Author

D. J. Hughes

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Immunology· 3 Microbiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Organism:human· 4 Research Focus:host-pathogen & immune response· 3 Assay:proteomics· 2 Approach:biophysical modeling· 1 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1

Frequent Co-Authors

A. Vasou· 2 shared C. G. Bamford· 2 shared J. Andrejeva· 2 shared J. McLauchlan· 2 shared M. P. Weekes· 2 shared R. E. Randall· 2 shared A. Whitehouse· 1 shared B. J. Ravenhill· 1 shared

Activity by Year

2019-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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2 shared papersImmunology

A. Vasou

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

Spatial proteomics identifies a novel CRTC-dependent viral sensing pathway that stimulates production of Interleukin-11

B. J. Ravenhill, M. Oliveira, G. Wood, Y. Di, C. Davies, Y. Lu, R. Antrobus, G. Elliott, N. Irigoyen, D. J. Hughes, P. Lyons, B. Y. Chung, G. Borner, M. P. Weekes

The paper identifies a novel CRTC-dependent viral sensing pathway that promotes interleukin-11 production during viral infection.

bioRxiv · Apr 4, 2024 · PreprintImmunology

Kv1.3 induced hyperpolarisation and Cav3.2-mediated calcium entry are required for efficientKaposi's sarcoma-associated herpesvirus lytic replication

H. Carden, M. Dallas, D. J. Hughes, J. D. Lippiat, J. D. Mankouri, A. Whitehouse

The paper identifies Kv1.3 and Cav3.2 ion channels as essential for KSHV lytic replication by promoting Ca2+ influx and NFAT activation.

bioRxiv · Sep 10, 2021 · PreprintMicrobiology

A co-opted ISG15-USP18 binding mechanism normally reserved for deISGylation controls type I IFN signalling

A. Vasou, K. Nightingale, V. Cetkovska, J. Scheler, C. G. Bamford, J. Andrejeva, U. Schwarz-Linek, R. E. Randall, J. McLauchlan, M. P. Weekes, D. Bogunovic, D. J. Hughes

The paper identifies a new function of ISG15 in stabilizing USP18 through non-covalent interactions, revealing a mechanism that controls type I IFN signalling.

bioRxiv · Jun 1, 2021 · PreprintImmunology

Direct antiviral activity of interferon stimulated genes is responsible for resistance to paramyxoviruses in ISG15-deficient cells

D. Holthaus, A. Vasou, C. G. Bamford, J. Andrejeva, C. Paulus, R. E. Randall, J. McLauchlan, D. J. Hughes

The paper shows that ISG15-deficient cells are resistant to paramyxovirus infection due to direct antiviral activity of ISGs, but prolonged IFN treatment causes resistance through translational inhibition.

bioRxiv · Dec 12, 2019Immunology