (Wnt7b). Furthermore, Tbr1 mutant corticothalamic neurons have reduced thalamic axonal arborization. LiCl and a GSK3ß inhibitor, two WNT-signaling agonists, robustly rescue the dendritic spines and the synaptic and axonal defects, suggesting that this could have relevance for therapeutic approaches in some forms of ASD.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas de Dominio T Box / Espinas Dendríticas / Vía de Señalización Wnt Límite: Animals / Female / Humans / Male Idioma: En Revista: Cell Rep Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas de Dominio T Box / Espinas Dendríticas / Vía de Señalización Wnt Límite: Animals / Female / Humans / Male Idioma: En Revista: Cell Rep Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos