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Journal Article
by Li, Jun and Woods, Susan L and Healey, Sue and Beesley, Jonathan and Chen, Xiaoqing and Lee, Jason S and Sivakumaran, Haran and Wayte, Nicci and Nones, Katia and Waterfall, Joshua J and Pearson, John and Patch, Anne-Marie and Senz, Janine and Ferreira, Manuel A and Kaurah, Pardeep and Mackenzie, Robertson and Heravi-Moussavi, Alireza and Hansford, Samantha and Lannagan, Tamsin R.M and Spurdle, Amanda B and Simpson, Peter T and da Silva, Leonard and Lakhani, Sunil R and Clouston, Andrew D and Bettington, Mark and Grimpen, Florian and Busuttil, Rita A and Di Costanzo, Natasha and Boussioutas, Alex and Jeanjean, Marie and Chong, George and Fabre, Aurélie and Olschwang, Sylviane and Faulkner, Geoffrey J and Bellos, Evangelos and Coin, Lachlan and Rioux, Kevin and Bathe, Oliver F and Wen, Xiaogang and Martin, Hilary C and Neklason, Deborah W and Davis, Sean R and Walker, Robert L and Calzone, Kathleen A and Avital, Itzhak and Heller, Theo and Koh, Christopher and Pineda, Marbin and Rudloff, Udo and Quezado, Martha and Pichurin, Pavel N and Hulick, Peter J and Weissman, Scott M and Newlin, Anna and Rubinstein, Wendy S and Sampson, Jone E and Hamman, Kelly and Goldgar, David and Poplawski, Nicola and Phillips, Kerry and Schofield, Lyn and Armstrong, Jacqueline and Kiraly-Borri, Cathy and Suthers, Graeme K and Huntsman, David G and Foulkes, William D and Carneiro, Fatima and Lindor, Noralane M and Edwards, Stacey L and French, Juliet D and Waddell, Nicola and Meltzer, Paul S and Worthley, Daniel L and Schrader, Kasmintan A and Chenevix-Trench, Georgia
American journal of human genetics, ISSN 0002-9297, 2016, Volume 98, Issue 5, pp. 830 - 842
Journal Article
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 1106 - 17
.... Adenomatous polyposis coli (APC) germline mutations cause aneuploidy and are responsible for familial adenomatous polyposis (FAP... 
PHOSPHORYLATION | BI 6727 | MULTIDISCIPLINARY SCIENCES | SUBCELLULAR-LOCALIZATION | SPINDLE ASSEMBLY CHECKPOINT | MUTATIONS | HEREDITARY COLORECTAL-CANCER | MITOTIC CENTROSOMES | BETA-CATENIN | POLO-LIKE KINASE | CHROMOSOMAL INSTABILITY | Colonic Neoplasms - genetics | Aurora Kinase B - metabolism | Mitosis | Humans | Male | Colonic Neoplasms - physiopathology | Adenomatous Polyposis Coli - enzymology | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Female | Adenomatous Polyposis Coli - genetics | Chromosomal Instability | Protein-Serine-Threonine Kinases - metabolism | Adenomatous Polyposis Coli Protein - genetics | Proto-Oncogene Proteins - metabolism | Aurora Kinase B - genetics | Tumor Suppressor Proteins - metabolism | Kinetochores - metabolism | Mice, Inbred C57BL | Adenomatous Polyposis Coli - physiopathology | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Proto-Oncogene Proteins - genetics | Mice, Knockout | Animals | Adenomatous Polyposis Coli Protein - metabolism | Cell Line, Tumor | Colonic Neoplasms - enzymology | Mice | Animal models | Cell survival | Stability | Polo-like kinase 1 | RNA-mediated interference | Familial adenomatous polyposis | Abnormalities | Colorectal cancer | Aneuploidy | Pharmacology | Kinases | Polyposis coli | Survival | Genomic instability | Adenomatous polyposis coli | Aurora B protein | Colon cancer | Colon | Inhibition | Mutation | Polyps | Cancer
Journal Article
PloS one, ISSN 1932-6203, 10/2013, Volume 8, Issue 10, p. e77257
Mutations in the central region of the signalling hub Adenomatous Polyposis Coli (APC... 
