|1.||Tanabe, Tsutomu: 1 article (01/2014)|
|2.||Sakurai, Eri: 1 article (01/2014)|
|3.||Kii, Isao: 1 article (01/2014)|
|4.||Kurihara, Takashi: 1 article (01/2014)|
|5.||Miyata, Atsuro: 1 article (01/2014)|
|6.||Hagiwara, Masatoshi: 1 article (01/2014)|
|7.||Kawamoto, Daisuke: 1 article (01/2014)|
|8.||Asada, Toshihide: 1 article (01/2014)|
|9.||Toyomoto, Masayasu: 1 article (01/2014)|
|10.||Yoshimura, Megumu: 1 article (01/2014)|
|1.||Breast Neoplasms (Breast Cancer)
03/20/2008 - "The identification of these two modes of inhibition of formation of the nm23-H1-h-prune protein complex pave the way toward new challenges, including translational studies using IC261 or this competitive peptide 'in vivo' to inhibit cellular motility induced by nm23-H1-h-prune complex formation during progression of breast cancer."
03/20/2008 - "The region of the nm23-h-prune interaction lies between S120 and S125 of nm23, where missense mutants show impaired binding; this region has been highly conserved throughout evolution, and can undergo serine phosphorylation by casein kinase I. Thus, the casein kinase I delta-epsilon specific inhibitor IC261 impairs the formation of the nm23-h-prune complex, which translates 'in vitro' into inhibition of cellular motility in a breast cancer cellular model. "
06/02/2011 - "This activity accounts for many of the diverse biological effects of IC261 and, most importantly, for its selective cancer cell killing."
06/02/2011 - "Unexpectedly, and unlike IC261, PF670 and PF480 were unable to induce cancer cell death. "
06/02/2011 - "RNA interference screens identified CK1ɛ as a pro-survival factor in cancer cells in vitro and the CK1δ/ɛ-specific inhibitor IC261 is remarkably effective at selective, synthetic lethal killing of cancer cells. "
06/02/2011 - "IC261 induces cell cycle arrest and apoptosis of human cancer cells via CK1δ/ɛ and Wnt/β-catenin independent inhibition of mitotic spindle formation."
06/02/2011 - "In contrast, while sub-micromolar concentrations of IC261 neither inhibited CK1δ/ɛ kinase activity nor blocked Wnt/β-catenin signaling in cancer cells, it caused a rapid induction of prometaphase arrest and subsequent apoptosis in multiple cancer cell lines. "
|3.||Pancreatic Neoplasms (Pancreatic Cancer)
|2.||Casein Kinase Idelta
|3.||Casein Kinase I (Casein Kinase 1)
|4.||Casein Kinases (Casein Kinase)
|5.||Staphylococcal Protein A (A, Protein)
|1.||Heterologous Transplantation (Xenotransplantation)