Bradford Willox
Brigham and Women's Hospital
4 Papers
Bradford Willox is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Promoter & Enhancer. The author has an hindex of 4, co-authored 4 publications.
Chat about Author
Papers
Epstein-Barr Virus Oncoprotein Super-enhancers Control B Cell Growth
Hufeng Zhou,Hufeng Zhou,Stefanie C.S. Schmidt,Stefanie C.S. Schmidt,Sizun Jiang,Sizun Jiang,Bradford Willox,Katharina Bernhardt,Katharina Bernhardt,Jun Liang,Jun Liang,Eric Johannsen,Peter V. Kharchenko,Benjamin E. Gewurz,Benjamin E. Gewurz,Elliott Kieff,Elliott Kieff,Bo Zhao,Bo Zhao +18 more
TL;DR: In insight into mechanisms of EBV-induced lymphoproliferation and potential therapeutic interventions, EBV super-enhancer-associated genes included the MYC and BCL2 oncogenes, which enable LCL proliferation and survival are provided.
179
The NF-κB genomic landscape in lymphoblastoid B cells.
Bo Zhao,Bo Zhao,Luis A. Barrera,Ina Ersing,Ina Ersing,Bradford Willox,Stefanie C.S. Schmidt,Stefanie C.S. Schmidt,Hannah Greenfeld,Hufeng Zhou,Hufeng Zhou,Sarah B. Mollo,Sarah B. Mollo,Tommy T. Shi,Kaoru Takasaki,Sizun Jiang,Sizun Jiang,Ellen Cahir-McFarland,Manolis Kellis,Martha L. Bulyk,Elliott Kieff,Elliott Kieff,Benjamin E. Gewurz,Benjamin E. Gewurz +23 more
TL;DR: A complex NF-κB-binding landscape was found, which did not readily reflect the two NF- κB pathway paradigms, and the oncogenic forkhead box protein FOXM1 co-occupied nearly half of NF-πA-binding sites and was identified in protein complexes with NF-σB on DNA.
Epstein–Barr virus nuclear antigen 3A partially coincides with EBNA3C genome-wide and is tethered to DNA through BATF complexes
Stefanie C.S. Schmidt,Sizun Jiang,Sizun Jiang,Hufeng Zhou,Hufeng Zhou,Bradford Willox,Amy M. Holthaus,Peter V. Kharchenko,Eric Johannsen,Elliott Kieff,Elliott Kieff,Bo Zhao,Bo Zhao +12 more
TL;DR: The data strongly support a model in which EBNA3A is tethered to DNA through a BATF-containing protein complexes to enable continuous cell proliferation in EBV-infected human lymphoblasts.
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 Zhou,Amy M. Holthaus,Anqi Wang,Tommy T. Shi,Seiji Maruo,Peter V. Kharchenko,Peter V. Kharchenko,Eric Johannsen,Elliott Kieff,Bo Zhao +11 more
TL;DR: 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 p14ARF and p16INK4A expression.