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Nathalie Lamarche-Vane, PhD

Senior Scientist, RI-MUHC, Glen site

Cancer Research Program

Professor, Department of Anatomy and Cell Biology, Faculty of Medicine, 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 Pubmed to see my current publications list

  • 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., in press.

  • DeGeer, J. and Lamarche-Vane, N. (2013) Rho GTPases and neurodegeneration diseases. Exp. Cell Res. 319, 2384-2394. PMID: 23830879.

  • Judith Antoine-Bertrand, Atefeh Ghogha, Fiona K. Bedford, Nathalie Lamarche-Vane (2011) The activation of ezrin-radixin-moesin (ERM) proteins is regulated by netrin-1 and is required for axon outgrowth. Mol. Biol. Cell 22, 3734-3746 PMID: 21849478.

  • Laura Southgate*, Rajiv D Machado*, Katie M Snape*, Martin Primeau, Dimitra Dafou, Deborah M Ruddy, Peter A. Branney, Malcolm Fisher, Grace J Lee, Yi He, Teisha Y Bradshaw, Bettina Blaumeiser, William S Winship, Willie Reardon, Eamonn R Maher, David R FitzPatrick, Wim Wuyts, Martin Zenker, Nathalie Lamarche-Vane & Richard C Trembath. (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 PMCID: PMC3146732.

  • He, Y., Northey, J.J, Primeau, M., Machado, R.D., Trembath, R., Siegel, P. and Lamarche-Vane, N. * (2011) CdGAP is required for Transforming Growth Factor-b and Neu-ErbB2-induced breast cancer cell motility and invasion, Oncogene 30, 1032-1045 PMID: 21042277.