David Schlaepfer is a California-born scientist known for his studies on cell migration and cancer metastasis. His early research focused on signaling by protein kinases, with a subsequent focus on the proteins that regulate the turnover of cell contacts with the extracellular matrix. In particular, Schlaepfer is well known for his studies on focal adhesion kinase (FAK).
Schlaepfer received his PhD in Biological Sciences after training in the laboratory of Harry Haigler at the University of California, Irvine in 1992, with early work focused on the function and regulation of protein kinase C (PKC). Schlaepfer then moved to the Salk Institute to train with Tony Hunter, a pioneer in the study of protein-tyrosine phosphorylation, where his work focused on FAK. In 1995, Schlaepfer won the Santa Cruz Biotechnology investigator award. By 1996, Schlaepfer was awarded a position as an assistant professor at The Scripps Research Institute in La Jolla, where he advanced to the associate professor level. In 2007, Schlaepfer joined the Department of Reproductive Medicine in the School of Medicine at the University of California, San Diego as a full professor.
As of 2010, Schlaepfer is a Professor in the Department of Reproductive Medicine in the School of Medicine at the University of California, San Diego.
Schlaepfer, D.D., Hanks, S.K., Hunter, T., and van der Geer, P. (1994). Integrin-mediated signal transduction linked to Ras Pathway by Grb2 Binding to Focal adhesion kinase. Nature 372: 786-791.
Ilic, D., Almeida, E.A., Schlaepfer, D.D., Dazin, P., Aizawa, S., and Damsky, C.H. (1998). Extracellular matrix survival signals transduced by focal adhesion kinase suppress p53-mediated apoptosis. J. Cell Biol. 143: 547-560.
Sieg, D.J., Hauck, C.R., Ilic, D., Klingbeil, C.K., Schaefer, E.. Damsky, C.H., and Schlaepfer, D.D. (2000). FAK integrates growth factor and integrin signals to promote cell migration. Nature Cell Biol. 2: 249-256.
Hauck, C.R., Hsia, D.A., Puente, X.S., Cheresh, D.A., and Schlaepfer, D.D. (2002). FRNK blocks v-Src-stimulated invasion and experimental metastases without effects on cell motility or growth. EMBO J. 21: 6289-6302.
Hsia, D.A., Mitra, S.K., Hauck, C.R., Streblow, D.N., Nelson, J.A., Ilic, D., Haung, S., Li, E., Nemerow, G.R., Leng, J., Spencer, K.S.R., Cheresh, D.A., and Schlaepfer, D. D. (2003). Differential regulation of cell motility and invasion by FAK. J. Cell Biol. 160: 753-767.
Hsia, D.A., Lim, S.T., Bernard-Trifilo, J.A., Mitra, S.K., Tanaka, S., den Hertog, J., Streblow, D.N., Ilic, D., Ginsberg, M.H., and Schlaepfer, D.D. (2005). Integrin a4b1 promotes FAK-independent cell motility via a4 cytoplasmic domain-specific activation of Src. Mol. Cell. Biol. 25: 9700-9712.
Mitra, S.K., Mikolon, D., Molina, J., Hsia, D.A., Hanson, D. A., Chi, A., Lim. S.T., Bernard-Trifilo, J.T., Ilic, D., Stupack, D.G., Cheresh, D.A., and Schlaepfer, D.D. (2006). Intrinsic FAK activity and Y925 phosphorylation facilitate an angiogenic switch in tumors. Oncogene 25: 5969-5984.
Lim Y, Lim ST, Tomar A, Gardel M, Bernard-Trifilo JA, Chen XL, Uryu SA, Canete-Soler R, Zhai J, Lin H, Schlaepfer WW, Nalbant P, Bokoch G, Ilic D, Waterman-Storer C, Schlaepfer DD.(2008) PyK2 and FAK connections to p190Rho guanine nucleotide exchange factor regulate RhoA activity, focal adhesion formation, and cell motility. J Cell Biol. 180:187-203.
Wu L, Bernard-Trifilo JA, Lim Y, Lim ST, Mitra SK, Uryu S, Chen M, Pallen CJ, Cheung NK, Mikolon D, Mielgo A, Stupack DG, Schlaepfer DD. (2008) Distinct FAK-Src activation events promote alpha5beta1 and alpha4beta1 integrin-stimulated neuroblastoma cell motility. Oncogene 27:1439-48.
