G
Gretchen L. Bentz
Researcher at University of North Carolina at Chapel Hill
Publications - 16
Citations - 1454
Gretchen L. Bentz is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Human cytomegalovirus & Monocyte. The author has an hindex of 14, co-authored 16 publications receiving 1290 citations. Previous affiliations of Gretchen L. Bentz include Mercer University & LSU Health Sciences Center Shreveport.
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Journal ArticleDOI
Exosomal HIF1α supports invasive potential of nasopharyngeal carcinoma-associated LMP1-positive exosomes.
Mitsuharu Aga,Gretchen L. Bentz,Salvatore Raffa,Maria Rosaria Torrisi,Satoru Kondo,Naohiro Wakisaka,Tomokazu Yoshizaki,Joseph S. Pagano,Julia Shackelford +8 more
TL;DR: It is hypothesized that exosome-mediated transfer of functional pro-metastatic factors by LMP1-positive NPC cells to surrounding tumor cells promotes cancer progression and is provided evidence that HIF1α itself participates in exosomes-mediated pro- Metastatic effects in recipient cells.
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Human Cytomegalovirus Induces Monocyte Differentiation and Migration as a Strategy for Dissemination and Persistence
TL;DR: It is reported that primary HCMV infection of monocytes induces transendothelial migration and monocyte-to-macrophage differentiation and that these HCMVs-differentiated macrophages are productive for viral replication.
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Human cytomegalovirus (HCMV) infection of endothelial cells promotes naive monocyte extravasation and transfer of productive virus to enhance hematogenous dissemination of HCMV.
Gretchen L. Bentz,Marta Jarquin-Pardo,Gary Chan,M. Shane Smith,Christian Sinzger,Andrew D. Yurochko +5 more
TL;DR: It is shown that HCMV infection of endothelial cells increased the recruitment and transendothelial migration of monocytes and the migrating monocytes were productively infected with the virus, providing evidence for an active role of the infected endothelium in H CMV dissemination and pathogenesis.
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Human CMV infection of endothelial cells induces an angiogenic response through viral binding to EGF receptor and β1 and β3 integrins
TL;DR: Because a proangiogenic response drives the neovascularization observed in atherosclerotic disease, the findings identify a possible mechanism for how HCMV infection contributes to vascular disease.
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TRAF6 and the Three C-Terminal Lysine Sites on IRF7 Are Required for Its Ubiquitination-Mediated Activation by the Tumor Necrosis Factor Receptor Family Member Latent Membrane Protein 1
TL;DR: The last three C-terminal lysine sites of human IRF7 variant A are determined to be essential for activation of IRF9 and support the hypothesis that regulatory ubiquitination of IRf7 is a prerequisite for its phosphorylation.