B Lymphocytes from Patients with a Hypomorphic Mutation in STAT3 Resist Epstein-Barr Virus-Driven Cell Proliferation
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Title
B Lymphocytes from Patients with a Hypomorphic Mutation in STAT3 Resist Epstein-Barr Virus-Driven Cell Proliferation
Authors
Keywords
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Journal
JOURNAL OF VIROLOGY
Volume 88, Issue 1, Pages 516-524
Publisher
American Society for Microbiology
Online
2013-10-31
DOI
10.1128/jvi.02601-13
References
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Related references
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- (2013) C. A. King JOURNAL OF VIROLOGY
- Autosomal Dominant STAT3 Deficiency and Hyper-IgE Syndrome
- (2012) Marie-Olivia Chandesris et al. MEDICINE
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- (2011) Abhik Saha et al. CANCER BIOLOGY & THERAPY
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- (2011) C.-P. Kung et al. JOURNAL OF VIROLOGY
- Signal transducer and activator of transcription 3 (STAT3) and survivin induction by varicella-zoster virus promote replication and skin pathogenesis
- (2011) N. Sen et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Identification of a sub-population of B cells that proliferates after infection with epstein-barr virus
- (2011) Cynthia Megyola et al. Virology Journal
- Epstein-Barr Virus Infection of Polarized Epithelial Cells via the Basolateral Surface by Memory B Cell-Mediated Transfer Infection
- (2011) Claire Shannon-Lowe et al. PLoS Pathogens
- Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines
- (2011) Joyce Hui-Yuen et al. Jove-Journal of Visualized Experiments
- B cell–intrinsic signaling through IL-21 receptor and STAT3 is required for establishing long-lived antibody responses in humans
- (2010) Danielle T. Avery et al. JOURNAL OF EXPERIMENTAL MEDICINE
- Transcription Profiling of Epstein-Barr Virus Nuclear Antigen (EBNA)-1 Expressing Cells Suggests Targeting of Chromatin Remodeling Complexes
- (2010) Ramakrishna Sompallae et al. PLoS One
- miR-34b Targets Cyclic AMP-Responsive Element Binding Protein in Acute Myeloid Leukemia
- (2009) M. Pigazzi et al. CANCER RESEARCH
- Upregulation of STAT3 Marks Burkitt Lymphoma Cells Refractory to Epstein-Barr Virus Lytic Cycle Induction by HDAC Inhibitors
- (2009) D. Daigle et al. JOURNAL OF VIROLOGY
- Features Distinguishing Epstein-Barr Virus Infections of Epithelial Cells and B Cells: Viral Genome Expression, Genome Maintenance, and Genome Amplification
- (2009) C. Shannon-Lowe et al. JOURNAL OF VIROLOGY
- Clinical Manifestations, Etiology, and Pathogenesis of the Hyper-IgE Syndromes
- (2009) Alexandra F Freeman et al. PEDIATRIC RESEARCH
- Early Events Associated with Infection of Epstein-Barr Virus Infection of Primary B-Cells
- (2009) Sabyasachi Halder et al. PLoS One
- AP-1 homolog BZLF1 of Epstein-Barr virus has two essential functions dependent on the epigenetic state of the viral genome
- (2009) M. Kalla et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Roles of unphosphorylated STATs in signaling
- (2008) Jinbo Yang et al. CELL RESEARCH
- Deficiency of Th17 cells in hyper IgE syndrome due to mutations inSTAT3
- (2008) Cindy S. Ma et al. JOURNAL OF EXPERIMENTAL MEDICINE
- Impaired TH17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome
- (2008) Joshua D. Milner et al. NATURE
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