James R. Boyne
University of Huddersfield
30 Papers
174 Citations
James R. Boyne is an academic researcher from University of Huddersfield. The author has contributed to research in topics: Nuclear export signal & Merkel cell polyomavirus. The author has an hindex of 16, co-authored 30 publications. Previous affiliations of James R. Boyne include National Health Service & St James's University Hospital.
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Papers
Recruitment of the complete hTREX complex is required for Kaposi's sarcoma-associated herpesvirus intronless mRNA nuclear export and virus replication.
TL;DR: The first direct evidence is provided that the complete hTREX complex is essential for the export of KSHV intronless mRNAs and infectious virus production.
The role of CAF derived exosomal microRNAs in the tumour microenvironment of melanoma.
M. Shelton,Chinedu Anthony Anene,Jérémie Nsengimana,Wayne Roberts,Julia Newton-Bishop,James R. Boyne +5 more
TL;DR: This review assesses the roles of melanoma exosomal miRNAs in CAF formation and how CAF exosome-mediated feedback signalling to melanoma lead to tumour progression and metastasis, and efforts to exploit exosomes-mediated network communication between tumour cells and their microenvironment.
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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.
Basic fibroblast growth factor-induced cell death is effected through sustained activation of p38MAPK and up-regulation of the death receptor p75NTR.
TL;DR: It is demonstrated that sustained activation of p38MAPK is essential for activation of the death cascade following exposure of Ewing's sarcoma family of tumors cells to bFGF and evidence that activated p38 MAPK results in an up-regulation of thedeath receptor p75NTR is provided.
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IQGAP and mitotic exit network (MEN) proteins are required for cytokinesis and re-polarization of the actin cytoskeleton in the budding yeast, Saccharomyces cerevisiae.
TL;DR: It is demonstrated that mutations in genes of the mitotic exit network (MEN) prevent cell separation and are synthetically lethal in combination with both cytokinesis and septation defective mutations, establishing a mechanistic dependency of cell separation upon an intermediate step requiring actomyosin ring assembly.
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