Brian R. Jackson
University of Leeds
27 Papers
144 Citations
Brian R. Jackson is an academic researcher from University of Leeds. The author has contributed to research in topics: Kaposi's sarcoma-associated herpesvirus & Biology. The author has an hindex of 13, co-authored 26 publications. Previous affiliations of Brian R. Jackson include University of East Anglia & University of Newcastle.
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Papers
Merkel Cell Polyomavirus Small T Antigen Targets the NEMO Adaptor Protein To Disrupt Inflammatory Signaling
David A. Griffiths,Hussein K . Abdul-Sada,Laura M. Knight,Brian R. Jackson,Kathryn H. Richards,Emma L. Prescott,A. Howard S. Peach,G. Eric Blair,Andrew Macdonald,Adrian Whitehouse +9 more
TL;DR: A new function of MCPyV small T antigen (ST) is identified as an inhibitor of NF-κB-mediated transcription, allowing establishment of early or persistent infection within the host cell.
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An interaction between KSHV ORF57 and UIF provides mRNA-adaptor redundancy in herpesvirus intronless mRNA export.
Brian R. Jackson,James R. Boyne,Marko Noerenberg,Adam Taylor,Guillaume M. Hautbergue,Matthew J. Walsh,Rachel Wheat,David J. Blackbourn,Stuart A. Wilson,Adrian Whitehouse +9 more
TL;DR: It is highlighted that redundancy exists in the eukaryotic system for certain hTREX components involved in the mRNA nuclear export of intronless KSHV mRNAs.
Using learning analytics to assess student engagement and academic outcomes in open access enabling programmes
Mirella Atherton,Mahsood Shah,Jenny Vazquez,Zoe Griffiths,Brian R. Jackson,Catherine Burgess +5 more
TL;DR: In this article, the authors confirm a correlation between student inclusion and academic support in Open Access Enabling courses and show that there is a strong correlation between students' inclusion and their academic support.
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NEDDylation is essential for Kaposi's sarcoma-associated herpesvirus latency and lytic reactivation and represents a novel anti-KSHV target.
TL;DR: This work shows that pharmacological inhibition of NEDDylation (using the small molecule inhibitor MLN4924) is cytotoxic to PEL cells by inhibiting NF-κB, and reveals novel mechanisms that regulate KSHV latency and reactivation.
A restricted spectrum of missense KMT2D variants cause a multiple malformations disorder distinct from Kabuki syndrome.
Sara Cuvertino,Verity L. Hartill,Verity L. Hartill,Alice Colyer,Terence Garner,Nisha Nair,Lihadh Al-Gazali,Natalie Canham,Víctor Faundes,Frances Flinter,Jozef Hertecant,Muriel Holder-Espinasse,Brian R. Jackson,Sally Ann Lynch,Fatima Nadat,Vagheesh M. Narasimhan,Michelle Peckham,Robert Sellers,Marco Seri,Francesca Montanari,Laura Southgate,Laura Southgate,Gabriella Maria Squeo,Richard C. Trembath,David A. van Heel,Santina Venuto,Daniel Weisberg,Karen Stals,Sian Ellard,Anne Barton,Susan J. Kimber,Eamonn Sheridan,Eamonn Sheridan,Giuseppe Merla,Adam Stevens,Colin A. Johnson,Siddharth Banka,Siddharth Banka +37 more
TL;DR: KMT2D MVs located in a specific region spanning exons 38 and 39 and affecting highly conserved residues cause a novel multiple malformations syndrome distinct from KS1, likely result in disease through a dominant negative mechanism.
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