O-GlcNAcylation of STAT5 controls tyrosine phosphorylation and oncogenic transcription in STAT5-dependent malignancies

• DOI: 10.1038/leu.2017.4
• Publication Date: 2017-01-11T07:43:01Z
• Authors: P Freund; M A Kerenyi; M Hager; T Wagner; B Wingelhofer; H T T Pham; M Elabd; X Han; P Valent; F Gouilleux; V Sexl; O H Krämer; B Groner; R Moriggl
• Keywords: STAT5

The signal transducer and activator of transcription 5 (STAT5) regulates differentiation, survival, proliferation transformation hematopoietic cells. Upon cytokine stimulation, STAT5 tyrosine phosphorylation (pYSTAT5) is transient, while in diverse neoplastic cells persistent overexpression enhanced pYSTAT5 are frequently found. Post-translational modifications might contribute to activation the context transformation, but strength duration incompletely understood. We found that O-GlcNAcylation act together trigger levels oncogenic expression a mutated hyperactive gain-of-function (GOF) without resulted decreased phosphorylation, oligomerization transactivation potential complete loss capacity. lack diminished phospho-ERK phospho-AKT levels. Our data show an important process contributes through driving myeloid transformation. could be required for nutrient sensing metabolism cancer