Nature Communications (Jun 2020)

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

  • 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

DOI
https://doi.org/10.1038/s41467-020-16786-5
Journal volume & issue
Vol. 11, no. 1
pp. 1 – 14

Abstract

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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.