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Basic Characteristics of Mutations
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Mutation Site
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S147A |
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Mutation Site Sentence
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Mutation of the LT beta-TrCP phosphodegron site (S147A) required for replication also did not show VP1 expression, indicative of replication loss, as previously reported. |
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Mutation Level
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Amino acid level |
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Mutation Type
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Nonsynonymous substitution |
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Gene/Protein/Region
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Large T |
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Standardized Encoding Gene
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MCPyV_gp3
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Genotype/Subtype
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- |
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Viral Reference
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JF813003
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Functional Impact and Mechanisms
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Disease
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Cell line
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Immune
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- |
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Target Gene
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FBXW7
SKP2
BTRC
VPS39
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Clinical and Epidemiological Correlations
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Clinical Information
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- |
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Treatment
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- |
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Location
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- |
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Literature Information
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PMID
|
35336880
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Title
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Replication Kinetics for a Reporter Merkel Cell Polyomavirus
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Author
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Abere B,Zhou H,Shuda M,Stolz DB,Rapchak K,Moore PS,Chang Y
|
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Journal
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Viruses
|
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Journal Info
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2022 Feb 25;14(3):473
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Abstract
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Merkel cell polyomavirus (MCV) causes one of the most aggressive human skin cancers, but laboratory studies on MCV replication have proven technically difficult. We report the first recombinase-mediated MCV minicircle (MCVmc) system that generates high levels of circularized virus, allowing facile MCV genetic manipulation and characterization of viral gene expression kinetics during replication. Mutations to Fbw7, Skp2, beta-TrCP and hVam6p interaction sites, or to the stem loop sequence for the MCV-encoded miRNA precursor, markedly increase viral replication, whereas point mutation to an origin-binding site eliminates active virus replication. To further increase the utility of this system, an mScarlet fusion protein was inserted into the VP1 c-terminus to generate a non-infectious reporter virus for studies on virus kinetics. When this reporter virus genome is heterologously expressed together with MCV VP1 and VP2, virus-like particles are generated. The reporter virus genome is encapsidated and can be used at lower biosafety levels for one-round infection studies. Our findings reveal that MCV has multiple, self-encoded viral restriction mechanisms to promote viral latency over lytic replication, and these mechanisms are now amenable to examination using a recombinase technology.
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Sequence Data
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-
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