E
Edward J. D. Greenwood
Researcher at University of Cambridge
Publications - 38
Citations - 999
Edward J. D. Greenwood is an academic researcher from University of Cambridge. The author has contributed to research in topics: Medicine & Simian immunodeficiency virus. The author has an hindex of 9, co-authored 31 publications receiving 723 citations. Previous affiliations of Edward J. D. Greenwood include University of Edinburgh.
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Journal ArticleDOI
Helminth secretions induce de novo T cell Foxp3 expression and regulatory function through the TGF-β pathway
John R. Grainger,Katie Smith,James P. Hewitson,Henry J. McSorley,Yvonne Harcus,Kara J. Filbey,Constance A. M. Finney,Edward J. D. Greenwood,David P. Knox,Mark S. Wilson,Yasmine Belkaid,Alexander Y. Rudensky,Rick M. Maizels +12 more
TL;DR: The intestinal parasite H. polygyrus secretes a TGF-β–like molecule that induces regulatory T cells, thus suppressing anti-parasitic effector T cell responses by the host.
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No evidence for basigin/CD147 as a direct SARS-CoV-2 spike binding receptor.
Jarrod Shilts,Thomas W M Crozier,Edward J. D. Greenwood,Paul J. Lehner,Gavin J. Wright,Gavin J. Wright +5 more
TL;DR: This paper found no evidence for a direct interaction between the SARS-CoV-2 spike protein to either of the two common isoforms of basigin and showed that removing basigenin from the surface of human lung epithelial cells by CRISPR/Cas9 results in no change in their susceptibility to SARS CoV2 infection.
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Temporal proteomic analysis of HIV infection reveals remodelling of the host phosphoproteome by lentiviral Vif variants
Edward J. D. Greenwood,Nicholas J Matheson,Kim Wals,Dick J. H. van den Boomen,Robin Antrobus,James C Williamson,Paul J. Lehner +6 more
TL;DR: The ability of Vif to target PPP2R5 subunits is found in primate and non-primate lentiviral lineages, and remodeling of the cellular phosphoproteome is therefore a second ancient and conserved Vif function.
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Promiscuous Targeting of Cellular Proteins by Vpr Drives Systems-Level Proteomic Remodeling in HIV-1 Infection.
Edward J. D. Greenwood,James C Williamson,Agata Sienkiewicz,Adi Naamati,Nicholas J Matheson,Paul J. Lehner +5 more
TL;DR: It is proposed that promiscuous targeting of multiple host factors underpins complex Vpr-dependent cellular phenotypes and validate this in the case of G2/M cell cycle arrest.
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The SMC5/6 complex compacts and silences unintegrated HIV-1 DNA and is antagonized by Vpr.
Liane Dupont,Stuart Bloor,James C Williamson,Sergio Martínez Cuesta,Raven Shah,Ana Teixeira-Silva,Adi Naamati,Edward J. D. Greenwood,Stefan G. Sarafianos,Nicholas J Matheson,Paul J. Lehner +10 more
TL;DR: In this paper, a targeted CRISPR-Cas9 library was used to identify SMC5-SMC6 complex localization factor 2 (SLF2) as the VPR target responsible for silencing HIV-1-like lentiviruses.