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 (-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.
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| http://dx.doi.org/10.1080/23723556.2020.1871172 | DOI Listing |
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