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PMID |
Sentence |
1 |
16824518
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A20 is a negative regulator of NF-kappaB activation and thus a potential therapeutic tool for the treatment of diseases where apoptosis and/or inflammatory responses are part of the pathogenic process.
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2 |
18329387
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A20 negatively regulates NFkappaB (nuclear factor kappaB) signaling induced by TNF receptor family and Toll-like receptors, but the mechanism of A20 action is poorly defined.
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3 |
19343319
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In addition to the upregulation of known pro-apoptotic genes, a number of anti-apoptotic genes including BIRC3, BCL2A1, TNFAIP3, CFLAR and TRAF1 were induced by cytokines through NF-kappaB.
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4 |
21151899
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High glucose and hyperglycemia reduced upregulation of the NF-?B inhibitory and atheroprotective protein A20 in human coronary endothelial (EC) and smooth muscle cell (SMC) cultures challenged with Tumor Necrosis Factor alpha (TNF), aortae of diabetic mice following Lipopolysaccharide (LPS) injection used as an inflammatory insult and in failed vein-grafts of diabetic patients.
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5 |
18952128
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The zinc finger-containing protein A20 is a negative regulator of TNF-induced JNK (c-Jun-N-terminal kinase) and NFkappaB (nuclear factor kappaB) signaling.
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6 |
18952128
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Although A20 is mostly localized in the cytosol, our recent studies reveal that a fraction of A20 can associate with a lysosome-interacting compartment in a manner that requires its carboxy terminal zinc fingers, but independent of its ubiquitin modifying activities.
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7 |
18952128
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This process is dependent on the membrane tethering zinc finger domains of A20, but does not require A20 ubiquitin modifying activity.
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8 |
10523611
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The inhibitory effect of A20 on cytokine-stimulated NO production is due to transcriptional blockade of inducible NO synthase (iNOS) induction; A20 inhibits the activation of the transcription factor nuclear factor kappaB at a level upstream of IkappaBalpha degradation.
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9 |
16936197
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Activation of NF-kappaB by TNF receptor-associated factor (TRAF) 2, TRAF6, NF-kappaB-inducing kinase, or protein kinase D, which transduce signals downstream of Toll-like receptors, TNF receptors, and free radicals, respectively, were all potent activators of the A20 promoter.
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10 |
16936197
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Finally, A20 expression was sufficient to protect beta-cells from TNF-induced apoptosis.
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11 |
16936197
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Further, A20 expression is NF-kappaB dependent, thus linking islet proinflammatory gene responses with protection from apoptosis.
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