Page 35 - Hormel Report 2023
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Our long-term goal is to understand how muta- tions in an H3.3 gene contribute to the generation of pediatric gliomas. Our central hypothesis is reduction in total available phosphorylatable H3.3 – caused by the heterozygous mutations
in residues flanking Ser31 in one of the two H3.3 genes – partially abrogates cell cycle checkpoint function.
ORCID iD: https://orcid.org/0000-0003-0091-3814
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Model for Ser31 phosphorylation and aneuploidy checkpoint
Cells following chromosome missegregation have high phosphor-Ser31 in their nuclei
PUBLICATION HIGHTLIGHTS:
• Zhang, L., Nesvick, C. L., Day, C. A., Choi, J., Lu, V. M., Peterson, T., Power, E. A., Anderson, J. B., Hamdan, F. H., Decker, P. A., Simons, R., Welby, J. P., Siada, R., Ge, J. Z., Kaptzan, T., Johnsen, S. A., Hinchcliffe, E. H., & Daniels, D. J. (2022). STAT3 is a biologically relevant therapeutic target in H3K27M-mutant diffuse midline glioma. Neuro-Oncology, 24(10), 1700-1711.
• Day, C. A., Hinchcliffe, E. H., & Robinson, J. P. (2022). H3K27me3 in Diffuse Midline Glioma and Epithelial Ovarian Cancer: Opposing Epigenetic Changes Leading to the Same Poor Outcomes. Cells, 11(21), 19.
