Mutations in the APC gene and their implications for protein structure and function
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Cited by (178)
USP7 inactivation suppresses APC-mutant intestinal hyperproliferation and tumor development
2023, Stem Cell ReportsExtract from Butea monosperma inhibits β-catenin/Tcf signaling in SW480 human colon cancer cells
2018, Gene ReportsCitation Excerpt :Among these two binding sites, the 20 aa repeat had high affinity upon phosphorylation whereas the functional significance of 15 aa residues is still obscure (Breitman et al., 2008). Most of the tumor associated mutations in APC have been mapped in the residues of 1286–1513 (Polakis, 1995). In results, the butrin and isobutrin were strongly bound with the 20 aa β-catenin regions as well as in the tumor associated mutated regions.
USP7 Is a Tumor-Specific WNT Activator for APC-Mutated Colorectal Cancer by Mediating β-Catenin Deubiquitination
2017, Cell ReportsCitation Excerpt :Its loss initiates adenoma formation through constitutive Wnt activation (The Cancer Genome Atlas Network, 2012; Nagase and Nakamura, 1993). Most APC somatic mutations occur in the “mutation cluster region” (MCR) between codons 1,286 and 1,513 (Polakis, 1995; Vogelstein and Kinzler, 2004). Region-specific APC mutations have been associated with distinct β-catenin transcriptional activity and tumor susceptibility (Gaspar and Fodde, 2004).
Colon and Rectal Cancer
2015, The Molecular Basis of Cancer: Fourth EditionCrystal structures of the armadillo repeat domain of adenomatous polyposis coli and its complex with the tyrosine-rich domain of Sam68
2011, StructureCitation Excerpt :Most of the tumor-associated mutations in the apc gene have been mapped within the central region (residues 1286–1513) (Miyaki et al., 1994; Miyoshi et al., 1992). Such apc mutations result in truncated APC proteins that lack all of the axin/conductin-binding SAMP motifs and some of the β-catenin-binding 20 amino acid repeats (Polakis, 1995). The Arm domain in the N-terminal region of APC binds a variety of proteins (Figure 1A), suggesting that APC may also be involved in the regulation of cell-cell adhesion, cell polarization, and cell migration.
Upregulation of Glycogen synthase kinase 3β in human colorectal adenocarcinomas correlates with accumulation of CTNNB1
2011, Clinical Colorectal CancerCitation Excerpt :This in turn, increased CTNNB1 phosphorylation and degradation. Other mechanisms independent of GSK3B also appear to regulate CTNNB1.5,53,54 A recent study in Drosophila, for example, demonstrated that human APC-CTNNB1 physical interactions did not require phosphorylation of APC by GSK3B.55