Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10870747 | FEBS Letters | 2014 | 6 Pages |
Abstract
In T cells mitochondria-derived reactive oxygen species (ROS) are indispensible for activation of the transcription factor NF-κB, expression of cytokines and the CD95 ligand (CD95L/FasL). Here we show that activation-induced ROS generation is dependent on mitochondrial fission. Inhibition of dynamin related protein 1 (Drp1) results in reduced ROS levels and transcriptional activity of NF-κB leading to diminished proliferation and CD95L-dependent activation-induced cell death (AICD). Upon stimulation Drp1 is S-nitrosylated, which is required for oxidative signalling, AICD and cytokine production. In conclusion, we describe a novel signalling pathway that links TCR-induced nitric oxide release to mitochondrial fission and oxidative signalling.
Keywords
PKCNMMAH2DCF-DACFSEphorbol 12-myristate 13-acetateDrp1AICDIP3TCr2′,7′-dichlorodihydrofluorescein diacetatePMAROSinterleukinApoptosisdiacylglycerolMitochondrial dynamicsDAGT cellactivation induced cell deathNAMEdynamin related protein 1Protein kinase Ccarboxyfluorescein succinimidyl esterReactive oxygen species (ROS)Reactive oxygen speciesT cell receptor
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Authors
Daniel Röth, Peter H. Krammer, Karsten Gülow,