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Article . 2000 . Peer-reviewed
Data sources: Crossref
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Mighty Deadly MyD88

Mighty Deadly MyD88

Abstract

Toll receptors are activated by bacterially produced pathogen-associated molecular pattern (PAMPs). Bacterial lipoproteins (BLPs) are PAMPs that activate the Toll-like receptor 2 (TLR2) through recruitment of the adaptor molecule MyD88. Transfection of a variety of dominant negative mutants allowed Aliprantis et al . to show that MyD88 is a common mediator for both the cell survival signal mediated by NF-κB activation and the apoptotic signal mediated through Fas-associated death domain protein (FADD). FADD activation is dependent on the death domain (DD) of MyD88, and the two proteins could be coimmunoprecipitated from transfected cells, confirming a physical interaction between them. Apoptosis was inhibited by mutant forms of caspase 8, FADD, or MyD88, confirming an apoptosis pathway from TLR2 to MyD88 to FADD to caspase 8. Aliprantis, A.O., Yang, R.-B., Weiss, D.S., Godowski, P., and Zychlinsky, A. (2000) The apoptotic signaling pathway activated by Toll-like receptor-2. EMBO J . 19 : 3325-3336. [Abstract] [Full Text]

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
0
Average
Average
Average
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