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  • 1
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    Functional genomic analysis of the Wnt-wingless signaling pathway (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-09
    Description: The Wnt-Wingless (Wg) pathway is one of a core set of evolutionarily conserved signaling pathways that regulates many aspects of metazoan development. Aberrant Wnt signaling has been linked to human disease. In the present study, we used a genomewide RNA interference (RNAi) screen in Drosophila cells to screen for regulators of the Wnt pathway. We identified 238 potential regulators, which include known pathway components, genes with functions not previously linked to this pathway, and genes with no previously assigned functions. Reciprocal-Best-Blast analyses reveal that 50% of the genes identified in the screen have human orthologs, of which approximately 18% are associated with human disease. Functional assays of selected genes from the cell-based screen in Drosophila, mammalian cells, and zebrafish embryos demonstrated that these genes have evolutionarily conserved functions in Wnt signaling. High-throughput RNAi screens in cultured cells, followed by functional analyses in model organisms, prove to be a rapid means of identifying regulators of signaling pathways implicated in development and disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DasGupta, Ramanuj -- Kaykas, Ajamete -- Moon, Randall T -- Perrimon, Norbert -- New York, N.Y. -- Science. 2005 May 6;308(5723):826-33. Epub 2005 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Howard Hughes Medical Institute (HHMI), Harvard Medical School, New Research Building, No. 339, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. rdasgupt@genetics.med.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15817814" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Line ; Cloning, Molecular ; Computational Biology ; Cytoskeletal Proteins/metabolism ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/*genetics/metabolism ; Embryo, Nonmammalian/metabolism ; Embryonic Development ; Epistasis, Genetic ; *Gene Expression Regulation ; Genes, Insect ; Genes, Reporter ; *Genomics ; Mutation ; Phenotype ; Phosphorylation ; Protein Kinases/metabolism ; Proteins/metabolism ; Proto-Oncogene Proteins/genetics/*metabolism ; *RNA Interference ; *Signal Transduction ; Trans-Activators/metabolism ; Transcription Factors/chemistry/genetics/metabolism ; Transfection ; Wnt Proteins ; Wnt1 Protein ; Wnt3 Protein ; Zebrafish ; Zebrafish Proteins ; beta Catenin ; rab5 GTP-Binding Proteins/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Wilms tumor suppressor WTX negatively regulates WNT/beta-catenin signaling (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-19
    Description: Aberrant WNT signal transduction is involved in many diseases. In colorectal cancer and melanoma, mutational disruption of proteins involved in the degradation of beta-catenin, the key effector of the WNT signaling pathway, results in stabilization of beta-catenin and, in turn, activation of transcription. We have used tandem-affinity protein purification and mass spectrometry to define the protein interaction network of the beta-catenin destruction complex. This assay revealed that WTX, a protein encoded by a gene mutated in Wilms tumors, forms a complex with beta-catenin, AXIN1, beta-TrCP2 (beta-transducin repeat-containing protein 2), and APC (adenomatous polyposis coli). Functional analyses in cultured cells, Xenopus, and zebrafish demonstrate that WTX promotes beta-catenin ubiquitination and degradation, which antagonize WNT/beta-catenin signaling. These data provide a possible mechanistic explanation for the tumor suppressor activity of WTX.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Major, Michael B -- Camp, Nathan D -- Berndt, Jason D -- Yi, Xianhua -- Goldenberg, Seth J -- Hubbert, Charlotte -- Biechele, Travis L -- Gingras, Anne-Claude -- Zheng, Ning -- Maccoss, Michael J -- Angers, Stephane -- Moon, Randall T -- New York, N.Y. -- Science. 2007 May 18;316(5827):1043-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Washington School of Medicine, Box 357370, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17510365" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adenomatous Polyposis Coli Protein/metabolism ; Animals ; Axin Protein ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; Genes, Wilms Tumor ; Humans ; Kidney Neoplasms/genetics ; Protein Binding ; Protein Interaction Mapping ; Proteomics ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/metabolism ; *Signal Transduction ; Transduction, Genetic ; Tumor Suppressor Proteins/chemistry/genetics/*metabolism ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Wilms Tumor/genetics ; Wnt Proteins/*metabolism ; Xenopus Proteins ; Zebrafish ; beta Catenin/*metabolism ; beta-Transducin Repeat-Containing Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Wnt5a control of cell polarity and directional movement by polarized redistribution of adhesion receptors (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-19
    Description: Mechanisms by which Wnt pathways integrate the organization of receptors, organelles, and cytoskeletal proteins to confer cell polarity and directional cell movement are incompletely understood. We show that acute responses to Wnt5a involve recruitment of actin, myosin IIB, Frizzled 3, and melanoma cell adhesion molecule into an intracellular structure in a melanoma cell line. In the presence of a chemokine gradient, this Wnt-mediated receptor-actin-myosin polarity (W-RAMP) structure accumulates asymmetrically at the cell periphery, where it triggers membrane contractility and nuclear movement in the direction of membrane retraction. The process requires endosome trafficking, is associated with multivesicular bodies, and is regulated by Wnt5a through the small guanosine triphosphatases Rab4 and RhoB. Thus, cell-autonomous mechanisms allow Wnt5a to control cell orientation, polarity, and directional movement in response to positional cues from chemokine gradients.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229220/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229220/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Witze, Eric S -- Litman, Elizabeth S -- Argast, Gretchen M -- Moon, Randall T -- Ahn, Natalie G -- F32-CA105796/CA/NCI NIH HHS/ -- F32-CA112847/CA/NCI NIH HHS/ -- R01 CA118972/CA/NCI NIH HHS/ -- R01 CA118972-01A2/CA/NCI NIH HHS/ -- R01 CA118972-02/CA/NCI NIH HHS/ -- R01-CA118972/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 18;320(5874):365-9. doi: 10.1126/science.1151250.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of Colorado, Boulder, CO80309, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18420933" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Antigens, CD146/metabolism ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cell Movement ; *Cell Polarity ; Chemokine CXCL12/metabolism ; Chemotaxis ; Endosomes/metabolism ; Golgi Apparatus/metabolism ; Humans ; Melanoma/*metabolism/pathology ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Nonmuscle Myosin Type IIB/metabolism ; Proto-Oncogene Proteins/*metabolism ; *Signal Transduction ; Transplantation, Heterologous ; Wnt Proteins/*metabolism ; rab4 GTP-Binding Proteins/metabolism ; rhoB GTP-Binding Protein/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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