http://purl.uniprot.org/citations/11781828 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/11781828 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/11781828 | http://www.w3.org/2000/01/rdf-schema#comment | "RelB is an unusual member of the Rel/NF-kappaB family of transcription factors which are involved in oncogenic processes. Due to a relaxed control by the IkappaBs, the cytosolic NF-kappaB inhibitors, RelB is constitutively expressed in the nuclei of lymphoid cells. We show here that RelB is inducibly degraded upon activation of T cells in a fashion similar to the IkappaBs. However, RelB degradation differs from that of IkappaBs since it is not induced by TNFalpha but only by T cell receptor or TPA/ionomycin stimulation. Moreover, RelB degradation occurs in three steps: (i) after stimulation RelB is rapidly phosphorylated at amino acids Thr84 and Ser552 followed by (ii) an N-terminal cut and, finally, (iii) the complete degradation in the proteasomes. Since mutation of the two phosphoacceptor sites to non-acceptor sites abolished RelB phosphorylation in vivo and led to the stabilization of the mutated RelB(DM), site-specific phosphorylation appears to be a necessary prerequisite for RelB degradation. RelB is a crucial regulator of NF-kappaB-dependent gene expression. Thus, the signal-induced degradation of RelB should be an important control mechanism of NF-kappaB activity."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.org/dc/terms/identifier | "doi:10.1038/sj.onc.1204884"xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.org/dc/terms/identifier | "doi:10.1038/sj.onc.1204884"xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/author | "Neumann M."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/author | "Neumann M."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/author | "Berberich-Siebelt F."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/author | "Berberich-Siebelt F."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/author | "Berberich I."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/author | "Berberich I."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/author | "Serfling E."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/author | "Serfling E."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/author | "Marienfeld R."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/author | "Marienfeld R."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/author | "Denk A."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/author | "Denk A."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/date | "2001"xsd:gYear |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/date | "2001"xsd:gYear |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/name | "Oncogene"xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/name | "Oncogene"xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/pages | "8142-8147"xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/pages | "8142-8147"xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/title | "Signal-specific and phosphorylation-dependent RelB degradation: a potential mechanism of NF-kappaB control."xsd:string |
http://purl.uniprot.org/citations/11781828 | http://purl.uniprot.org/core/title | "Signal-specific and phosphorylation-dependent RelB degradation: a potential mechanism of NF-kappaB control."xsd:string |