IndraLab

Statements

TNFAIP3 activates autophagy. 15 / 16
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"The above results suggested that TNFAIP3 induces autophagy through inhibiting mTOR signaling."
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"It has been reported that Zinc finger protein A20 and TNFAIP3 (A20) can inhibit the activity of the NF-kappaB pathway and promote autophagy."
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"These results demonstrated that TNFAIP3 may induce autophagy in the LPS stimulated human NPCs."
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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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"In summary, overexpressed TNFAIP3 can promote autophagy and reduce inflammation in LPS induced human NPCs."
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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 survival of CD4 T cells by restricting MTOR and promoting autophagy."
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"TNFAIP3 and DEPTOR together rapidly promoted autophagy after LPS treatment to prevent NLRP3 inflammasome formation."
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"TNFAIP3 promotes autophagy in LPS stimulated human NPCs."
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"TNFAIP3 promotes autophagy by inhibiting mTOR signaling in inflammatory 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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"TNFAIP3 inhibited inflammatory response and enhanced autophagy, thereby alleviating PD in mice."
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"TNFAIP3 inhibited inflammatory response and enhanced autophagy , thereby alleviating PD in mice ."
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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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"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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