- Non-homologous end joining-mediated DNA misrepair in quiescent HSCs is associated with the acquisition of genomic rearrangements, which persist in vivo and contribute to clonal expansion of abnormal HSCs.
- The unfolded protein response in mitochondria (UPRmt) mediates the metabolic remodeling required for HSC entry to and exit from quiescence and the loss of Sirtuin 7 leads to the dysregulation of the UPRmt and promotes HSC aging.
- A regulator of local, but not systemic, insulin-like growth factor 1 (IGF-1) signaling has dramatic effects on HSCs and their myeloid progeny, which may have therapeutic implications clonal hematopoiesis and myeloproliferative neoplasms and their associated comorbidities.
Monday, June 10, 2019 - 12:00pm to 1:00pm
Mary E. Mohrin, PhD
900 East 57th StreetKCBD Auditorium 1103
Chicago, IL 60637
- 1.00 AMA PRA Category 1 Credit™
- 1.00 Participation