JAW-JOU KANG2018-09-102018-09-102006http://www.scopus.com/inward/record.url?eid=2-s2.0-33744951784&partnerID=MN8TOARShttp://scholars.lib.ntu.edu.tw/handle/123456789/320714Daxx, a human cell death-associated protein, was isolated as a Tcf4-interacting protein, using a yeast two-hybrid screen. Co- immunoprecipitation in HEK-293T cells and yeast two-hybrid screen in Y190 cells were performed to identify the interaction between Tcf4 with Daxx and to map the binding regions of Tcf4. In the nucleus, Daxx reduced DNA binding activity of Tcf4 and repressed Tcf4 transcriptional activity. Overexpression of Daxx altered the expression of genes downstream of Tcf4, including cyclin D1 and Hath-1, and induced G1 phase arrest in colon cancer cells. A reduction in Daxx protein expression was also observed in colon adenocarcinoma tissue when compared with normal colon tissue. This evidence suggests a possible physiological function of Daxx, via interaction with Tcf4, to regulate proliferation and differentiation of colon cells. ? 2006 by The American Society for Biochemistry and Molecular Biology, Inc.[SDGs]SDG3Carcinogens; Cell culture; DNA; Genes; Tissue culture; Tumors; Colon cancer cells; Daxx protein expression; Tcf4-interacting protein; Proteins; cyclin D1; Daxx protein; DNA binding protein; protein tcf4; unclassified drug; article; cancer cell; cell cycle arrest; cell cycle G1 phase; colon cancer; controlled study; gene overexpression; human; human cell; priority journal; protein expression; Adaptor Proteins, Signal Transducing; Base Sequence; Basic Helix-Loop-Helix Transcription Factors; beta Catenin; Binding Sites; Cell Differentiation; Cell Line, Tumor; Cell Proliferation; Colonic Neoplasms; DNA, Complementary; DNA, Neoplasm; G1 Phase; Gene Expression; Genes, bcl-1; Humans; Multiprotein Complexes; Nuclear Proteins; Protein Binding; Recombinant Proteins; TCF Transcription Factors; Two-Hybrid System TechniquesPhysiological and functional interactions between Tcf4 and Daxx in colon cancer cellsjournal article10.1074/jbc.M601807200