IndraLab

Statements

TNFAIP3 activates autophagy. 20 / 21
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"TNFAIP3 inhibited inflammatory response and enhanced autophagy, thereby alleviating PD in mice."
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"In CD4 + T cells, TNFAIP3 promotes autophagy and survival following T-cell receptor activation by suppression of mTOR signaling through direct interaction of TNFAIP3 with mTOR [144] ."
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"It has been reported that Zinc finger protein A20 / TNFAIP3 ( A20 ) can inhibit the activity of the NF-kappaB pathway and promote autophagy ."
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"The reduced mitochondrial content could result from increased autophagy mediated by the upregulation of Tnfaip3, since Tnfaip3 deficiency has been shown to increase mitochondrial content in CD4 cells by promoting autophagy , or from reduced CD4 cell growth.Pathway analysis further supports a compromised effector function of CD4 cells from MMTV-Her2 mice."
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"A recent study showed that TNFAIP3 promoted autophagy after T cell receptor stimulation in CD4 T cells [ 16 ]."
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"TNFAIP3 promotes survival of CD4 T cells by restricting MTOR and promoting autophagy."
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"Besides, TNFAIP3 induced autophagy via modulating the TLR4/MyD88/nuclear factor kappa B (NF-κB) signaling pathway."
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"TNFAIP3 promotes survival of CD4 T cells by restricting MTOR and promoting autophagy."
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"In normal monocytes, TNFAIP3 induced autophagy, which restricted inflammasome activation to the early stage of LPS stimulation."
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"TNFAIP3 and DEPTOR together rapidly promoted autophagy after LPS treatment to prevent NLRP3 inflammasome formation."
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"TNFAIP3 inhibited inflammatory response and enhanced autophagy , thereby alleviating PD in mice ."
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"In summary, overexpressed TNFAIP3 can promote autophagy and reduce inflammation in LPS induced human NPCs."
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"Moreover, autophagy triggered by TNFAIP3 can ameliorate the degeneration of inflammatory human NPCs, providing a potential and an attractive therapeutic strategy for degenerative disease."
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"These results indicate that TNFAIP3 promotes autophagy after T cell receptor (TCR) stimulation in CD4 T cells."
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"TNFAIP3 promotes autophagy in LPS stimulated human NPCs."
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"Taken together, our findings illustrate that TNFAIP3 restricts MTOR signaling and promotes autophagy, providing new insight into the manner in which MTOR and autophagy regulate survival in CD4 T cells."
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"These results demonstrated that TNFAIP3 may induce autophagy in the LPS stimulated human NPCs."
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"TNFAIP3 promotes autophagy by inhibiting mTOR signaling in inflammatory human NPCs."
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"Interestingly, another study revealed that TNFAIP3 restricts mTOR signaling and promotes autophagy, regulating survival in CD4 T cells [64]."
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"The above results suggested that TNFAIP3 induces autophagy through inhibiting mTOR signaling."
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