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Akihiro Furusaka

Researcher at Jikei University School of Medicine

Publications -  14
Citations -  1145

Akihiro Furusaka is an academic researcher from Jikei University School of Medicine. The author has contributed to research in topics: Hepatitis C virus & Insulin receptor. The author has an hindex of 10, co-authored 14 publications receiving 1118 citations. Previous affiliations of Akihiro Furusaka include Tokyo Medical University.

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Journal ArticleDOI

Efficient replication of the genotype 2a hepatitis C virus subgenomic replicon

TL;DR: The genotype 2a subgenomic replicon was established in Huh7 cells and replicated efficiently with or without G418 selection in a transient replication assay, providing a powerful new tool for researching HCV.
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Sequence analysis of hepatitis C virus isolated from a fulminant hepatitis patient.

TL;DR: HCV was isolated from a fulminant hepatitis patient and its entire genome was recovered; a clustering around genotype 2a was observed, but the sequence deviated especially in 5′UTR, core, NS3, and NS5A; and monoclonality of the HVR sequence was found not only in the fulminants hepatitis patient but in a certain percentage of chronic hepatitis patients.
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Hepatitis C virus JFH-1 strain infection in chimpanzees is associated with low pathogenicity and emergence of an adaptive mutation

TL;DR: This study shows that the HCV JFH‐1 strain causes attenuated infection and low pathogenicity in chimpanzees and is capable of adapting in vivo with a unique mutation conferring an enhanced replicative phenotype.
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Association of insulin receptor substrate proteins with Bcl-2 and their effects on its phosphorylation and antiapoptotic function.

TL;DR: It is shown that IRS-1 associates with the loop domain of Bcl-2 and synergistically up-regulates antiapoptotic function of B Cl-2, thus regulating cell survival probably through regulating phosphorylation of B cl-2.
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Processing of hepatitis C virus core protein is regulated by its C-terminal sequence.

TL;DR: Compared between clones isolated from two patients with fulminant hepatitis and from five patients with chronic hepatitis, the data suggest that core protein processing is regulated by C‐terminus mutations.