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http://purl.uniprot.org/citations/25169422http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25169422http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25169422http://www.w3.org/2000/01/rdf-schema#comment"Previously, it has been reported that HN1 is involved in cytoplasmic retention and degradation of androgen receptor in an AKT dependent manner. As HN1 is a hormone inducible gene, and has been shown that it is upregulated in various cancers, we studied the importance of HN1 function in β-catenin signaling in prostate cancer cell line, PC-3 and mammary cancer cell line MDA-MB231. Here, we demonstrated that HN1 physically associates with GSK3β/β-catenin destruction complex and abundantly localizes to cytoplasm, especially when the GSK3β is phosphorylated on S9 residue. Further, ectopic HN1 expression results an increase in the β-catenin degradation leading to loss of E-cadherin interaction, concurrently contributing to actin re-organization, colony formation and migration in cancer cell lines. Thus, we report that HN1 is an essential factor for β-catenin turnover and signaling, augments cell growth and migration in prostate cancer cells."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.org/dc/terms/identifier"doi:10.1002/jcb.24956"xsd:string
http://purl.uniprot.org/citations/25169422http://purl.org/dc/terms/identifier"doi:10.1002/jcb.24956"xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/author"Akyuz G.K."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/author"Akyuz G.K."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/author"Korkmaz K.S."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/author"Korkmaz K.S."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/author"Ozturk B.E."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/author"Ozturk B.E."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/author"Varisli L."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/author"Varisli L."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/name"J. Cell. Biochem."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/name"J. Cell. Biochem."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/pages"170-178"xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/pages"170-178"xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/title"HN1 negatively influences the beta-catenin/E-cadherin interaction, and contributes to migration in prostate cells."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/title"HN1 negatively influences the beta-catenin/E-cadherin interaction, and contributes to migration in prostate cells."xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/volume"116"xsd:string
http://purl.uniprot.org/citations/25169422http://purl.uniprot.org/core/volume"116"xsd:string
http://purl.uniprot.org/citations/25169422http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25169422
http://purl.uniprot.org/citations/25169422http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25169422