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Regulation of inflammatory signaling by TBL1/TBLR1

DC FieldValueLanguage
dc.contributor.author이미희-
dc.date.accessioned2015-12-24T08:49:31Z-
dc.date.available2015-12-24T08:49:31Z-
dc.date.issued2012-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/134308-
dc.descriptionDept. of Medical Science/석사-
dc.description.abstractDysregulation of inflammatory signaling has been implicated in the development of human diseases. Nuclear factor κB (NF-κB) plays a key role in regulating inflammatory signaling through controlling the NF-κB target genes. Recently, the formation of NF-κB and transducin β-like protein (TBL1) complex upon tumor necrosis factor-alpha (TNF-α) has been reported; however, little is known about how the corepressor TBL1 activates NF-κB function. Here, we show that both TBL1 and its related protein (TBLR1) are SUMOylated in a NF-κB mediated inflammatory signaling-dependent manner, and this modification is selectively reversed by SUMO-specific protease I (SENP1). SUMOylation of TBL1-TBLR1 increased the expression of NF-κB target genes by interacting with NF-κB and consequently led to activation of NF-κB-mediated inflammation. Conversely, SENP1 inhibited SUMOylation of TBL1-TBLR1, leading to reduction of NF-κB-mediated transcription. Finally, knockdown of TBL1 greatly impaired the production of interleukin (IL)-1beta, IL-6, and IL-8 in androgen-independent prostate cancer, PC-3 cells. Thus, our data reveal a mechanism for regulation of NF-κB mediated inflammation signal via the reversible SUMOylation of TBL1 and TBLR1.-
dc.description.statementOfResponsibilityprohibition-
dc.publisherGraduate School, Yonsei University-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleRegulation of inflammatory signaling by TBL1/TBLR1-
dc.title.alternativeTBL1/TBLR1에 의한 염증 신호 체계 조절 규명-
dc.typeThesis-
dc.contributor.alternativeNameLee, Mee Hee-
dc.type.localThesis-
Appears in Collections:
1. College of Medicine (의과대학) > Others (기타) > 2. Thesis

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