Overcoming cancer cell resistance to Smac mimetic induced apoptosis by modulating cIAP-2 expression

Smac mimetics target cancer cells in a TNFα-dependent manner, partly via proteasome degradation of cellular inhibitor of apoptosis 1 (cIAP1) and cIAP2. Degradation of cIAPs triggers the release of receptor interacting protein kinase (RIPK1) from TNF receptor I (TNFR1) to form a caspase-8 activating...

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Detaylı Bibliyografya
Asıl Yazarlar: Petersen, Sean L., Peyton, Michael, Minna, John D., Wang, Xiaodong
Materyal Türü: Artigo
Dil:Inglês
Baskı/Yayın Bilgisi: National Academy of Sciences 2010
Konular:
Biological Sciences
Online Erişim:https://ncbi.nlm.nih.gov/pmc/articles/PMC2900705/
https://ncbi.nlm.nih.gov/pubmed/20547836
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.1005667107
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