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Grant: Operating Grant

McGill University

$679,190.00

Molecular mechanisms of CdGAP (Cdc42 GTPase-activating protein), a negative regulator of the oncogenic small GTPases Rac1 and Cdc42

EF 2011-12

Résumé
Cancer is the result of deregulated cellular processes such as cell proliferation (increased number of cells, "nodule"), cell morphology (the shape and color of the cell are changed), cell movement and attachment (the cell will move from one site to another site or organ, "metastasis"). My laboratory is studying small molecules, named Rho GTPases, which are implicated in the regulation of these cellular processes. They act as switches that can be turned on or off, and are important both in the functions of a normal cell as well as in the regulation of processes leading to cancer. I have previously identified a novel protein, named CdGAP, which can turn off the Rho GTPases. CdGAP is the member of a large family of proteins and there is now much evidence suggesting that these proteins are affected in human cancers. Moreover, we have recently demonstrated CdGAP as a positive modulator of breast cancer cells. Therefore, we are using molecular and cellular approaches to better understand the role of CdGAP in breast cancer. The goal of this research proposal is to understand at the molecular and cellular level how CdGAP functions in the cell. Understanding how CdGAP is regulated and functions in the cell will provide novel molecular targets for therapeutic agents against breast cancer and will provide invaluable tools to screen human cancers for this protein. This will lead to the reduction of the incidence, morbidity, and mortality from cancer.
Programme
Operating Grant
Bénéficiaire
Emplacement
Quebec, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database

Tel que publié

Id
238425
Name
Lamarche-Vane Nathalie
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Molecular & Cellular Biology of Cancer
Projecttitle
Molecular mechanisms of CdGAP (Cdc42 GTPase-activating protein), a negative regulator of the oncogenic small GTPases Rac1 and Cdc42
Programtype2
Operating Grants
Orgnameinp2
McGill University
Cihramount2
$679,190
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Breast Cancer; Live Cell Imaging; Rho Gtpases; Rhogaps; Signal Transduction; Tgfbeta Signaling
Abstract
Cancer is the result of deregulated cellular processes such as cell proliferation (increased number of cells, "nodule"), cell morphology (the shape and color of the cell are changed), cell movement and attachment (the cell will move from one site to another site or organ, "metastasis"). My laboratory is studying small molecules, named Rho GTPases, which are implicated in the regulation of these cellular processes. They act as switches that can be turned on or off, and are important both in the functions of a normal cell as well as in the regulation of processes leading to cancer. I have previously identified a novel protein, named CdGAP, which can turn off the Rho GTPases. CdGAP is the member of a large family of proteins and there is now much evidence suggesting that these proteins are affected in human cancers. Moreover, we have recently demonstrated CdGAP as a positive modulator of breast cancer cells. Therefore, we are using molecular and cellular approaches to better understand the role of CdGAP in breast cancer. The goal of this research proposal is to understand at the molecular and cellular level how CdGAP functions in the cell. Understanding how CdGAP is regulated and functions in the cell will provide novel molecular targets for therapeutic agents against breast cancer and will provide invaluable tools to screen human cancers for this protein. This will lead to the reduction of the incidence, morbidity, and mortality from cancer.
Competitiondate
201109
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Lamarche-Vane, Nathalie
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $679,190~ $0~