Epstein–Barr Virus Nuclear Antigen 3C binds to BATF/IRF4 or SPI1/IRF4 composite sites and recruits Sin3A to repress CDKN2A

Sizun Jiang; Bradford Willox; Hufeng ZhouAmy M. HolthausAnqi WangTommy T. ShiSeiji MaruoPeter V. KharchenkoEric C. JohannsenElliott KieffBo Zhao

首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Epstein–Barr Virus Nuclear Antigen 3C binds to BATF/IRF4 or SPI1/IRF4 composite sites and recruits Sin3A to repress CDKN2A

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Epstein–Barr Virus Nuclear Antigen 3C binds to BATF/IRF4 or SPI1/IRF4 composite sites and recruits Sin3A to repress CDKN2A

机译：Epstein–Barr Virus Nuclear Antigen 3C binds to BATF/IRF4 or SPI1/IRF4 composite sites and recruits Sin3A to repress CDKN2A

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Epstein–Barr virus nuclear antigen 3C (EBNA3C) repression of CDKN2A p14~(ARF) and p16~(INK4A) is essential for immortal human B-lymphoblastoid cell line (LCL) growth. EBNA3C ChIP-sequencing identified >13,000 EBNA3C sites in LCL DNA. Most EBNA3C sites were associated with active transcription; 64 were strong H3K4me1- and H3K27ac-marked enhancers and 16 were active promoters marked by H3K4me3 and H3K9ac. Using ENCODE LCL transcription factor ChIP-sequencing data, EBNA3C sites coincided (±250 bp) with RUNX3 (64), BATF (55), ATF2 (51), IRF4 (41), MEF2A (35), PAX5 (34), SPI1 (29), BCL11a (28), SP1 (26), TCF12 (23), NF-κB (23), POU2F2 (23), and RBPJ (16). EBNA3C sites separated into five distinct clusters: (i) Sin3A, (ii) EBNA2/RBPJ, (iii) SPI1, and (iv) strong or (v) weak BATF/IRF4. EBNA3C signals were positively affected by RUNX3, BATF/IRF4 (AICE) and SPI1/IRF4 (EICE) cooccupancy. Gene set enrichment analyses correlated EBNA3C/Sin3A promoter sites with transcription down-regulation (P < 1.6 × 10~(?4)). EBNA3C signals were strongest at BATF/IRF4 and SPI1/IRF4 composite sites. EBNA3C bound strongly to the p14~(ARF) promoter through SPI1/IRF4/BATF/RUNX3, establishing RBPJ-, Sin3A-, and REST-mediated repression. EBNA3C immune precipitated with Sin3A and conditional EBNA3C inactivation significantly decreased Sin3A binding at the p14~(ARF) promoter (P < 0.05). These data support a model in which EBNA3C binds strongly to BATF/IRF4/SPI1/RUNX3 sites to enhance transcription and recruits RBPJ/Sin3A- and REST/ NRSF-repressive complexes to repress p14~(ARF) and p16~(INK4A) expression.

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《Proceedings of the National Academy of Sciences of the United States of America》 |2014年第1期|421-426|共6页
作者
Sizun Jiang; Bradford Willox; Hufeng ZhouAmy M. HolthausAnqi WangTommy T. ShiSeiji MaruoPeter V. KharchenkoEric C. JohannsenElliott KieffBo Zhao;
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作者单位

Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115;

Department of Medicine and McArdle Laboratory for Cancer Research, University of Wisconsin–Madison, Madison, WI 53706;

Department of Tumor Virology, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, JapanCenter for Biomedical Informatics, Harvard Medical School, Boston, MA 02115;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种英语
中图分类自然科学总论;
关键词
EBV; tumor suppressor; resting B lymphocyte; lymphoma;

Epstein–Barr Virus Nuclear Antigen 3C binds to BATF/IRF4 or SPI1/IRF4 composite sites and recruits Sin3A to repress CDKN2A

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