Novel mechanisms of cellular antiviral defense through the PARP-13 shorter isoform, ZAPS

2016 Fiscal Year Final Research Report

• Project/Area Number: 25713032
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Partial Multi-year Fund
• Research Field: Respiratory organ internal medicine
• Research Institution: Tokyo Medical and Dental University (2014-2016); Hokkaido University (2013)
• Principal Investigator: HAYAKAWA Sumio 東京医科歯科大学, 難治疾患研究所, 助教 (00368292)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: インターフェロン / インフルエンザウイルス / 抗ウイルス

Outline of Final Research Achievements

Type I IFN are produced in response to viral infection and are key cytokines for the activation of innate immunity. The pathogen invasion is sensed by pattern-recognition receptors(PRRs) of innate immune system through the recognition of pathogen associated molecular patterns(PAMPs). The PRRs trigger the activation of intracellular signaling pathway, which leads to the induction of antimicrobial genes. RIG-I is the key PRR for detection of positive- and negative strand RNA viruses in the cytoplasm of cells and has an important triggering response to viruses, such as influenza A virus. However, the NS1 from influenza virus counters host antiviral defenses. In this study, the interaction of RIG-I and ZAPS is one of the keypoints, wherein NS1 inhibits RIG-I-mediated antiviral activity.

Free Research Field

生化学