The nuclear lamina binds the EBV genome during latency and regulates viral gene expression | PLOS Pathogens
CYB561A3 is the key lysosomal iron reductase required for Burkitt B-cell growth and survival - ScienceDirect
DNA methylation enzymes and PRC1 restrict B-cell Epstein–Barr virus oncoprotein expression | Nature Microbiology
Biomolecules | Free Full-Text | Stress-Induced Epstein-Barr Virus Reactivation | HTML
EBV latency gene expression in different latency states. This figure... | Download Scientific Diagram
Epstein–Barr virus oncoprotein–driven B cell metabolism remodeling | PLOS Pathogens
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Epstein–Barr virus latency programs dynamically sensitize B cells to ferroptosis | PNAS
IKKα-Mediated Noncanonical NF-κB Signaling Is Required To Support Murine Gammaherpesvirus 68 Latency In Vivo | Journal of Virology
Ben Gewurz on Twitter: "(5/6) By contrast, latency I Burkitt B cells were particularly vulnerable to ferroptosis induction by blockade of either cystine import, glutathione synthesis or glutathione peroxidase 4 (GPX4). Eric
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See @BenGewurz's Tweet on Twitter / Twitter
1 Establishment of EBV latency in memory B cells of the peripheral... | Download Scientific Diagram
MYC Controls the Epstein-Barr Virus Lytic Switch - ScienceDirect
UHRF1 maintains EBV latency promotor methylation a, Schematic diagram... | Download Scientific Diagram
ICF, the missing ingredient of TF-IDF | by Ori Abramovsky | CodeX | Medium
Benjamin Gewurz | Harvard Catalyst Profiles | Harvard Catalyst
IKKα-Mediated Noncanonical NF-κB Signaling Is Required To Support Murine Gammaherpesvirus 68 Latency In Vivo | Journal of Virology
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EBV latency types found in EBV-driven malignancies. Cell morphology... | Download Scientific Diagram
Ben Gewurz on Twitter: "(5/6) By contrast, latency I Burkitt B cells were particularly vulnerable to ferroptosis induction by blockade of either cystine import, glutathione synthesis or glutathione peroxidase 4 (GPX4). Eric
Frontiers | Immune Landscape of CMV Infection in Cancer Patients: From “Canonical” Diseases Toward Virus-Elicited Oncomodulation
