"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..."
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.
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