RIPK3 binds RIPK1

Stable Identifier
R-HSA-5213462
Type
Reaction [binding]
Species
Homo sapiens
Compartment
Locations in the PathwayBrowser
General
SVG |   | PPTX  | SBGN
Click the image above or here to open this reaction in the Pathway Browser
The layout of this reaction may differ from that in the pathway view due to the constraints in pathway layout

When caspase-8 (CASP8) activity is inhibited, receptor-interacting protein 1 and 3 (RIPK1 and RIPK3) form a complex also known as the necrosome (Sun X et al. 2002; Li J et al. 2012). The RIP homotypic interaction motifs (RHIMs) of RIPK1 and RIPK3 mediate their interaction.

RIPK3 was found to be essential for the regulated necrosis. RIPK3 knockdown in human colorectal adenocarcinoma (HT-29) cell line, that stably expressed a shRNA targeting RIPK3, lead to blockage of TNF-alpha, TRAIL or FAS-induced pronecrotic signaling pathway (He S et al. 2009). Knockdown of RIPK3 in human keratinocyte HaCaT cells blocked TLR3-mediated necroptosis without affecting the apoptotic response. Moreover, overexpression of RIPK3 in human epithelial carcinoma cell line HeLa led to increased caspase-independent TLR3-induced cell death in the absence of IAPs (Feoktistova M et al. 2011).

Literature References
PubMed ID Title Journal Year
19524512 Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha

He, S, Wang, L, Miao, L, Wang, T, Du, F, Zhao, L, Wang, X

Cell 2009
22817896 The RIP1/RIP3 necrosome forms a functional amyloid signaling complex required for programmed necrosis

Li, J, McQuade, T, Siemer, AB, Napetschnig, J, Moriwaki, K, Hsiao, YS, Damko, E, Moquin, D, Walz, T, McDermott, A, Chan, FK, Wu, H

Cell 2012
Participants
Participant Of
This event is regulated
Orthologous Events
Authored
Reviewed
Created