作者: Bert Vogelstein , Kenneth W. Kinzler , Zhenghe Wang
DOI:
关键词: Cancer cell 、 Cell 、 Cancer research 、 Mutation 、 Beta-catenin 、 Catenin 、 Phosphorylation 、 Biology 、 Genetic model 、 Signal transduction
摘要: Several previous studies in a variety of systems have suggested that phosphorylation at S45 beta-catenin is essential for subsequent more NH(2)-terminal residues. Using genetic models expressing under endogenous regulation, we find not required residues S33, S37, or T41 human colon cancer cells, contrast to prevailing models. These findings suggest there are important cell- and organism-specific differences even the most highly conserved signaling pathways emphasize importance examining these cell types which actually deregulated.