unclassified drug | gel permeation chromatography | structure analysis | in vitro study | gene cluster | missense mutation | protein structure | creatine kinase BB | protein unfolding | regulatory mechanism | creatine kinase BB epsilon | conformational transition | disease activity | genetic susceptibility | human | point mutation | colon polyposis | gene structure | Wnt signaling pathway | human tissue | protein phosphorylation | article | Caenorhabditis elegans | protein secondary structure | alpha helix | controlled study | mutational analysis | nonhuman | protein degradation | INTRINSIC DISORDER | AXIN | APC | BETA-CATENIN DEGRADATION | ARMADILLO REPEAT DOMAIN | STRUCTURAL BASIS | PHOSPHORYLATION | CRYSTAL-STRUCTURE | MULTIDISCIPLINARY SCIENCES | TUMOR-SUPPRESSOR PROTEIN | SCAFFOLD PROTEINS | Adenomatous Polyposis Coli Protein - genetics | Phosphorylation | Protein Structure, Secondary | Signal Transduction | Protein Unfolding | Humans | Hot Temperature | Wnt Proteins - metabolism | Adenomatous Polyposis Coli - metabolism | Adenomatous Polyposis Coli Protein - chemistry | Point Mutation | Animals | Wnt Proteins - genetics | Proteolysis | Adenomatous Polyposis Coli Protein - metabolism | Mutation | Adenomatous Polyposis Coli - genetics | Polyposis, Familial | Genetic aspects | Gene mutations | Size exclusion chromatography | Wnt protein | Amino acids | Breast cancer | Secondary structure | Polyposis coli | Kinases | Chromatography | Cell adhesion & migration | Adenomatous polyposis coli | Proteins | Signaling | Missense mutation | Bioinformatics | Protein structure | Conformation
Journal Article
Journal Article
PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 7, p. e68072
Truncating mutations affect the adenomatous polyposis coli (APC) gene in most cases of colon cancer, resulting in the stabilization of beta-catenin and uncontrolled cell proliferation... 
WNT SIGNALING PATHWAY | COLORECTAL TUMORS | TRUNCATED APC | EPITHELIAL-CELLS | GENE | MUTATION CLUSTER REGION | MULTIDISCIPLINARY SCIENCES | TUMOR-SUPPRESSOR | IDENTIFICATION | SOMATIC MUTATIONS | DROSOPHILA | Adenomatous Polyposis Coli Protein - genetics | Protein Structure, Tertiary | Phosphorylation | Cytoskeletal Proteins - genetics | Humans | Rectum - metabolism | Transcriptional Activation | Gene Expression Regulation, Neoplastic | Cytoskeletal Proteins - chemistry | beta Catenin - metabolism | Colon - metabolism | beta Catenin - genetics | Adenomatous Polyposis Coli - metabolism | Genes, APC | Repetitive Sequences, Amino Acid | Proteolysis | Adenomatous Polyposis Coli Protein - metabolism | Cell Line, Tumor | Cytoskeletal Proteins - metabolism | Adenomatous Polyposis Coli - genetics | Adenomatous Polyposis Coli - chemistry | Amino acids | Polyposis, Familial | Genetic aspects | Colon cancer | Comparative analysis | Cell proliferation | Immunoprecipitation | Familial adenomatous polyposis | Colorectal cancer | Biology | Kinases | Polyposis coli | Cell adhesion & migration | Degradation | Proteins | β-catenin | Ubiquitination | Complementation | Colon | Adenomatous polyposis coli protein | RNA-mediated interference | Interference | Amino acid sequence | Tumor cell lines | Ribonucleic acid--RNA | Adenomatous polyposis coli | Medicine | Acids | Insects | Stem cells | Mutation | Tumors | Cancer | RNA | Ribonucleic acid
Journal Article
American journal of human genetics, ISSN 0002-9297, 2016, Volume 99, Issue 2, pp. 337 - 351
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2014, Volume 9, Issue 4, p. e94413
Wnt signalling is prevented by the proteosomal degradation of beta-catenin, which occurs in a destruction complex containing adenomatous polyposis coli (APC), APC-like (APCL), Axin and Axin2... 
WNT SIGNALING PATHWAY | COLORECTAL TUMORS | FUNCTIONAL INTERACTION | BETA-CATENIN DEGRADATION | DESTRUCTION COMPLEX | MUTATION CLUSTER REGION | MULTIDISCIPLINARY SCIENCES | APC TUMOR-SUPPRESSOR | GENE-PRODUCT | SOMATIC MUTATIONS | NEGATIVE REGULATOR | Phosphorylation | Epithelial Cells - metabolism | Axin Protein - genetics | Cytoskeletal Proteins - genetics | Humans | Protein Multimerization | Gene Expression Regulation, Neoplastic | Molecular Sequence Data | Adenomatous Polyposis Coli - pathology | Axin Protein - metabolism | Repetitive Sequences, Amino Acid | Cell Transformation, Neoplastic - genetics | HEK293 Cells | Cytoskeletal Proteins - metabolism | Adenomatous Polyposis Coli - genetics | Binding Sites | Adenomatous Polyposis Coli Protein - genetics | Protein Structure, Tertiary | Signal Transduction | Epithelial Cells - pathology | Cytoskeletal Proteins - chemistry | Cell Transformation, Neoplastic - metabolism | beta Catenin - metabolism | beta Catenin - genetics | Adenomatous Polyposis Coli - metabolism | Adenomatous Polyposis Coli Protein - chemistry | Sequence Alignment | Adenomatous Polyposis Coli Protein - metabolism | Cell Line, Tumor | Protein Binding | Cytoskeleton | Care and treatment | Colorectal cancer | Physiological aspects | Amino acids | Polyposis, Familial | Diagnosis | Risk factors | Wnt protein | Destruction | Serine | Kinases | Polyposis coli | Proteins | β-catenin | Cell growth | Colon cancer | Cell cycle | Tumorigenesis | Colon | Adenomatous polyposis coli protein | Amino acid sequence | Adenomatous polyposis coli | Medicine | Signaling | Acids | Mutation | Binding sites | Tumors
Journal Article