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D

Dai Iwakiri

Researcher at Hokkaido University

Publications -  23
Citations -  2019

Dai Iwakiri is an academic researcher from Hokkaido University. The author has contributed to research in topics: Epstein–Barr virus & RNA silencing. The author has an hindex of 17, co-authored 23 publications receiving 1861 citations. Previous affiliations of Dai Iwakiri include Kobe University.

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EB virus-encoded RNAs are recognized by RIG-I and activate signaling to induce type I IFN.

TL;DR: Results indicate that EBERs are recognized by RIG‐I and activate signaling to induce type I IFN in EBV‐infected cells.
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Epstein-Barr virus (EBV)-encoded small RNA is released from EBV-infected cells and activates signaling from Toll-like receptor 3

TL;DR: It is reported that EBER induces signaling from the Toll-like receptor 3 (TLR3), which is a sensor of viral double-stranded RNA (dsRNA) and induces type I IFN and proinflammatory cytokines and EBER-induced activation of innate immunity would account for immunopathologic diseases caused by active EBV infection.
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Editing of Epstein-Barr Virus-encoded BART6 MicroRNAs Controls Their Dicer Targeting and Consequently Affects Viral Latency

TL;DR: MiR-BART6-5p RNAs suppress the EBNA2 viral oncogene required for transition from immunologically less responsive type I and type II latency to the more immunoreactive type III latency as well as Zta and Rta viral proteins essential for lytic replication, revealing the regulatory function of miR- BART6 in EBV infection and latency.
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Epstein-Barr virus-encoded small RNA induces IL-10 through RIG-I-mediated IRF-3 signaling.

TL;DR: A new mechanism of dsRNA signaling pathway that triggers the expression of IL-10, which acts as an autocrine growth factor in BL cells is suggested.
Journal Article

Autocrine Growth of Epstein-Barr Virus-Positive Gastric Carcinoma Cells Mediated by an Epstein-Barr Virus-Encoded Small RNA

TL;DR: It is reported that EBV infection induces expression of insulin-like growth factor 1 (IGF-I) in the GC-derived EBV-negative cell line NU-GC-3 and that the secreted IGF-I acts as an autocrine growth factor.