Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 정희용 | - |
dc.date.accessioned | 2018-03-23T05:25:57Z | - |
dc.date.available | 2018-03-23T05:25:57Z | - |
dc.date.issued | 2014-11 | - |
dc.identifier.citation | JOURNAL OF CLINICAL INVESTIGATION, 권: 124, 호: 11, 페이지: 4976-4988 | en_US |
dc.identifier.issn | 0021-9738 | - |
dc.identifier.issn | 1558-8238 | - |
dc.identifier.uri | https://www.jci.org/articles/view/75667 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/51271 | - |
dc.description.abstract | The signai-responsive E3 ubiquitin ligase pellino 1 (PELI1) regulates TLR and T cell receptor (TCR) signaling and contributes to the maintenance of autoimmunity; however, little is known about the consequence of mutations that result in upregulation of PELI1. Here, we developed transgenic mice that constitutively express human PELI1 and determined that these mice have a shorter lifespan due to tumor formation. Constitutive expression of PEW resulted in ligand-independent hyperactivation of B cells and facilitated the development of a wide range of lymphoid tumors, with prominent B cell infiltration observed across multiple organs. PELI1 directly interacted with the oncoprotein B cell chronic lymphocytic leukemia (BCL6) and induced lysine 63-mediated BCL6 polyubiquitination. In samples from patients with diffuse large B-cell lymphomas (DLBCLs), PELI1 expression levels positively correlated with BCL6 expression, and PELI1 overexpression was closely associated with poor prognosis in DLBCLs. Together:these results suggest that increased PELI1 expression and subsequent induction of BCL6 promotes lymphomagenesis and that this pathway may be a potential target for therapeutic strategies to treat B cell lymphomas. | en_US |
dc.description.sponsorship | We thank Tae-Jin Kim, Myung Soo Kang, and Hong Tae Kim (Sungkyunkwan University) for providing materials and the Samsung Biomedical Research Institute for providing equipment, technical assistance, and financial support. This study was supported by National Research Foundation grants funded by the Korean government (MEST; 2011-0030043 and 2012M3A9A8053102) and by research grant no. 1220220 from the National R&D Program for Cancer Control, Ministry of Health and Welfare, Republic of Korea. | en_US |
dc.language.iso | en | en_US |
dc.publisher | AMER SOC CLINICAL INVESTIGATION INC, 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA | en_US |
dc.subject | TOLL-LIKE RECEPTORS | en_US |
dc.title | Pellino 1 promotes lymphomagenesis by deregulating BCL6 polyubiquitination | en_US |
dc.type | Article | en_US |
dc.relation.no | 11 | - |
dc.relation.volume | 124 | - |
dc.identifier.doi | 10.1172/JCI75667 | - |
dc.relation.page | 4976-4988 | - |
dc.relation.journal | JOURNAL OF CLINICAL INVESTIGATION | - |
dc.contributor.googleauthor | Park, Hye-Young | - |
dc.contributor.googleauthor | Go, Heounjeong | - |
dc.contributor.googleauthor | Song, Ha Rim | - |
dc.contributor.googleauthor | Kim, Suhyeon | - |
dc.contributor.googleauthor | Ha, Geun-Hyoung | - |
dc.contributor.googleauthor | Jeon, Yoon-Kyung | - |
dc.contributor.googleauthor | Kim, Ji-Eun | - |
dc.contributor.googleauthor | Lee, Ho | - |
dc.contributor.googleauthor | Cho, Hyeseong | - |
dc.contributor.googleauthor | Chung, Hee-Young | - |
dc.relation.code | 2014032716 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | hychung | - |
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