A kinase-deficient NTRK2 splice variant predominates in glioma and amplifies several oncogenic signaling pathways

A kinase-deficient NTRK2 splice variant predominates in glioma and amplifies several oncogenic signaling pathways

Tropomyosin receptor kinase B (TrkB), encoded by the neurotrophic tyrosine receptor kinase 2 (NTRK2) gene, exhibits intricate splicing patterns and post-translational modifications. Here, the authors perform whole gene and transcript-level analyses and report the TrkB.T1 splice variant enhances PDGF...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Siobhan S. Pattwell, Sonali Arora, Patrick J. Cimino, Tatsuya Ozawa, Frank Szulzewsky, Pia Hoellerbauer, Tobias Bonifert, Benjamin G. Hoffstrom, Norman E. Boiani, Hamid Bolouri, Colin E. Correnti, Barbara Oldrini, John R. Silber, Massimo Squatrito, Patrick J. Paddison, Eric C. Holland
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2020
Materias:
Science
Q
Acceso en línea:https://doaj.org/article/e76b737ec4c34d949cb32dc9395b4f44
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
Descripción
Sumario:Tropomyosin receptor kinase B (TrkB), encoded by the neurotrophic tyrosine receptor kinase 2 (NTRK2) gene, exhibits intricate splicing patterns and post-translational modifications. Here, the authors perform whole gene and transcript-level analyses and report the TrkB.T1 splice variant enhances PDGF-driven gliomas in vivo and augments PI3K signaling cascades in vitro.

Ejemplares similares