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http://purl.uniprot.org/citations/20060811http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20060811http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20060811http://www.w3.org/2000/01/rdf-schema#comment"The endoplasmic reticulum (ER) emanates context-dependent signals, thereby mediating cellular response to a variety of stresses. However, the underlying molecular mechanisms have been enigmatic. To better understand the signaling capacity of the ER, we focused on roles played by mitsugumin23 (MG23), a protein residing predominantly in this organelle. Overexpression of MG23 in human embryonic kidney 293T cells specifically enhanced apoptosis triggered by etoposide, a DNA-damaging anti-cancer drug. Conversely, genetic deletion of MG23 reduced susceptibility of thymocytes to DNA damage-induced apoptosis, which was demonstrated by whole-body irradiation experiments. In this setting, induction of the tumor-suppressor gene p53 was attenuated in MG23-knockout thymocytes as compared with their wild-type counterparts, consistent with the elevated radioresistance. It is therefore suggested that MG23 is an essential component of ER-generated lethal signals provoked upon DNA damage, specifying cell fate under pathophysiological conditions."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.org/dc/terms/identifier"doi:10.1016/j.bbrc.2010.01.013"xsd:string
http://purl.uniprot.org/citations/20060811http://purl.org/dc/terms/identifier"doi:10.1016/j.bbrc.2010.01.013"xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/author"Sasaki N."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/author"Sasaki N."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/author"Takeshima H."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/author"Takeshima H."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/author"Yamazaki T."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/author"Yamazaki T."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/author"Nishi M."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/author"Nishi M."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/name"Biochem. Biophys. Res. Commun."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/name"Biochem. Biophys. Res. Commun."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/pages"196-200"xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/pages"196-200"xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/title"Facilitation of DNA damage-induced apoptosis by endoplasmic reticulum protein mitsugumin23."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/title"Facilitation of DNA damage-induced apoptosis by endoplasmic reticulum protein mitsugumin23."xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/volume"392"xsd:string
http://purl.uniprot.org/citations/20060811http://purl.uniprot.org/core/volume"392"xsd:string
http://purl.uniprot.org/citations/20060811http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/20060811
http://purl.uniprot.org/citations/20060811http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/20060811