scholarly journals A Novel Zinc Finger Protein Interacts with Receptor-interacting Protein (RIP) and Inhibits Tumor Necrosis Factor (TNF)- and IL1-induced NF-κB Activation

2002 ◽  
Vol 277 (18) ◽  
pp. 15985-15991 ◽  
Author(s):  
Danying Chen ◽  
Xiaoyan Li ◽  
Zhonghe Zhai ◽  
Hong-Bing Shu
Keyword(s):  
Tumor Necrosis Factor ◽  
Zinc Finger ◽  
Tumor Necrosis ◽  
Zinc Finger Protein ◽  
Interacting Protein ◽  
Finger Protein ◽  
Necrosis Factor

scholarly journals The A20 zinc finger protein protects cells from tumor necrosis factor cytotoxicity.

1992 ◽  
Vol 267 (18) ◽  
pp. 12424-12427
Author(s):  
A W Opipari ◽  
H.M. Hu ◽  
R Yabkowitz ◽  
V.M. Dixit
Keyword(s):  
Tumor Necrosis Factor ◽  
Zinc Finger ◽  
Tumor Necrosis ◽  
Zinc Finger Protein ◽  
Finger Protein ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor induces rapid down-regulation of TXNIP in human T cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Trine B. Levring ◽  
Martin Kongsbak-Wismann ◽  
Anna K. O. Rode ◽  
Fatima A. H. Al-Jaberi ◽  
Daniel V. Lopez ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Glucose Uptake ◽  
Tumor Necrosis ◽  
Gradient Centrifugation ◽  
Tumor Necrosis Factor Receptor ◽  
Down Regulation ◽  
Interacting Protein ◽  
Human T Cells ◽  
Necrosis Factor

Abstract In addition to antigen-driven signals, T cells need co-stimulatory signals for robust activation. Several receptors, including members of the tumor necrosis factor receptor superfamily (TNFRSF), can deliver co-stimulatory signals to T cells. Thioredoxin interacting protein (TXNIP) is an important inhibitor of glucose uptake and cell proliferation, but it is unknown how TXNIP is regulated in T cells. The aim of this study was to determine expression levels and regulation of TXNIP in human T cells. We found that naïve T cells express high levels of TXNIP and that treatment of blood samples with TNF results in rapid down-regulation of TXNIP in the T cells. TNF-induced TXNIP down-regulation correlated with increased glucose uptake. Furthermore, we found that density gradient centrifugation (DGC) induced down-regulation of TXNIP. We demonstrate that DGC induced TNF production that paralleled the TXNIP down-regulation. Treatment of blood with toll-like receptor (TLR) ligands induced TNF production and TXNIP down-regulation, suggesting that damage-associated molecular patterns (DAMPs), such as endogenous TLR ligands, released during DGC play a role in DGC-induced TXNIP down-regulation. Finally, we demonstrate that TNF-induced TXNIP down-regulation is dependent on caspase activity and is caused by caspase-mediated cleavage of TXNIP.

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