Email: hjw14@columbia.edu
Muchir, A., Shan, J., Bonne, G., Lehnart, S. E. and Worman, H. J. Inhibition of extracellular signal-regulated kinase signaling to prevent cardiomyopathy caused by mutation in the gene encoding A-type lamins. Hum. Mol. Genet. 2009;18:241-247.
Ostlund, C., Folker, E. S., Choi, J. C., Gomes, E. R., Gundersen, G. G. and Worman, H. J. Dynamics and molecular interactions of linker of nucleoskeleton and cytoskeleton (LINC) complex proteins. J. Cell Sci. 2009;122:4099-4108
Wu, W., Shan, J., Bonne, G., Worman, H. J. and Muchir, A. Pharmacological inhibition of c- Jun N-terminal kinase signaling prevents cardiomyopathy caused by mutation in LMNA gene. Biochim. Biophys. Acta 2010;1802:632-638.
Wang, Y., Ostlund, C. and Worman, H. J. Blocking protein farnesylation improves nuclear shape abnormalities in keratinocytes of mice expressing the prelamin A variant in Hutchinson-Gilford progeria syndrome. Nucleus 2010;1:432-439.
Kond, E., Bourgeois, B., Tellier-Lebegue, C., Wu, W., Prez, J., Caputo, S. M., Attanda, W., Gasparini, S., Charbonnier, J. B., Gilquin, B., Worman, H. J. and Zinn-Justin, S. Structural analysis of the Smad2-MAN1 interaction that regulates transforming growth factor-beta signaling at the inner nuclear membrane. Biochemistry 2010;49:8020-8032.
Folker, E. S., Ostlund, C., Luxton, G. W. G., Worman, H. J. and Gundersen, G. G. Lamin A variants that cause striated muscle disease are defective in anchoring transmembrane actin-associated nuclear lines for nuclear movement. Proc. Natl. Acad. Sci. USA 2011;in press.
Wu, W., Muchir, A., Shan, J., Bonne, G and Worman, H. J. Mitogen activated protein kinase inhibitors improve heart function and prevent fibrosis in cardiomyopathy caused by lamin A/C gene mutation. Circulation 2011;in press.