A Genetic Screen Reveals an Unexpected Role for Yorkie Signaling in JAK/STAT-Dependent Hematopoietic Malignancies in Drosophila melanogaster.

ABSTRACT: A gain-of-function mutation in the tyrosine kinase JAK2 (JAK2^V617F ) causes human myeloproliferative neoplasms (MPNs). These patients present with high numbers of myeloid lineage cells and have numerous complications. Since current MPN therapies are not curative, there is a need to find new regulators and targets of Janus kinase/Signal transducer and activator of transcription (JAK/STAT) signaling that may represent additional clinical interventions . Drosophila melanogaster offers a low complexity model to study MPNs as JAK/STAT signaling is simplified with only one JAK [Hopscotch (Hop)] and one STAT (Stat92E). hop^{Tumorous-lethal(Tum-l)} is a gain-of-function mutation that causes dramatic expansion of myeloi

SUBMITTER: Anderson AM 

PROVIDER: S-EPMC5555452 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature