IndraLab

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TNFAIP3 inhibits apoptotic process. 33 / 33
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"TNF alpha induced protein 3 (TNFAIP3, A20) is a tumor enhancer in glioma [ xref ] and inhibits apoptosis in glioblastoma [ xref ]."
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"A20 inhibits TNF-induced apoptosis in fibroblasts, blocks necroptosis in fibroblasts and T cells, and paradoxically promotes Fas-dependent death in activated B cells ( xref ; xref ; xref )."
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"One critical finding from this study is that A20 not only completely blocked the transcription of other NF-kappaB target genes known to antagonize JNK signaling , but also effectively suppressed TNF-induced JNK activation and apoptotic cell death in NF-kappaB activation-deficient MEFs ( Figure 2 ) ."
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"Consistently, IEC specific deletion of TNFAIP3 (encoding A20), a gene mutated in Crohn 's disease that encodes an E3 ligase editing enzyme involved in dampening NF-kappaB signaling and TNF induced apoptosis, leads to massive IEC apoptosis and increased susceptibility to experimental colitis."
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"Our first set of experiments utilizing P. gingivalis as a model organism showed that while A20 competent cells remained resistant to bacteria-induced apoptotic response , A20 depletion triggered apoptosis upon exposure to bacteria ."
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"In contrast, ATRA induces the expression of BIRC3 and TNFAIP3, which inhibit Fas and TNFalpha mediated apoptosis signaling pathway by the interaction with TRAF2, and thus may prevent apoptosis."
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"We found that overexpression of miR-19b-3p or knockout of TNFAIP3 decreased apoptosis rates of NPC cell lines after irradiation."
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"In contrast, A20 inhibits apoptosis, at least partially, by binding to TXBP151, which inhibits TNF-α-induced apoptosis."
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"A20 can inhibit TNF-induced apoptosis in many cell types."
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"A20 restricts apoptosis in gingival keratinocytes following P. gingivalis infection ."
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"Additionally , the same group has reported that TNFAIP3 can endogenously suppress ASK1 and reduce apoptosis , lipid accumulation , and inflammation [ 116 ] ."
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"These results demonstrate that A20 not only inhibits TNF-induced apoptosis but also TNF-induced necrosis, suggesting that it interferes with an early step in TNF signalling which is required for both types of cell death."
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"As A20 can inhibit TNF-induced apoptosis in some cell types xref , xref , xref – xref , and A20 levels are elevated in GSCs, we hypothesized that GSCs are resistant to TNFα-induced apoptosis."
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"Additionally, the same group has reported that TNFAIP3 can endogenously suppress ASK1 and reduce apoptosis, lipid accumulation, and inflammation [XREF_BIBR]."
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"A20 inhibits apoptosis in several cell types, enhances cell survival and has implications for cellular senescence and aging."
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"Unlike A20, which inhibits TNF-induced apoptosis, overexpression of ZNF216 sensitized cells to TNF-induced apoptosis."
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"The inhibition of TNFα-induced apoptosis by A20 correlates with the inhibition of phospholipase A2, reduced production of reactive oxygen species (ROS), diminished collapse of mitochondrial membrane potential, decreased activation of caspase-3-like proteases and inhibition of JNK (Jäättelä et al., xref ; Wissing et al., xref ; Lademann et al., xref ; Daniel et al., xref ; Won et al., xref )."
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"Studies in Jurkat T-cells demonstrated that A20 inhibits TNFα-induced apoptosis by disrupting the recruitment of TRADD and RIP to TNFR-1 complex [ xref ]."
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"TNF alpha induced protein 3 (TNFAIP3, A20) is a tumor enhancer in glioma [XREF_BIBR] and inhibits apoptosis in glioblastoma [XREF_BIBR]."
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"However, fenretinide specifically induced Fas and TNFalpha mediated apoptosis by increasing the expression of pro apoptotic genes i.e., DEDD2, CASP8, CASP4, and HSPA1A/B; whereas, ATRA induced the expression of BIRC3 and TNFAIP3, which inhibit apoptosis by interacting with TRAF2."
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"TNFAIP3 can inhibit both NF-kappaB signaling and apoptosis, but the role of TNFAIP3 in vivo is likely cell and context dependent, owing to the ability of NF-kappaB to concomitantly induce transcription of inflammatory and anti-apoptotic genes."
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"However, the antagonists TNFAIP3, FLIP and cIAP, which respectively inhibit apoptosis via TRAF6, caspases 8, 9, 10 and TRAF-2 directly or indirectly are also prominent amongst the up-regulated genes [ xref - xref ]."
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"Apoptosis and pyroptosis of NP cells increased gradually treated with LPS for 12 h , 24 h , and 48 h. Differently , the level of mitophagy increased first and then decreased , and was the highest at LPS treatment for 12 h. Overexpression or knockdown of A20 in NP cells revealed that A20 attenuated the pyroptosis , apoptosis , and production of inflammatory cytokines of NP cells induced by LPS , while A20 sponsored mitophagy , reduced ROS production and collapse of mitochondrial membrane potential ( DeltaPsim ) ."
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"In pancreatic islets, A20 inhibited both apoptosis and NF-κB activation induced by cytokines, suggesting that NF-κB may actually mediate apoptosis [58] ."
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"This study suggests a distinct role of ZNF216 from A20, which inhibits TNF-induced apoptosis (Figure xref )."
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"TNFAIP3 inhibits NF-κB activation as well as TNFα-mediated apoptosis by binding to TRAF family adaptor proteins (Heyninck , 1999) ."
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"Besides its well documented NF-κB inhibitory function, A20 also inhibits TNF-induced apoptosis ( xref ; xref ; xref )."
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"TNFAIP3 functions to inhibit NFκB activation and TNFα-mediated apoptosis [32,33]."
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"Furthermore, A20 may inhibit apoptosis through the suppression of pro-inflammatory cytokines (Nagamachi et al., xref )."
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"A20 inhibits apoptosis induced by TNF by interfering with the formation of complex I. The concomitant increase in both A20 and cFLIP which would lead to inhibition of complex I and complex II, respectively, may be required for complete protection against apoptosis induced by TNF."
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"Moreover, A20 may inhibit apoptosis through the suppression of pro-inflammatory cytokines ( xref )."
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"TNFAIP3 inhibits NF-κB activation as well as TNFα-mediated apoptosis by binding to TRAF family adaptor proteins (Heyninck et al., 1999)."
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"The downregulation of TNFAIP3 facilitates hyperactive NF-kappaB signaling, chronic inflammation, and reduced apoptosis, all characteristics of SLE."
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