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- Nathalie Lamarche-Vane, PhD
null Nathalie Lamarche-Vane, PhD
Senior Scientist, RI-MUHC, Glen site
Cancer Research ProgramCentre for Translational Biology
Professor, Department of Anatomy and Cell Biology, Faculty of Medicine and Health Sciences, McGill University
Keywords
Rho GTPases • cell migration • signal transduction • neuronal development • breast cancer
Research Focus
My research focuses on the signaling pathways mediated by the Rho family of small GTPases. Rho GTPases play a critical role in many aspects of cell biology, in cell migration, cell adhesion, cell morphology and cell growth. These cellular events are crucial for the normal development and physiology in humans. For instance, in the adult, migration events are involved in the normal physiology as well as in pathology such as metastasis. In embryogenesis, cell migration is an important feature of the development of the nervous system. Using molecular and cellular approaches, we are interested to delineate the role of Rho GTPases in cell migration, in particular, in neuronal development and in the cellular processes leading to cancer metastasis. Understanding the molecular mechanisms underlying the Rho proteins in cell migration and cell adhesion will be helpful to identify novel drug targets for tumor therapy and neurodegenerative diseases.
Selected Publications
Click on to see my current publications list
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DeGeer, J., Kaplan, A., Mattar, P., Morabito, M., Stochaj, U., Kennedy, T.E., Debant, A., Cayouette, M., Fournier, AE., and Lamarche-Vane, N. (2015) Hsc70 chaperone activity underlies Trio GEF function in axon growth and guidance induced by netrin-1. J. Cell Biol. 210, 817-832.
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C. Caron, J. DeGeer, PM. Duquette, P. Fournier, V. Luangrath, H. Ishii, F. Karimzadeh, *N. Lamarche-Vane and *I. Royal. (2016), CdGAP/ARHGAP31, a Cdc42/Rac1 GTPase regulator, is critical for vascular development and VEGF-mediated angiogenesis. Sc. Rep. 6:27485. doi: 10.1038/srep27485.
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Yi He, Jason J. Northey, Ariane Pelletier, Zuzana Kos, Liliane Meunier, Benjamin Haibe-Kains, Anne-Marie Mes-Masson, Jean-François Côté, Peter M. Siegel, and Nathalie Lamarche-Vane. (2017) The Cdc42/Rac1 regulator CdGAP is a novel E-cadherin transcriptional co-repressor with Zeb2 in breast cancer. Oncogene 36, 3490-3503.
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Southgate*, L., Machado, RD*, Snape, KM*, Primeau, M., Dafou, D., Ruddy, DM., Branney, PA., Fisher, M., Lee, GJ., He, Y., Bradshaw, TY., Blaumeiser, B., Winship, WS., Reardon, W., Maher, ER., FitzPatrick, DR., Wuyts, W., Zenker, M., Lamarche-Vane, N., and Trembath, RC (2011) Gain-of-Function mutations of ARHGAP31 (CdGAP), a Rho family GTPase regulator, cause Syndromic Cutis Aplasia and limb anomalies. Am. J. Hum. Gen. 88, 574-585.
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C. Mehra, JH. Chung, Y. He, M.L. Márquez, MA Goyette, N. Boufaied, V. Barrès, V. Ouellet, KP Guérard, C. Delliaux, F. Saad, J. Lapointe, JF Côté, DP. Labbé*, N. Lamarche-Vane* (2021) The Rac1/Cdc42 regulator CdGAP promotes prostate cancer metastasis by regulating epithelial-to-mesenchymal transition, cell cycle progression, and apoptosis. Commun. Biol. accepted.