dept of biochem


homefacultyresearch areasgraduate programpostdocscoursesseminarsresourcescontact uslinksdirectory

Larry A. Feig

Jaharis 613
150 Harrison Ave.
Boston, MA 02111


larry.feig@tufts.edu

office: 617-636-6956
lab: 617-636-6955

Larry A. Feig, Ph.D.

Director, Biochemistry Graduate Program

Professor, Tufts Department of Biochemistry


 

Links:


Research


Lab Members


Recent Publications

 

Research Summary:

We study the role of the Ras family of GTPases in the development of CANCER and in mediating CALCIUM SIGNALING IN NEURONS. Studies on Ras proteins and cancer focus on how Ras induces oncogenic transformation of primary human cells through activation of the Ral GTPases, and on how R-Ras proteins contribute to breast cancer.

Studies on Ras function in neurons focus on Ras-GRF proteins, which are brain-specific Ras activators that mediate calcium activation of Erk/Map kinase by both NMDA and AMPA glutamate receptors. Knockout mice are used as a model system to investigate the role of Ras-GRF proteins in both learning and memory and neuronal excitotoxicity.



Research:

For more details, please see the publications below.


Lab Members

Feig Lab

Assistant Research Professor

Postdoctoral Associates

Graduate Students

Technicians


Recent Publications

  1. Arai, J., Li, S., Hartley, D.M. and Feig, L.A. (2009). Transgenerational rescue of a genetic defect in long-term potentiation and memory formation by juvenile enrichment. J. Neuroscience. 29:1496-1502. (see Commentaries in Nature News and Scientific American )

  2. Hao, Y., Wong, R. and Feig, L.A. (2008). RalGDS couples growth factor signaling to Akt activation. Mol. Cell. Biol. 28:2851-2859.

  3. Li, S., Feig, L.A., and Hartley, D.M. 2007. A brief, but repeated, swimming protocol is sufficient to overcome amyloid B-protein inhibition of hippocampal long-term potentiation. Eur J. Neuro. 26:1289-1298.

  4. Li, S., Tian, X., Hartley, D.M. and Feig, L.A. 2006. The environment versus genetics in controlling the contribution of MAP kinases to synaptic plasticity. Current Biology. 16:1-11.

  5. Tian, X., and Feig, L.A. 2006. “Age-dependent Participation of Ras-GRF Proteins in Coupling Calcium-permeable AMPA Glutamate Receptors to Ras/Erk Signaling in Cortical Neurons.” Journal of Biological Chemistry 281(11): 7578-7582

  6. Yu, Y., Hao, Y, and Feig, L.A. 2006. The R-Ras GTPase mediates cross talk between estrogen and insulin signaling in breast cancer cells. Mol. Cell. Biol. 26:6372-6380.

  7. Li, Shaomin; Tian, Xuejun; Hartley, Dean M; Feig, Larry A. (2006). “Distinct Roles for Ras-Guanine Nucleotide-Releasing Factor 1 (Ras-GRF1) and Ras-GRF2 in the Induction of Long-Term Potentiation and Long-Term Depression.” Journal of Neuroscience 26(6): 1721-1729

  8. Feig, Larry A. (2006). “The Odyssey of K-Ras.” Molecular Cell 21(4): 447-449

  9. Wei, Jie; Fain, Sebastian; Harrison, Celia; Feig, Larry A; Baleja, James D. (2006). “Molecular Dissection of Rab11 Binding from Coiled-Coil Formation in the Rab11-FIP2 C-Terminal Domain.” Journal of the American Chemical Society, in press.

  10. Lim Kian-Huat, Baines, A., Fiordalisi, J.J, Shipitsin, M., Feig, L.A., Cox, A.D., Der, C.J., Counter, C.M. 2005. Activation of RalA is critical for Ras-induced tumorigenesis of human cells. Cancer Cell. 7:533-545.

  11. Rusanescu, G., Yeng, W. Bai, A., Neel, B.G. and Feig, L.A. 2005. Tyrosine phosphatase SHP-2 is a mediator of activity dependent neuronal excitotoxicity. EMBO J. 24:1-10.

  12. Shipitsin, M. and Feig, L.A. 2004. RalA but not RalB enhances polarized membrane delivery of E-cadherin to the basolateral surface of MDCK cells. Mol. Cell. Biol. 24:5746-5756.

  13. Tian, X, Gotoh, T., Tsuji, K, Lo, E., Su, H. and Feig, L.A. 2004 Developmentally regulated role for Ras-GRFs in coupling NMDA glutamate receptors to Ras/Erk/CREB. EMBO J. 23:1567-1575.

  14. Feig, L.A., 2003, The Ral GTPases: Approaching their 15 minutes of fame. Trends in Cell Biology 13:419-425.

  15. Buchbaum, R.J., Connoly, B.A. and Feig, L.A. 2003 Regulation of p70 S6 kinase by complex formation between the Rac GEF Tiam1 and the scaffold spinophilin. J. Biol. Chem. 278: 18833-18841.

  16. Polzin A, Shipitsin M, Goi T, Feig LA, Turner TJ., 2002 Ral-GTPase influences the regulation of the readily releasable pool of synaptic vesicles. Mol Cell Biol. 22:1714-22.

  17. Yu, Y. and Feig, L.A.2002 Involvement of R-Ras and Ral GTPases in estrogen-independent proliferation of cancer cells . Oncogene. 21:7557-756831.

  18. Tian X, Rusanescu G, Hou W, Schaffhausen B, and Feig LA., 2002. PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism EMBO J. 21:1327-38.

  19. Feig, L.A. and Buchsbaum, R. 2002 Cell Signaling: Life or death decisions of Ras proteins Current Biology 12:259-61.

  20. Goi, T., Shipistin, M., Lu, Z., Foster D.A., Klinz, S. and Feig, L.A. 2000, An EGF receptor/Ral-GTPase signaling regulates c-Src activity and substrate specificity. EMBO J. 19, 623-630.

  21. Farnsworth, C.L., Freshney, N.W., Rosen, L.B., Ghosh, A., Greenberg, M.E. and Feig, L.A. 1995 calcium activation of Ras mediated by neuronal exchange factor Ras-GRF, Nature, 376, 524-527.

  22. Jiang, H., Luo, J.-Q., Urano, T., Frankel, P., Lu, Z., Foster, D.A., and Feig, L.A. 1995 Involvement of Ral GTPase in v-Src-induced phospholipase D activation. Nature, 378, 409-412.


             

Sackler Home