Grant: Operating Grant - Priority Announcement: Infection and Immunity (Bridge Funding)
Memorial University of Newfoundland
$100,000.00
Downregulation of IFN-inducible genes by Ras/Raf/MEK
FY 2008-09
Summary
Upon virus infection, hosts produce proteins called interferons (IFNs) that play critical roles as the first line of defense. IFNs activate antiviral machinery in infected and neighboring cells and inhibit amplification of viruses. However, IFNs do not always work effectively. In this proposal, we will study cellular environments that reduce the efficacy of IFN to activate the antiviral machinery. Our goal is to identify cellular mechanisms that regulate the function of IFN negatively. Our study will provide a novel insight into the future development of effective strategies that improve the function of host IFN system to fight against virus infection.
Department
Program
Operating Grant - Priority Announcement: Infection and Immunity (Bridge Funding)
Recipient
Location
Newfoundland and Labrador, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
178300
Name
Hirasawa Kensuke
Region
Newfoundland and Labrador
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Infection and Immunity
Theme2
Biomedical
Prcname2
Biochemistry & Molecular Biology - B
Projecttitle
Downregulation of IFN-inducible genes by Ras/Raf/MEK
Programtype2
Operating Grants
Orgnameinp2
Memorial University of Newfoundland
Cihramount2
$100,000
Cihrequipment2
$0
Programname2
Operating Grant - Priority Announcement: Infection and Immunity (Bridge Funding)
Keyworddelim
Cell Signaling; Interferon (Ifn); Nr4a Receptors; Ras/Raf/Mek; Transcription; Virus Infection
Abstract
Upon virus infection, hosts produce proteins called interferons (IFNs) that play critical roles as the first line of defense. IFNs activate antiviral machinery in infected and neighboring cells and inhibit amplification of viruses. However, IFNs do not always work effectively. In this proposal, we will study cellular environments that reduce the efficacy of IFN to activate the antiviral machinery. Our goal is to identify cellular mechanisms that regulate the function of IFN negatively. Our study will provide a novel insight into the future development of effective strategies that improve the function of host IFN system to fight against virus infection.
Competitiondate
200809
Approvedterm2
1 yr 0 mth
Pinamesdelim
Hirasawa, Kensuke
Approvedterm
1 an 0 mois
Cihrcontribution2
~ $100,000~ $0~
