Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이수영 | * |
dc.contributor.author | 김재상 | * |
dc.date.accessioned | 2018-05-02T08:15:39Z | - |
dc.date.available | 2018-05-02T08:15:39Z | - |
dc.date.issued | 2004 | * |
dc.identifier.issn | 0021-9258 | * |
dc.identifier.other | OAK-2191 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/242761 | - |
dc.description.abstract | Nuclear factor-κB (NF-κB) is a transcription factor critical for key cellular processes, including immune response, apoptosis, and cell cycle progression. A yeast two-hybrid screening, using the Rel homology domain (RHD) of the p65 subunit (RelA) of NF-κB as bait, led to the isolation of PIAS3, previously identified as a specific inhibitor of STAT3. We show that PIAS3 can directly associate with p65 using an in vitro pull-down and in vivo coimmunoprecipitation assays. When overexpressed, PIAS3 inhibits NF-κB-dependent transcription induced by treatment with tumor necrosis factor α (TNF-α) or interleukin-1β or by overexpression of TNF family receptors such as RANK, TNFR1, and CD30 or signal transducers of TNF receptor-associated factors (TRAFs), including TRAF2, TRAF5, and TRAF6. Down-regulation of PIAS3 by RNA interference reverses its effect on TNF-α-mediated NF-κB activation. We found that an N-terminal region of PIAS3 is necessary for both the interaction with p65 and the transcriptional suppression activity. In addition, we found that an LXXLL coregulator signature motif located within the N-terminal region of PIAS3 is the minimal requirement for the interaction with p65. Furthermore, we demonstrate that PIAS3 interferes with p65 binding to the CBP coactivator, thereby resulting in a decreased NF-κB-dependent transcription. Taken together, these data suggest that PIAS3 may function in vivo as a modulator in suppressing the transcriptional activity of p65. | * |
dc.language | English | * |
dc.title | PIAS3 suppresses NF-κB-mediated transcription by interacting with the p65/RelA subunit | * |
dc.type | Article | * |
dc.relation.issue | 23 | * |
dc.relation.volume | 279 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 24873 | * |
dc.relation.lastpage | 24880 | * |
dc.relation.journaltitle | Journal of Biological Chemistry | * |
dc.identifier.doi | 10.1074/jbc.M313018200 | * |
dc.identifier.wosid | WOS:000221702500119 | * |
dc.identifier.scopusid | 2-s2.0-2642520591 | * |
dc.author.google | Jang H.D. | * |
dc.author.google | Yoon K. | * |
dc.author.google | Shin Y.J. | * |
dc.author.google | Kim J. | * |
dc.author.google | Lee S.Y. | * |
dc.contributor.scopusid | 이수영(53980218900;7409697278) | * |
dc.contributor.scopusid | 김재상(8643335800) | * |
dc.date.modifydate | 20240415140424 | * |