Eric Johannsen, MD
Position title: Associate Professor, Department of Medicine
6531 Wisconsin Institutes for Medical Research
- Lab Website
- Johannsen Lab
Our research focuses on the molecular biology of Epstein-Barr virus (EBV) nuclear proteins, their role in the virus lifecycle and the pathogenesis of EBV associated malignancies. Herpesviruses infect their hosts for life and EBV precisely manipulates growth and survival signaling pathways of B lymphocytes, resulting in their immortalization. Understanding the mechanisms that EBV has evolved to exploit infected cells is an important basis for therapy of EBV associated diseases and offers a unique vantage from which to view and understand complex cellular pathways.
1993 Howard Hughes Medical Institute Medical Student Fellow
2001 K08 Mentored Clinical Scientist Development Award
2002 Finland Research Award
2007 Howard Hughes Medical Institute Physician Scientist Early
- Ohashi M, Holthaus AM, Calderwood MA, Lai CY, Krastins B, Sarracino D, Johannsen E. “The EBNA3 Family of Epstein-Barr Virus Nuclear Proteins Associates with the USP46/USP12 Deubiquitination Complexes to Regulate Lymphoblastoid Cell Line Growth.” PLoS Pathog. 2015 Apr 9;11(4):e1004822.
- Zhou H, Schmidt SC, Jiang S, Willox B, Bernhardt K, Liang J, Johannsen EC, Kharchenko P, Gewurz BE, Kieff E, Zhao B. “Epstein-Barr Virus Oncoprotein Super-enhancers Control B Cell Growth.” Cell Host Microbe. 2015 Feb 11;17(2):205-16. PMID: 25639793
- Johannsen E, Lambert PF “Epigenetics of human papillomaviruses.” Virology 2013 Oct;45(1-2):205-12. PMCID: PMC3822409
- Duarte M, Wang L, Calderwood MA, Adelmant G, Ohashi M, Roecklein-Canfield J, Marto JA, Hill DE, Deng H, Johannsen E. “An RS motif within the Epstein-Barr virus BLRF2 tegument protein is phosphorylated by SRPK2 and is important for viral replication.” PLoS One 2013; 8(1):e53512. PMID: 23326445. PMCID: PMC3541133.
- Jiang S, Willox B, Zhou H, Holthaus AM, Wang A, Shi TT, Maruo S, Kharchenko PV, Johannsen EC, Kieff E., Zhao B. “Epstein-Barr Virus Nuclear Antigen 3C binds to BATF/IRF4 or SPI1/IRF4 composite sites and recruits Sin3A to repress CDKN2A.” Proc Natl Acad Sci U S A. 2014; 111(1):421-6. PMID: 24344258. PMCID: