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The NF-κB genomic landscape in lymphoblastoid B cells.
Zhao, Bo; Barrera, Luis A; Ersing, Ina; Willox, Bradford; Schmidt, Stefanie C S; Greenfeld, Hannah; Zhou, Hufeng; Mollo, Sarah B; Shi, Tommy T; Takasaki, Kaoru; Jiang, Sizun; Cahir-McFarland, Ellen; Kellis, Manolis; Bulyk, Martha L; Kieff, Elliott; Gewurz, Benjamin E.
Afiliación
  • Zhao B; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
  • Barrera LA; Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Committee on Higher Degrees in Biophysics, Harvard University, Cambridge, MA 02138, USA; Harvard-MIT Division of Health Sciences and Technology, Harvard M
  • Ersing I; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
  • Willox B; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
  • Schmidt SC; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
  • Greenfeld H; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
  • Zhou H; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
  • Mollo SB; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
  • Shi TT; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
  • Takasaki K; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
  • Jiang S; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
  • Cahir-McFarland E; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
  • Kellis M; Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Bulyk ML; Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Committee on Higher Degrees in Biophysics, Harvard University, Cambridge, MA 02138, USA; Harvard-MIT Division of Health Sciences and Technology, Harvard M
  • Kieff E; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
  • Gewurz BE; Division of Infectious Disease, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: bgewurz@partners.org.
Cell Rep ; 8(5): 1595-606, 2014 Sep 11.
Article en En | MEDLINE | ID: mdl-25159142
The nuclear factor κB (NF-κΒ) subunits RelA, RelB, cRel, p50, and p52 are each critical for B cell development and function. To systematically characterize their responses to canonical and noncanonical NF-κB pathway activity, we performed chromatin immunoprecipitation followed by high-throughput DNA sequencing (ChIP-seq) analysis in lymphoblastoid B cell lines (LCLs). We found a complex NF-κB-binding landscape, which did not readily reflect the two NF-κB pathway paradigms. Instead, 10 subunit-binding patterns were observed at promoters and 11 at enhancers. Nearly one-third of NF-κB-binding sites lacked κB motifs and were instead enriched for alternative motifs. The oncogenic forkhead box protein FOXM1 co-occupied nearly half of NF-κB-binding sites and was identified in protein complexes with NF-κB on DNA. FOXM1 knockdown decreased NF-κB target gene expression and ultimately induced apoptosis, highlighting FOXM1 as a synthetic lethal target in B cell malignancy. These studies provide a resource for understanding mechanisms that underlie NF-κB nuclear activity and highlight opportunities for selective NF-κB blockade.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Linfocitos B / Genoma Humano / FN-kappa B / Elementos de Facilitación Genéticos / Redes Reguladoras de Genes Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Cell Rep Año: 2014 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Linfocitos B / Genoma Humano / FN-kappa B / Elementos de Facilitación Genéticos / Redes Reguladoras de Genes Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Cell Rep Año: 2014 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos