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Michael A. Skinner

Researcher at Imperial College London

Publications -  144
Citations -  7593

Michael A. Skinner is an academic researcher from Imperial College London. The author has contributed to research in topics: Virus & Fowlpox virus. The author has an hindex of 44, co-authored 144 publications receiving 7214 citations. Previous affiliations of Michael A. Skinner include Medical Research Council & University of Reading.

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Human immunodeficiency virus 1 tat protein binds trans-activation-responsive region (TAR) RNA in vitro

TL;DR: Tat, the trans-activator protein for human immunodeficiency virus 1 (HIV-1), has been expressed in Escherichia coli from synthetic genes and binds specifically to HIV-1 trans-activation-responsive region (TAR) RNA in gel-retardation, filter-binding, and immunoprecipitation assays.
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HIV-1 tat protein stimulates transcription by binding to a U-rich bulge in the stem of the TAR RNA structure.

TL;DR: There is a direct correlation between the ability of tat to bind to TAR RNA and to activate HIV transcription, and Viral LTRs carrying TAR sequences encoding any of the mutations known to produce transcripts which bind tat weakly, are not stimulated efficiently by tat in vivo.
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HIV-1 regulator of virion expression (Rev) protein binds to an RNA stem-loop structure located within the Rev response element region

TL;DR: A approximately 33 nucleotide fragment is protected from ribonuclease T1 digestion by the binding of Rev to RRE RNA, suggesting that Rev binds with high affinity to only a restricted region of the RRE.
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mda-5, but not RIG-I, is a common target for paramyxovirus V proteins.

TL;DR: It is shown that 12 other paramyxoviruses also target mda-5 by a direct interaction between the conserved cysteine-rich C-terminus of their V proteins and the helicase domain of mDA-5, and that the inhibition of m da-5 function is also not restricted to mammalian cells.
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New model for the secondary structure of the 5' non-coding RNA of poliovirus is supported by biochemical and genetic data that also show that RNA secondary structure is important in neurovirulence.

TL;DR: The sequence of a neurovirulent revertant of an attenuated mutant provides additional evidence for an interaction between a region known to be important for neurovirulence, sequence 471-483, and nucleotides 528 to 538.