Grant: Operating Grant
Université Laval
$821,551.00
MRE11-RAD50-NBS1: at the crossroads of DNA double-strand break repair and Fanconi anemia
EF 2009-10
Résumé
Cancer is a constant treath for humans. All organisms have evolved mechanisms that allow the maintenance of genomic integrity. The consequences of damaged DNA, and especially double-strand breaks, may be disastrous and lead to cancer if left unrepaired. All organisms can suffer DNA damage, during normal cellular processes or as a consequence of DNA damaging agents such as ultraviolet light and ionizing radiation.
The present project involves the characterization of key enzymes (MRE11-RAD50-NBS1) involved in the repair of double-strand breaks but also Fanconi anemia. Understanding how these proteins function in cell is critical to improve radiotherapy on cancer cells. Moreover, it will greatly improve our knowledge on several genetic disorders (such as Ataxia telangiectasia like-disorder and Fanconi Anemia) that are characterized by defective DNA damage responses.
Programme
Operating Grant
Bénéficiaire
Emplacement
Quebec, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
188788
Name
Masson Jean-Yves
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Genetics
Theme2
Biomedical
Prcname2
Cancer Biology & Therapeutics
Projecttitle
MRE11-RAD50-NBS1: at the crossroads of DNA double-strand break repair and Fanconi anemia
Programtype2
Operating Grants
Orgnameinp2
Université Laval
Cihramount2
$821,551
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Biochemical And Cellular Assays; Cancer Research; Dna Repair; Double-Strand Breaks; Fanconi Anemia; Mre11-Rad50-Nbs1
Abstract
Cancer is a constant treath for humans. All organisms have evolved mechanisms that allow the maintenance of genomic integrity. The consequences of damaged DNA, and especially double-strand breaks, may be disastrous and lead to cancer if left unrepaired. All organisms can suffer DNA damage, during normal cellular processes or as a consequence of DNA damaging agents such as ultraviolet light and ionizing radiation.
The present project involves the characterization of key enzymes (MRE11-RAD50-NBS1) involved in the repair of double-strand breaks but also Fanconi anemia. Understanding how these proteins function in cell is critical to improve radiotherapy on cancer cells. Moreover, it will greatly improve our knowledge on several genetic disorders (such as Ataxia telangiectasia like-disorder and Fanconi Anemia) that are characterized by defective DNA damage responses.
Competitiondate
200909
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Masson, Jean-Yves
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $821,551~ $0~
