Scott M. Stoeger, Ph.D.
Affiliations: | 2007 | University of Nebraska Medical Center, Omaha, NE, United States |
Area:
Pharmacology, OncologyGoogle:
"Scott Stoeger"Parents
Sign in to add mentor| Kenneth H. Cowan | grad student | 2007 | University of Nebraska Medical Center | |
| (Role of the ERK1/2 MAP kinase pathway on the cellular response to anticancer chemotherapy.) | ||||
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Publications
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| Razidlo GL, Johnson HJ, Stoeger SM, et al. (2018) Correction: KSR1 is required for cell cycle reinitiation following DNA damage. The Journal of Biological Chemistry. 293: 19136 |
| Razidlo GL, Johnson HJ, Stoeger SM, et al. (2009) KSR1 is required for cell cycle reinitiation following DNA damage. The Journal of Biological Chemistry. 284: 6705-15 |
| Stoeger SM, Cowan KH. (2009) Characterization of kinase suppressor of Ras-1 expression and anticancer drug sensitivity in human cancer cell lines. Cancer Chemotherapy and Pharmacology. 63: 807-18 |
| Kim M, Yan Y, Kortum RL, et al. (2005) Expression of kinase suppressor of Ras1 enhances cisplatin-induced extracellular signal-regulated kinase activation and cisplatin sensitivity. Cancer Research. 65: 3986-92 |
| Yan Y, Spieker RS, Kim M, et al. (2005) BRCA1-mediated G2/M cell cycle arrest requires ERK1/2 kinase activation. Oncogene. 24: 3285-96 |
| Sgagias MK, Wagner KU, Hamik B, et al. (2004) Brca1-deficient murine mammary epithelial cells have increased sensitivity to CDDP and MMS. Cell Cycle (Georgetown, Tex.). 3: 1451-6 |