Northwestern Medicine scientists have made significant strides in understanding myeloproliferative neoplasms (MPNs), rare blood cancers associated with JAK2/STAT pathway activation. Their study reveals that PPIL2 interacts with PLEK2, leading to the degradation of the tumor suppressor protein p53, thereby facilitating cancer progression. Blocking PPIL2 using cyclosporin A not only increased p53 levels but also reduced abnormal blood cell proliferation in MPN models. These findings provide a potential therapeutic avenue for treating MPNs by targeting protein interactions within the PLEK2 signalosome.
These diseases are often driven by abnormal activation of a protein called JAK2. In earlier research, we discovered that another protein, PLEK2, acts downstream of JAK2...
Collection
[
|
...
]