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Published online
doi:10.1083/jcb.200706097
The Journal of Cell Biology, Vol. 179, No. 1, 23-31
The Rockefeller University Press, 0021-9525 $30.00
© Ma et al.
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p66Shc mediates anoikis through RhoA



Zhenyi Ma, David P. Myers, Ru Feng Wu, Fiemu E. Nwariaku, and Lance S. Terada

The University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390

Correspondence to L. Terada: lance.terada{at}utsouthwestern.edu

Detachment of parenchymal cells from a solid matrix switches contextual cues from survival to death during anoikis. Marked shape changes accompany detachment and are thought to trigger cell death, although a working model to explain the coordination of attachment sensation, shape change, and cell fate is elusive. The constitutive form of the adapter Shc, p52Shc, confers survival properties, whereas the longer p66Shc signals death through association with cytochrome c. We find that cells that lack p66Shc display poorly formed focal adhesions and escape anoikis. However, reexpression of p66Shc restores anoikis through a mechanism requiring focal adhesion targeting and RhoA activation but not an intact cytochrome c–binding motif. This pathway stimulates the formation of focal adhesions and stress fibers in attached cells and tension-dependent cell death upon detachment. p66Shc may thus report attachment status to the cell by imposing a tension test across candidate anchorage points, with load failure indicating detachment.

Abbreviations used in this paper: BDM, 2,3 butanedione monoxime; CH, collagen homologous; FAK, focal adhesion kinase; FAT, focal adhesion targeting; HUVEC, human umbilical vein endothelial cells; PTB, phosphotyrosine-binding; RBD, rho-binding domain; SH, Src homology; TIRF, total internal reflection fluorescence; wt, wild type.


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