In TNF-stimulated Cells, RIPK1 Promotes Cell Survival by Stabilizing TRAF2 and cIAP1, which Limits Induction of Non-canonical NF-κB and Activation of Caspase-8-Reference-Cited by-同舟云学术

In TNF-stimulated Cells, RIPK1 Promotes Cell Survival by Stabilizing TRAF2 and cIAP1, which Limits Induction of Non-canonical NF-κB and Activation of Caspase-8

Published:2011-04 Issue:15 Volume:286 Page:13282-13291
ISSN:0021-9258
Container-title:Journal of Biological Chemistry
language:en
Short-container-title:Journal of Biological Chemistry

Author:

Gentle Ian E.,Wong W. Wei-Lynn,Evans Joseph M.,Bankovacki Alexandra,Cook Wendy D.,Khan Nufail R.,Nachbur Ulrich,Rickard James,Anderton Holly,Moulin Maryline,Lluis Josep Maria,Moujalled Donia M.,Silke John,Vaux David L.

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference40 articles.

1. RIPK1 is not essential for TNFR1-induced activation of NF-κB

2. The Death Domain Kinase RIP Mediates the TNF-Induced NF-κB Signal

3. TRAF2 Must Bind to Cellular Inhibitors of Apoptosis for Tumor Necrosis Factor (TNF) to Efficiently Activate NF-κB and to Prevent TNF-induced Apoptosis

4. Both cIAP1 and cIAP2 regulate TNF -mediated NF- B activation

5. cIAP1 and cIAP2 Facilitate Cancer Cell Survival by Functioning as E3 Ligases that Promote RIP1 Ubiquitination

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