bioRxiv · 10.1101/058156
Hipk is required for JAK/STAT activity and promotes hemocyte-derived tumorigenesis
Abstract
Dysregulation of key signaling molecules and pathways are causative of many Human diseases and cancers. A point mutation in the Drosophila Janus kinase (called hop) causes constitutive activation of the JAK/STAT pathway and results in blood cell tumours. We provide robust genetic evidence that Hipk is required for endogenous JAK/STAT activity. Overexpression of Hipk can phenocopy the effects of overactive JAK/STAT mutations and lead to melanized tumors and loss of Hipk can suppress the effects of hyperactive JAK/STAT. Furthermore, Hipk expression in blood cell progenitors causes tumors. PLA experiments show that Hipk can interact with the pathway effector Stat92E. Together our results show that Hipk is a novel factor required for effective JAK/STAT signaling.\n\nSummary StatementLoss of hipk impairs JAK/STAT activity in multiple tissue types and elevated Hipk leads to the formation of blood cell tumors in Drosophila.
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Jessica A. Blaquiere, Nathan B. Wray, Esther M. Verheyen. 2016-06-10. Hipk is required for JAK/STAT activity and promotes hemocyte-derived tumorigenesis. https://doi.org/10.1101/058156
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