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TRADD is critical for resistance to TRAIL-induced cell death through NF-κB activation.

Authors
JY, Kim; JY, Lee; DG, Kim; GB, Koo; JW, Yu; YS, Kim
Citation
FEBS letters, 585(14):2144-2150, 2011
Journal Title
FEBS letters
ISSN
0014-57931873-3468
Abstract
One major obstacle in the clinical application of TRAIL as a cancer therapeutic agent is the acquisition of TRAIL resistance. We found that deficiency of TRADD sensitizes cells to TRAIL-induced apoptosis. Enhanced cell death in TRADD(-/-) MEFs is associated with defective NF-κB activation, indicating that the pro-survival function of TRADD in TRAIL signaling is mediated at least in part via NF-κB activation. Moreover, siRNA knock-down of TRADD in cancer cells sensitizes them to TRAIL-induced apoptosis. Thus, TRADD has a survival role in TRAIL signaling and may be one potential target for overcoming TRAIL resistance in cancer therapy.
MeSH terms
AnimalsApoptosis/*physiologyCaspase 3/metabolismCaspase 8/metabolismCell Line, TumorCells, CulturedEnzyme ActivationExtracellular Signal-Regulated MAP Kinases/metabolismFibroblasts/cytology/physiologyHumansJNK Mitogen-Activated Protein Kinases/metabolismMiceMice, KnockoutNF-kappa B/*metabolismPoly(ADP-ribose) Polymerases/metabolismRNA, Small Interfering/genetics/metabolismSignal Transduction/physiologyTNF Receptor-Associated Death Domain Protein/genetics/*metabolismTNF-Related Apoptosis-Inducing Ligand/genetics/*metabolism
DOI
10.1016/j.febslet.2011.05.034
PMID
21627969
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
AJOU Authors
김, 유선
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