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Summary
| Description |
English: Role of rECP in TNF-α apoptosis signaling. rECP increases BEAS-2B cells TNF-α production and release. The release of TNF-α binding to TNF receptor results in receptor internalization and activates caspase-8. Caspase-8-induced apoptosis can either trigger mitochondrial response or directly cause PARP activation by caspase-3. However, rECP-induced apoptosis shows no effects on mitochondrial responses. Accordingly, we suggest that rECP induces mitochondria-independent apoptosis. |
| Date | |
| Source | BioMed Central |
| Author | Chang K, Lo C, Fan T, Chang M, Shu C, Chang C, Chung C, Fang S, Chao C, Tsai J, Lai Y |
| Permission (Reusing this file) |
© 2010 Chang et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
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| current | 04:37, 20 May 2010 | | 661 × 1,107 (69 KB) | IxSerenityxi | {{Information |Description={{en|1=Role of rECP in TNF-α apoptosis signaling. rECP increases BEAS-2B cells TNF-α production and release. The release of TNF-α binding to TNF receptor results in receptor internalization and activates caspase-8. Caspase-8- |
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