What question did this study set out to answer?

To determine how cellular inhibitor of apoptosis proteins (cIAPs) and cFLIP isoforms regulate intracellular cell death complexes and pathways.

July 9, 2011Molecular CellOpen Access

cIAPs Block Ripoptosome Formation, a RIP1/Caspase-8 Containing Intracellular Cell Death Complex Differentially Regulated by cFLIP Isoforms

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Authors

MFMaria FeoktistovaRWTH Aachen University PGPeter GeserickBerlin Institute of Health at Charité - Universitätsmedizin Berlin BKBeate KellertMax Planck Society

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Implication

Experimental study reveals that cIAP loss triggers 2-MDa Ripoptosome assembly in cellular models, highlighting a molecular switch governing apoptotic versus necroptotic death during inflammation.

Key Points

To determine how cellular inhibitor of apoptosis proteins (cIAPs) and cFLIP isoforms regulate intracellular cell death complexes and pathways.
Evaluated the intracellular formation of cell death platforms following the loss of cIAPs in cellular models.
Characterized the molecular composition and regulatory dynamics of the 2-MDa complex, focusing on RIP1, FADD, caspase-8/10, and cFLIP isoforms.
Examined downstream cell death mechanisms during membrane receptor activation using Toll-like receptor 3 (TLR3) stimulation.
Loss of cIAPs prompted the spontaneous assembly of a 2-MDa complex named the Ripoptosome, containing RIP1, FADD, caspase-8, caspase-10, and cFLIP isoforms.
cFLIP(L) inhibited Ripoptosome formation, while cFLIP(S) promoted complex assembly, establishing caspase activity as a molecular rheostat between RIP3-dependent necroptosis and caspase-dependent apoptosis.
Ripoptosome core formation driven by RIP1 crucially dictated the outcome of membrane-bound receptor signaling, including TLR3-mediated inflammatory responses.

Cite This Study

Feoktistova et al. (2011) studied this question.

synapsesocial.com/papers/6a70c689e5469ee92be17445 https://doi.org/10.1016/j.molcel.2011.06.011

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Implication

Experimental study reveals that cIAP loss triggers 2-MDa Ripoptosome assembly in cellular models, highlighting a molecular switch governing apoptotic versus necroptotic death during inflammation.

cIAPs Block Ripoptosome Formation, a RIP1/Caspase-8 Containing Intracellular Cell Death Complex Differentially Regulated by cFLIP Isoforms

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Implication

Key Points

Cite This Study

cIAPs Block Ripoptosome Formation, a RIP1/Caspase-8 Containing Intracellular Cell Death Complex Differentially Regulated by cFLIP Isoforms

Discussion

Member takes

Implication

Key Points

Cite This Study

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