Our laboratory is interested in investigating the signal transduction and gene regulation in bacterial infection- and genotoxic stress-associated colonic inflammation and tumorigenesis, using a combination of genetic, immunological, molecular, and cellular approaches. We are studying the molecular/cellular mechanisms and pathophysiological significance of the novel and critical pathogen-host interactions and DNA damage responses that can be mechanistically linked to colon cancer etiology in mouse and human.
Fu K, Sun X, Wier EM, Hodgson A, Liu Y, Sears CL, Wan F. Sam68/KHDRBS1 is critical for colon tumorigenesis by regulating genotoxic stress-induced NF-κB activation. Elife. 2016 PubMed PMID: 27458801.
Hodgson A, Wier EM, Fu K, Sun X, Yu H, Zheng W, Sham HP, Johnson K, Bailey S, Vallance BA, Wan F. Metalloprotease NleC suppresses host NF-κB/inflammatory responses by cleaving p65 and interfering with the p65/RPS3 interaction. PLoS Pathog. 2015 PubMed PMID: 25756944.
Fu K, Sun X, Zheng W, Wier EM, Hodgson A, Tran DQ, Richard S, Wan F. Sam68 modulates the promoter specificity of NF-κB and mediates expression of CD25 in activated T cells. Nat Commun. 2013 PubMed PMID: 23715268.
Wan F, Weaver A, Gao X, Bern M, Hardwidge PR, Lenardo MJ. IKKβ phosphorylation regulates RPS3 nuclear translocation and NF-κB function during infection with Escherichia coli strain O157:H7. Nat Immunol. 2011 PubMed PMID: 21399639.
Wan F, Anderson DE, Barnitz RA, Snow A, Bidere N, Zheng L, Hegde V, Lam LT, Staudt LM, Levens D, Deutsch WA, Lenardo MJ. Ribosomal protein S3: a KH domain subunit in NF-kappaB complexes that mediates selective gene regulation. Cell. 2007 PubMed PMID: 18045535.