Fengyi Wan, PhD
- Assistant Professor
- Biochemistry and Molecular Biology (Primary)
- Molecular Microbiology and Immunology (Joint)
- School of Medicine (Joint)
615 N. Wolfe Street
Baltimore, Maryland 21205
PhD, Chinese Academy of Sciences, 2003
BS, Wuhan University, 1999
Our laboratory is interested in investigating the signal transduction and gene regulation in bacterially induced colonic infection, inflammation, and tumorigenesis. Nuclear factor kappa B (NF-kB) signaling pathways are crucial for host defense against bacterial infections and play an important role in tumorigenesis in the colon. We are studying the molecular/cellular mechanisms and pathophysiological significance of impaired NF-kB signal transduction and gene transactivation in bacterial infection-associated colonic inflammation and tumorigenesis, using a combination of genetic, immunological, molecular, and cellular approaches. In particular, we are interested to examine how the virulence proteins (effectors) from attaching/effacing pathogens interfere with NF-kB signaling and subvert inflammatory responses in colon epithelial cells, to elucidate the key immune cell signaling that orchestrates innate and adaptive immune responses to colonic bacterial infection, and to explore the critical pathogen-host interactions that can be mechanistically linked to microbially induced colon cancer etiology in mice.
Postdoc positions are available. Please contact Fengyi Wan (firstname.lastname@example.org) for the details.
Honors and Awards
Yong-Ling Liu Award, Chinese Academy of Sciences (2002); Director Award, Chinese Academy of Sciences (2003); Howard Temin Pathway to Independence Award in Cancer Research, NCI (2008); AAI-Invitrogen Trainee Achievement Award, American Association of Immunologists (2009); American Cancer Society Research Scholar, ACS (2013)
- signal transduction
- gene regulation
- pathogen-host interactions
- RNA-binding proteins
- autoimmune diseases.
Most recent publications
- Fu K, Sun X, Wier EM, Hodgson A, Liu Y, Sears CL, Wan F. (2016) Sam68/KHDRBS1 is critical for colon tumorigenesis by regulating genotoxic stress-induced NF-kB activation. Elife 5: e15018.
- Hodgson A, Wier EM, Fu K, Sun X, Yu H, Zheng W, Sham HP, Johnson K, Bailey S, Vallance BA, Wan F (2015) Metalloprotease NleC suppresses host NF-kB/inflammatory responses by cleaving p65 and interfering with the p65/RPS3 interaction. PLOS Pathog. 11: e1004705
- Fu K, Sun X, Zheng W, Wier EM, Hodgson A, Tran DQ, Richard S, Wan F (2013) Sam68 modulates the promoter specificity of NF-kB and mediates expression of CD25 in activated T cells. Nat. Commun. 4: 1909
- Wier EM, Neighoff J, Sun X, Fu K, Wan F (2012) Identification of an N-terminal truncation of the NF-kB p65 subunit that specifically modulates ribosomal protein S3-dependent NF-kB gene expression. J. Biol. Chem. 287: 43019-43029
- Wan F, Weaver A, Gao X, Bern M, Hardwidge PR, Lenardo MJ (2011) IKKb phosphorylation regulates RPS3 nuclear translocation and NF-kB function during infection with Escherichia coli strain O157:H7. Nat. Immunol. 12: 335-343