IndraLab

Statements

NFkappaB increases the amount of TNFAIP3. 10 / 10
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"TNFAIP3 expression is induced by NFkappaB 31."
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"In our work, we found that NF-kappaB induced the expression of CXCL1, ICAM1 and TNFAIP3 after doxorubicin treatment only in a subset of tumors, suggesting that differences in responses may exist among tumor subtypes."
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"In addition, TRPC1 activation enhanced NF-κB-dependent expression of the anti-apoptotic zinc finger protein A20, while silencing of TRPC1 promoted expression of pro-apoptotic proteins Bax and caspase-[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"NF-kappaB signaling also induces TNFAIP3 expression, thus providing a further feedback loop that modifies inflammation."
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"Furthermore, persistent endothelial NF-kappaB activation by vFLIP induces expression of the NF-kappaB regulator A20 and TNFAIP3, which represses vFLIP induced NF-kappaB activation and augments IKK1 protein expression [XREF_BIBR]."
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"Our results suggest a new function for A20 in the regulation of extrinsic cell death pathways in T cells, by facilitating optimal repression of RIPK1 mediated cell death by IKK complex and that is controlled by NF-κB dependent expression of Tnfaip3 during activation."
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"We ascribe a transcriptional mechanism to this change in death signalling, resulting from a failure of activated IKK2 deficient T cells to restore NF-κB dependent expression of Tnfaip3 ."
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"NF-kappaB signaling induces transcription of the TNFAIP3 gene, encoding a ubiquitin modifying enzyme (also known as A20) that negatively regulates the NF-kappaB signaling pathway [XREF_BIBR - XREF_BIBR]."
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"TNFAIP3 expression is up-regulated by NF-kB activation, and acts in a negative feedback to control NF-kβ-dependent gene expression."
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"In accord, HUVECs challenged with a prolonged exposure to thrombin activate the transcriptional pro-inflammatory program, but do not undergo apoptosis, due to concomitant NF-κB-dependent A20 expression [ xref ]."
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