IndraLab

Statements



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"A co-occupied intronic TNFAIP3 regulatory element mediated cooperative enhancement of transcription by GR and NF-kappaB that required the presence of a functional GR binding site (GBS)."

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"Research indicates that zinc plays a regulatory role in NF-κB transcription, mediated by the zinc-finger protein TNF-α-induced protein 3 (TNFAIP3) and the receptor signalling pathway activated by peroxisome proliferator-activated receptor (PPAR) [57,58]."

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"Interestingly, TNFAIP3 also enhances signal transducer and activator of transcription 3, which binds the distal region of the C/EBP b promoter to upregulate LIP but downregulate LAP expression [44,45]."

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"Multiple downstream components of TNF signaling have been associated in autoimmunity, most notably the tumor necrosis factor inducible protein A20 (TNFAIP3), which terminates TNF- and pattern recognition receptor induced responses of the transcription factor NF-kappaB."