Junjie Chen, PhD
Professor, Department of Therapeutic Radiology
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junjie.chen@yale.edu Phone: 203-785-3758 Fax: 203-785-7482 Yale University School of Medicine Department of Therapeutic Radiology P.O. Box 208040 HRT 213C New Haven, Connecticut 06520-8040 |
Degrees/Education:
B.S., Genetics and Genetic Engineering, Fudan University, Shanghai, People’s Republic of China (1988)
Ph.D., Cell and Molecular Biology Program, University of Vermont (1994)
Post Doctoral Fellow, Department of Cancer Biology, Dana Farber Cancer Institute, Harvard Medical School (1996)
Post Doctoral Fellow, Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School (1999)
Faculty Appointments:
Assistant Professor, Mayo Clinic College of Medicine, Biochem/Molecular Biology (dates-from-1999 to 2003)
Associate Professor, Mayo Clinic College of Medicine, Pharmacology (dates- from-2004 to 2006)
Professor, Yale University School of Medicine, Therapeutic Radiology (2006-present)
Certifications/Honors:
DOD breast cancer research career Development award
DOD Breast Cancer Research Program-Era of Hope Scholar Award
Research Interests:
We are interested in the molecular mechanisms that control genomic stability, tumor suppression and longevity.
Genomic instability is a common feature of all human cancers. The maintenance of genomic integrity following DNA damage depends on the coordination of the DNA repair system and cell cycle checkpoint controls. Similar to mitogenic signaling pathways, the DNA damage-induced signaling pathway consists of kinase-dependent signaling cascades that regulate cell cycle progression, DNA repair and apoptosis following DNA damage. It is the coordination of these events that ensures genomic stability. We have just begun to understand how this coordination is accomplished in mammalian cells.
ATM (ataxia telangiectasia mutated protein) and ATR (ataxia telangiectasia-related protein), two phosphatidylinositol 3-kinase-related protein kinases, are essential components in this DNA damage-signaling pathway. ATM and ATR activate the downstream checkpoint kinases Chk1 and Chk2/Cds1. Collectively, these four protein kinases phosphorylate a number of downstream effector proteins, including tumor suppressors p53 and BRCA1, where they coordinate DNA repair, cell cycle progression, transcriptional regulation and apoptosis in response to various DNA-damaging events. By focusing on several key regulators (ATM, 53BP1, Chk2, MDC1 and BRCA1) in this pathway and using biochemical and genetic approaches, we attempt to understand the roles of this DNA damage pathway in tumorigenesis and in anti-tumor therapy.
In the last two years, we have also our interests to the roles of mitotic checkpoint control and telomere maintenance in genomic instability. Additionally, we have ongoing research pursuing the link between DNA damage/repair, the regulation of chromatin structures and aging. Overall, the lab is interested in the pathways that control genomic stability and how the dysregulation of these pathways contributes to cancer, aging and other common illnesses.
Selected pubmed article listing A - Selected pubmed article listing B
