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, Hobbs RP, Wan F. Sam68/KHDRBS1-dependent NF-?B activation confers radioprotection to the colon epithelium in ?-irradiated mice. Elife 2016 PMID: 27996939.
Sun X, Fu K, Hodgson A, Wier EM, Wen MG, Kamenyeva O, Xia X, Koo LY, Wan F. Sam68 is required for DNA damage responses via regulating poly(ADP-ribosyl)ation. PLoS Biol 2016 PMID: 27635653.
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-kB activation. Elife 2016. 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-kB/inflammatory responses by cleaving p65 and interfering with the p65/RPS3 interaction. PLoS Pathog 2015 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-kB and mediates expression of CD25 in activated T cells. Nat. Commun. 2013. PMID: 23715268.