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lüll Re-evaluating the role of Frat in Wnt-signal transduction van Amerongen R; Berns ACell Cycle 2005[Aug]; 4 (8): 1065-72Frat proteins are potent activators of canonical Wnt-signal transduction. By binding to GSK3, Frat prevents the phosphorylation and concomitant degradation of beta-catenin and allows the activation of downstream target genes by beta-catenin/TCF complexes. The identification of the Xenopus Frat homologue GBP as an essential component of the maternal Wnt-pathway during embryonic axis formation suggested that Frat might fulfill a similar role in higher vertebrates. As a result most, if not all, studies addressing Frat function have focused on its ability to bind GSK3 and induce signaling through beta-catenin/TCF. Consequently, Frat has been advocated as the "missing link" that bridged signaling from Dishevelled to GSK3 in the canonical Wnt-pathway. Recent mouse-knockout studies however, call for a reevaluation of the physiological role of Frat. Mice that lack all Frat-family members appear to be normal and display no obvious defects in beta-catenin/TCF signaling. This observation reopens the question as to how GSK3 activity is controlled in vertebrate canonical Wnt-signal transduction in view of the apparent dispensability of Frat. Here we will review the studies that have been conducted on Frat proteins to date, with a specific focus on those that implicate a role for Frat in Wnt-signal transduction. In addition, we will discuss potential alternatives for the endogenous function of Frat.|*Gene Expression Regulation[MESH]|*Signal Transduction[MESH]|Adaptor Proteins, Signal Transducing[MESH]|Alleles[MESH]|Amino Acid Motifs[MESH]|Animals[MESH]|Caenorhabditis elegans[MESH]|Cell Line, Tumor[MESH]|Drosophila[MESH]|Genes, Reporter[MESH]|Glycogen Synthase Kinase 3/metabolism[MESH]|Humans[MESH]|Intracellular Signaling Peptides and Proteins/*physiology[MESH]|Luciferases/metabolism[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Models, Biological[MESH]|Phosphorylation[MESH]|Protein Conformation[MESH]|Proto-Oncogene Proteins/*physiology[MESH]|Wnt Proteins/*metabolism[MESH]|Xenopus[MESH]|beta Catenin/metabolism[MESH] |