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A JAK of all trades: how global phosphoproteomics reveal the Achilles heel of MPNs.

Tina M SchnoederFlorian PernerFlorian H Heidel
Published in: Molecular & cellular oncology (2021)
While Janus-kinase (JAK)-inhibitors effectively reduce the inflammatory phenotype of myeloproliferative neoplasms (MPN), they do not affect disease burden or presence of the mutated clone to a major extent. Here, we show how Janus-kinase 2 (JAK2)-mutated cells persist through maintenance of the mitogen-activated protein kinase Interacting Serine/Threonine Kinase 1 (MKNK1) - Extracellular Signal-regulated Kinase (ERK)-axis by hijacking the splicing machinery through post-translational modifications.
Keyphrases
  • protein kinase
  • tyrosine kinase
  • cell proliferation
  • transcription factor
  • gene expression
  • risk factors
  • single cell
  • cell cycle arrest
  • dna methylation
  • cell death
  • endoplasmic reticulum stress