IDP mediated transcriptional stabilization as a cause of AML
Full Description
PROJECT SUMMARY
High expression of the intrinsically disordered protein Meningioma-1 (MN1) is common in AML,
and associated with a poor prognosis. Forced expression of MN1 in murine hematopoietic
progenitors induces an aggressive leukemia. We recently discovered that the primary interaction
partner of MN1 is the BAF nucleosome-positioning complex. MN1 stabilizes BAF on chromatin.
MN1 binding is associated with sustained active enhancer chromatin at enhancers regulating a
hematopoietic stem/progenitor program. Intriguingly, MN1’s entire coding frame is disordered. We
hypothesize that MN1 causes AML by overstabilizing transcriptional hubs by increasing multi-
valent, low affinity interactions that result in high local concentrations of BAF and early
hematopoietic transcription factors. A better understanding of how MN1 causes leukemia may
identify opportunities for targeted therapies in a patient population who is failing conventional AML
therapy.
Grant Number: 5R01CA269788-05
NIH Institute/Center: NIH
Principal Investigator: KATHRIN BERNT
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