William T. Senapedis, Ph.D.
Affiliations: | 2011 | Harvard University, Cambridge, MA, United States |
Area:
Intracellular CompartmentationGoogle:
"William Senapedis"Parents
Sign in to add mentor| Pamela A. Silver | grad student | 2011 | Harvard | |
| (Forkhead at the Crossroads of Cancer and Healthy Lifespan.) | ||||
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Publications
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| Li N, Lopez MA, Linares M, et al. (2018) Dual PAK4-NAMPT inhibition impacts growth and survival, and increases sensitivity to DNA-damaging agents in Waldenstrom Macroglobulinemia. Clinical Cancer Research : An Official Journal of the American Association For Cancer Research |
| Kashyap T, Argueta C, Unger T, et al. (2018) Selinexor reduces the expression of DNA damage repair proteins and sensitizes cancer cells to DNA damaging agents. Oncotarget. 9: 30773-30786 |
| Gravina GL, Senapedis W, McCauley D, et al. (2014) Nucleo-cytoplasmic transport as a therapeutic target of cancer. Journal of Hematology & Oncology. 7: 85 |
| Senapedis WT, Kennedy CJ, Boyle PM, et al. (2011) Whole genome siRNA cell-based screen links mitochondria to Akt signaling network through uncoupling of electron transport chain. Molecular Biology of the Cell. 22: 1791-805 |
| Aldaye FA, Senapedis WT, Silver PA, et al. (2010) A structurally tunable DNA-based extracellular matrix. Journal of the American Chemical Society. 132: 14727-9 |
| Gómez-Baldó L, Schmidt S, Maxwell CA, et al. (2010) TACC3-TSC2 maintains nuclear envelope structure and controls cell division. Cell Cycle (Georgetown, Tex.). 9: 1143-55 |
| Astrinidis A, Senapedis W, Henske EP. (2006) Hamartin, the tuberous sclerosis complex 1 gene product, interacts with polo-like kinase 1 in a phosphorylation-dependent manner Human Molecular Genetics. 15: 287-297 |
| Astrinidis A, Senapedis W, Coleman TR, et al. (2003) Cell Cycle-regulated Phosphorylation of Hamartin, the Product of the Tuberous Sclerosis Complex 1 Gene, by Cyclin-dependent Kinase 1/Cyclin B Journal of Biological Chemistry. 278: 51372-51379 |
| Khare L, Astrinidis A, Senapedis W, et al. (2002) Expression of wild type and mutant TSC2, but not TSC1, causes an increase in the G1 fraction of the cell cycle in HEK293 cells Journal of Medical Genetics. 39: 676-680 |