| http://purl.uniprot.org/citations/28687276 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/28687276 | http://www.w3.org/2000/01/rdf-schema#comment | "Nuclear factor-κB (NF-κB) participates in apoptosis signaling pathway under various pathophysiological conditions. It exerts transcriptional control on the anti-apoptotic Bcl-2 family, such as Bcl-2, Bcl-xl, and Mcl-1, which act on the mitochondrial outer membrane. Previously, we described that NF-κB is negatively regulated by diacylglycerol kinase ζ (DGKζ), an enzyme that phosphorylates a lipid second messenger diacylglycerol. DGKζ downregulation enhances inhibitors of NF-κB α (IκBα) degradation and p65 subunit phosphorylation, leading to enhanced NF-κB transcriptional activity. Transcriptional machinery is tightly regulated by assembly/disassembly and modification of nucleosomal components. Of those, the human NAP1-like protein (NAP1L) family functions in the transport, assembly/disassembly of nucleosome core particles. We previously identified NAP1L1 and NAP1L4 as novel DGKζ binding partners, but the mechanism by which NAP1Ls are involved in NF-κB signaling pathway remains unclear. Here we show that knockdown of NAP1L1 suppresses IκBα degradation and nuclear transport of p65 subunit after treatment with TNF-α stimulation, leading to attenuation of the NF-κB transcriptional activity, whereas NAP1L4 knockdown remains silent. Moreover, ChIP assay reveals that NAP1L1 knockdown attenuates p65 binding to the Mcl-1 promoter after TNF-α stimulation. This attenuation leads to reduced expression of anti-apoptotic Mcl-1, thereby decreasing the mitochondrial membrane potential and subsequent apoptosis after treatment with TNF-α and CHX. Collectively, results of this study suggest that NAP1L1 downregulation renders the cell vulnerable to apoptotic cell death through attenuation of NF-κB transcriptional activity on the anti-apoptotic Mcl-1 gene."xsd:string |
| http://purl.uniprot.org/citations/28687276 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbamcr.2017.06.021"xsd:string |
| http://purl.uniprot.org/citations/28687276 | http://purl.uniprot.org/core/author | "Goto K."xsd:string |
| http://purl.uniprot.org/citations/28687276 | http://purl.uniprot.org/core/author | "Tanaka T."xsd:string |
| http://purl.uniprot.org/citations/28687276 | http://purl.uniprot.org/core/author | "Iino M."xsd:string |
| http://purl.uniprot.org/citations/28687276 | http://purl.uniprot.org/core/author | "Hozumi Y."xsd:string |
| http://purl.uniprot.org/citations/28687276 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/28687276 | http://purl.uniprot.org/core/name | "Biochim Biophys Acta Mol Cell Res"xsd:string |
| http://purl.uniprot.org/citations/28687276 | http://purl.uniprot.org/core/pages | "1759-1768"xsd:string |
| http://purl.uniprot.org/citations/28687276 | http://purl.uniprot.org/core/title | "NAP1L1 regulates NF-kappaB signaling pathway acting on anti-apoptotic Mcl-1 gene expression."xsd:string |
| http://purl.uniprot.org/citations/28687276 | http://purl.uniprot.org/core/volume | "1864"xsd:string |
| http://purl.uniprot.org/citations/28687276 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/28687276 |
| http://purl.uniprot.org/citations/28687276 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/28687276 |
| http://purl.uniprot.org/uniprot/#_A0A087WT64-mappedCitation-28687276 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28687276 |
| http://purl.uniprot.org/uniprot/#_A0A087X0W8-mappedCitation-28687276 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28687276 |
| http://purl.uniprot.org/uniprot/#_Q07820-mappedCitation-28687276 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28687276 |
| http://purl.uniprot.org/uniprot/#_A8CGI3-mappedCitation-28687276 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28687276 |
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| http://purl.uniprot.org/uniprot/#_B4DS05-mappedCitation-28687276 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28687276 |
| http://purl.uniprot.org/uniprot/#_B7Z4K9-mappedCitation-28687276 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28687276 |
| http://purl.uniprot.org/uniprot/#_B4DU51-mappedCitation-28687276 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28687276 |
| http://purl.uniprot.org/uniprot/#_B4E3L8-mappedCitation-28687276 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28687276 |
| http://purl.uniprot.org/uniprot/#_B4E082-mappedCitation-28687276 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28687276 |
| http://purl.uniprot.org/uniprot/#_B4DLY8-mappedCitation-28687276 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28687276 |