| http://purl.uniprot.org/citations/12972599 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12972599 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12972599 | http://www.w3.org/2000/01/rdf-schema#comment | "Csn2 (Trip15/Cops2/Alien) encodes the second subunit of the COP9 signalosome (CSN), an eight-subunit heteromeric complex homologous to the lid subcomplex of the 26S proteasome. CSN is a regulator of SCF (Skp1-cullin-F-box protein)ubiquitin ligases, mostly through the enzymatic activity that deconjugates the ubiquitin-like protein Nedd8 from the SCF Cul1 component. In addition, CSN associates with protein kinase activities targeting p53, c-Jun, and IkappaB for phosphorylation. Csn2 also interacts with and regulates a subset of nuclear hormone receptors and is considered a novel corepressor. We report that targeted disruption of Csn2 in mice caused arrest of embryo development at the peri-implantation stage. Csn2(-/-) blastocysts failed to outgrow in culture and exhibited a cell proliferation defect in inner cell mass, accompanied by a slight decrease in Oct4. In addition, lack of Csn2 disrupted the CSN complex and resulted in a drastic increase in cyclin E, supporting a role for CSN in cooperating with the SCF-ubiquitin-proteasome system to regulate protein turnover. Furthermore, Csn2(-/-) embryos contained elevated levels of p53 and p21, which may contribute to premature cell cycle arrest of the mutant."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.org/dc/terms/identifier | "doi:10.1128/mcb.23.19.6790-6797.2003"xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.org/dc/terms/identifier | "doi:10.1128/mcb.23.19.6790-6797.2003"xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/author | "Menon S."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/author | "Menon S."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/author | "Deng X.-W."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/author | "Deng X.-W."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/author | "Lykke-Andersen K."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/author | "Lykke-Andersen K."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/author | "Wei N."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/author | "Wei N."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/author | "Schaefer L."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/author | "Schaefer L."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/author | "Miller J.B."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/author | "Miller J.B."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/name | "Mol. Cell. Biol."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/name | "Mol. Cell. Biol."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/pages | "6790-6797"xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/pages | "6790-6797"xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/title | "Disruption of the COP9 signalosome Csn2 subunit in mice causes deficient cell proliferation, accumulation of p53 and cyclin E, and early embryonic death."xsd:string |
| http://purl.uniprot.org/citations/12972599 | http://purl.uniprot.org/core/title | "Disruption of the COP9 signalosome Csn2 subunit in mice causes deficient cell proliferation, accumulation of p53 and cyclin E, and early embryonic death."xsd:string |