Loren G. Fong
Department of Medicine
University of California
Los Angeles
CA 90095
USA
Name/email consistency: high
- Activating the synthesis of progerin, the mutant prelamin A in Hutchinson-Gilford progeria syndrome, with antisense oligonucleotides. Fong, L.G., Vickers, T.A., Farber, E.A., Choi, C., Yun, U.J., Hu, Y., Yang, S.H., Coffinier, C., Lee, R., Yin, L., Davies, B.S., Andres, D.A., Spielmann, H.P., Bennett, C.F., Young, S.G. Hum. Mol. Genet. (2009)
- A protein farnesyltransferase inhibitor ameliorates disease in a mouse model of progeria. Fong, L.G., Frost, D., Meta, M., Qiao, X., Yang, S.H., Coffinier, C., Young, S.G. Science (2006)
- Prelamin A and lamin A appear to be dispensable in the nuclear lamina. Fong, L.G., Ng, J.K., Lammerding, J., Vickers, T.A., Meta, M., Coté, N., Gavino, B., Qiao, X., Chang, S.Y., Young, S.R., Yang, S.H., Stewart, C.L., Lee, R.T., Bennett, C.F., Bergo, M.O., Young, S.G. J. Clin. Invest. (2006)
- Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice. Fong, L.G., Ng, J.K., Meta, M., Coté, N., Yang, S.H., Stewart, C.L., Sullivan, T., Burghardt, A., Majumdar, S., Reue, K., Bergo, M.O., Young, S.G. Proc. Natl. Acad. Sci. U.S.A. (2004)
