Grant: Master's Award: Canada Graduate Scholarships
University of Winnipeg
$17,500.00
Re-activation of human endogenous retrovirus-K in Amyotrophic Lateral Sclerosis: A consequence of genetic mutations in TDP43 and Optineurin.
FY 2012-13
Summary
Over 8% of our DNA contains ancient retroviruses, such as human endogenous retrovirus-K (ERVK). These viruses are normally silent, but can be re-activated during inflammatory disease, such as Amyotrophic Lateral Sclerosis (ALS). We do not understand what signals re-activate these retroviruses. Two key proteins known to be mutated in ALS patients - Optineurin and TDP43 - are known to modulate inflammatory pathways through Nuclear Factor-kappa B (NF-kB) signalling. Our preliminary results show that NF-kB can induce ERVK in human cells. The proposed study will examine how Optineurin and TDP43 might contribute to ERVK expression and neuroinflammation in ALS. We will use a combination of molecular biology and imaging techniques to address this research question. Our findings will allow us to identify potential therapeutic targets which modulate either the retrovirus or the immune system, thus preventing the development and clinical symptoms of ALS.
Department
Program
Master's Award: Canada Graduate Scholarships
Recipient
Location
Manitoba, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
280964
Name
Manghera Mamneet
Region
Manitoba
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Infection and Immunity
Theme2
Biomedical
Prcname2
Canada Graduate Scholarships Master's Awards A
Projecttitle
Re-activation of human endogenous retrovirus-K in Amyotrophic Lateral Sclerosis: A consequence of genetic mutations in TDP43 and Optineurin.
Programtype2
Studentship Programs
Orgnameinp2
University of Winnipeg
Cihramount2
$17,500
Cihrequipment2
$0
Programname2
Master's Award: Canada Graduate Scholarships
Keyworddelim
Amyotrophic Lateral Sclerosis; Confocal Microscopy; Functional Polymorphisms; Human Endogenous Retrovirus-K; Inflammatory Disease; Inflammatory Transcription Factors; Innate Immunity; Interferon Response Factors; Neurovirology; Nuclear Factor-Kappa B Signaling
Abstract
Over 8% of our DNA contains ancient retroviruses, such as human endogenous retrovirus-K (ERVK). These viruses are normally silent, but can be re-activated during inflammatory disease, such as Amyotrophic Lateral Sclerosis (ALS). We do not understand what signals re-activate these retroviruses. Two key proteins known to be mutated in ALS patients - Optineurin and TDP43 - are known to modulate inflammatory pathways through Nuclear Factor-kappa B (NF-kB) signalling. Our preliminary results show that NF-kB can induce ERVK in human cells. The proposed study will examine how Optineurin and TDP43 might contribute to ERVK expression and neuroinflammation in ALS. We will use a combination of molecular biology and imaging techniques to address this research question. Our findings will allow us to identify potential therapeutic targets which modulate either the retrovirus or the immune system, thus preventing the development and clinical symptoms of ALS.
Competitiondate
201302
Approvedterm2
1 yr 0 mth
Pinamesdelim
Manghera, Mamneet
Approvedterm
1 an 0 mois
Cihrcontribution2
~ $17,500~ $0~
