This grand round has already taken place.
Previous research in the laboratory has established an important role for sphingomyelin synthase 1 (SGMS1) in sustaining proliferation of cells expressing the Bcr-Abl oncogene, causative agent of chronic myelogenous leukemia (CML). It was found that SGMS1 expression was greatly elevated in these cells and upon investigating the mechanism responsible for the SMS1 up-regulation, we identified a novel oncogenic-driven mechanism of protein up-regulation involving the utilization of a novel alternative transcriptional start site (TSS). To uncover the molecular mechanism involved, the promoter regulating this novel TSS was isolated and analyzed in detail. This led to the identification of the transcription factor GATA-1 as a novel regulator of SMS1 expression, with important implications for GATA1 positive malignancies.
Dates and Times
Start: 1/14/2021 12:00 PM
End: 1/14/2021 1:00 PM
To learn about a novel oncogenic-driven mechanism of protein regulation revealed by Bcr-abl1 regulation of the sphingomyelin synthase 1 gene.
To appreciate the role of the GATA1 transcription factor in normal erythropoiesis and its potential role in GATA positive leukemias.
To learn about Sphingomyelin Synthase 1 as a potential viable target in GATA1 positive malignancies.
The School of Medicine, State University of New York at Stony Brook, is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.
The School of Medicine, State University of New York at Stony Brook designates this live activity for a maximum of 1.00 AMA PRA Category 1 Credit(s) ™. Physicians should only claim the credit commensurate with the extent of their participation in the activity.