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Article

Ruxolitinib mediated paradoxical JAK2 hyperphosphorylation is due to the protection of activation loop tyrosines from phosphatases.

Leukemia - 1 Jul 2025

Gorantla Sivahari P, Oelschläger Lorenz, Prince Gerin, Osius Jasmin, Kolluri Suresh Babu, Maluje Yamil, Fähnrich Anke, Ernst Nancy, Barbosa Gulde Alanis, Ludwig Ralf Joachim, Gemoll Timo, Fliedner Stephanie, Walter Wencke, Haferlach Torsten, Gebauer Niklas, Busch Hauke, Duyster Justus, von Bubnoff Nikolas

Abstract excerpt

Myelofibrosis (MF) in 50% of cases is driven by an activating JAK2 mutation, mostly V617F. Ruxolinitib is approved for the treatment of MF. Responses to ruxolitinib in MF are of limited duration. Unexpectedly, treatment of JAK2-V617F expressing cells with ruxolitinib causes paradoxical hyperphosphorylation of JAK2 at activation loop Tyr1007/Tyr1008. The significance of ruxolitinib-induced JAK2...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 40269271
DOI: 10.1038/s41375-025-02594-7
PMCID: PMC12208895

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JAK2

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