Bim and Mcl-1 exert key roles in regulating JAK2V617F cell survival.

ABSTRACT:

Background

The JAK2V617F mutation plays a major role in the pathogenesis of myeloproliferative neoplasms and is found in the vast majority of patients suffering from polycythemia vera and in roughly every second patient suffering from essential thrombocythemia or from primary myelofibrosis. The V617F mutation is thought to provide hematopoietic stem cells and myeloid progenitors with a survival and proliferation advantage. It has previously been shown that activated JAK2 promotes cell survival by upregulating the anti-apoptotic STAT5 target gene Bcl-xL. In this study, we have investigated the role of additional apoptotic players, the pro-apoptotic protein Bim as well as the anti-apoptotic protein Mcl-1.

Methods

Pharmacological inhibition of JAK2/STAT5 signaling in JAK2V617F

SUBMITTER: Rubert J 

PROVIDER: S-EPMC3037340 | biostudies-literature | 2011 Jan

REPOSITORIES: biostudies-literature