Research sheds light on regulation of JAK2
Janus kinase 2, abbreviated JAK2, is a non-receptor kinase and is part of the JAK-STAT signaling pathway, which regulates immunity, proliferation, differentiation, apoptosis and oncogenesis. JAK2 is especially important for modulating the production of blood cells from hematopoietic stem cells, and JAK2 mutations have been found in patients suffering leukemia. Although JAK2 is a prominent oncogenic driver of blood cancers, how the protein is regulated is incompletely understood.
Now a research published in the journal Genes and Development sheds light on this subject. Conducted by scientists at Children's Hospital of Philadelphia, Progenra, Inc., the University of Pennsylvania, University of Nebraska Medical Center and University of Western Australia, the research identifies a new signaling axis that regulates JAK2 and provides novel treatment strategies for blood cancers.
Dr. Wei Tong, lead researcher of this study, and colleagues performed extensive experiments in cell lines and animal models. They identified two proteins -- CBL and LNK (or called SH2B3) -- that play a critical role in down-regulating JAK2 stability and signaling. Depletion of either of the two proteins led to extended JAK2 half-life, enhanced JAK2 signaling, and increased cell growth in mouse hematopoietic stem/progenitor cells and in human cell lines.
Further investigation demonstrated that JAK inhibition could decrease abnormal hematopoietic stem/progenitor cells and attenuate the development of leukemia in a mouse model of aggressive myeloid leukemia caused by CBL loss. The finding indicates that CBL mutant myeloid malignancies might be treated with drugs that inhibit JAK2, but more research is required to test this hypothesis.
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