Nature Communications (Dec 2018)

SRPK1 maintains acute myeloid leukemia through effects on isoform usage of epigenetic regulators including BRD4

  • Konstantinos Tzelepis,
  • Etienne De Braekeleer,
  • Demetrios Aspris,
  • Isaia Barbieri,
  • M. S. Vijayabaskar,
  • Wen-Hsin Liu,
  • Malgorzata Gozdecka,
  • Emmanouil Metzakopian,
  • Hamish D. Toop,
  • Monika Dudek,
  • Samuel C. Robson,
  • Francisco Hermida-Prado,
  • Yu Hsuen Yang,
  • Roya Babaei-Jadidi,
  • Dimitrios A. Garyfallos,
  • Hannes Ponstingl,
  • Joao M. L. Dias,
  • Paolo Gallipoli,
  • Michael Seiler,
  • Silvia Buonamici,
  • Binje Vick,
  • Andrew J. Bannister,
  • Roland Rad,
  • Rab K. Prinjha,
  • John C. Marioni,
  • Brian Huntly,
  • Jennifer Batson,
  • Jonathan C. Morris,
  • Cristina Pina,
  • Allan Bradley,
  • Irmela Jeremias,
  • David O. Bates,
  • Kosuke Yusa,
  • Tony Kouzarides,
  • George S. Vassiliou

DOI
https://doi.org/10.1038/s41467-018-07620-0
Journal volume & issue
Vol. 9, no. 1
pp. 1 – 13

Abstract

Read online

SRPK1, a kinase involved in splicing regulation, is a potential therapeutic target for AML patients. Here, the authors show that SRPK1 inhibition changes isoform levels of key epigenetic regulators, including BRD4, and it has anti-tumor effects specifically against MLL-rearranged AML cells.