Physiological consequences of programmed necrosis, an alternative form of cell demise-Reference-Cited by-同舟云学术

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Physiological consequences of programmed necrosis, an alternative form of cell demise

Published:2010-03-31 Issue:4 Volume:29 Page:327-332
ISSN:1016-8478
Container-title:Molecules and Cells
language:en
Short-container-title:Mol Cells

Author:

Cho Young Sik,Park Seung Yeon,Shin Hee Suk,Chan Francis Ka-Ming

Publisher

Springer Science and Business Media LLC

Subject

Cell Biology,Molecular Biology,General Medicine

Link

http://link.springer.com/content/pdf/10.1007/s10059-010-0066-3.pdf

Reference34 articles.

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2. Agostinis, P., Buytaert, E., Breyssens, H., and Hendrickx, N. (2004). Regulatory pathways in photodynamic therapy induced apoptosis. Photochem. Photobiol. Sci. 3, 721–729.

3. Cauwels, A., Janssen, B., Waeytens, A., Cuvelier, C., and Brouckaert, P. (2003). Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2. Nat. Immunol. 4, 387–393.

4. Chan, F.K., Shisler, J., Bixby, J.G., Felices, M., Zheng, L., Appel, M., Orenstein, J., Moss, B., and Lenardo, M.J. (2003). A role for tumor necrosis factor receptor-2 and receptor-interacting protein in programmed necrosis and antiviral responses. J. Biol. Chem. 278, 51613–51621.

5. Cho, Y.S., Challa, S., Moquin, D., Genga, R., Ray, T.D., Guildford, M., and Chan, F.K. (2009). Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virusinduced inflammation. Cell 137, 1112–1123.

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