Postdoctoral Research Fellow – Cancer Research
A postdoctoral fellow position is available in the group of Dr. Yuichi Machida at Mayo Clinic in Rochester, MN to study abnormal proliferation and genome instability in cancer. The laboratory studies ubiquitin-mediated regulation of the cell cycle and DNA repair. This position will focus on the roles of nuclear proteases in DNA repair and genome maintenance.
Dr. Machida’s team was one of the first groups that identified the novel metalloprotease, Spartan, which removes proteins covalently crosslinked to genomic DNA. Due to its bulky nature, DNA-protein crosslinks (DPCs) interferer with DNA replication machineries and thereby cause DNA breaks and genomic instability. Dr. Machida’s work has demonstrated that genetically modified mice with reduced levels of Spartan exhibited genomic instability, premature aging, and liver cancer, recapitulating the phenotypes of the Ruijs-Aalfs Syndrome, a human disease caused by mutations in the Spartan gene (Nat Commun 5:5744, PMID: 25501849; Nucleic Acids Res 45:4564-4576, PMID: 28199696).
The successful candidate will investigate the mechanisms of DPC repair as well as its implications in tumor suppression and sensitivities to chemotherapeutic drugs using molecular biology, mouse genetics, organoids, and CRISPR/Cas9-based genetic screens.
To learn more about Dr. Machida’s program, please view his faculty information page at:
Qualified candidates must have a Ph.D. in a field deemed relevant by the program. Candidates with experience in cancer biology, molecular biology or mouse genetics are encouraged to apply.
Applications, including curriculum vitae and bibliography, and the names and email addresses of three references should be sent to:
Yuichi Machida, Ph.D.
Department of Oncology
Division of Oncology Research
Key words: DNA damage; DNA repair; DNA replication; cancer; tumor; chromatin; histone; ubiquitin; genome; chromosome; genomic instability; mutation; checkpoint; proliferation; cell cycle; mitosis; protease; CRISPR; CRISPR screen; liver; hepatocellular carcinoma; aging; premature aging; progeria; stem cell; senescence; mouse; genetics; development; organoids; carcinogenesis; chemotherapy; inhibitors
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