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TNFAIP3 inhibits MAP3K5. 12 / 12
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"Zhang et al. [ 57 ] found that TNFAIP3 could inhibit the activity of ASK1 and downstream JNK/p38 by the deubiquitination of ASK1 under pathological conditions, effectively preventing the development o[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Taken together , the results from this study reveal a novel anti-apoptotic mechanism of A20 in TNF signaling pathway : A20 binds to ASK1 and mediates ASK1 degradation , leading to suppression of JNK activation and eventually blockage of apoptosis ."
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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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"TNFAIP3 was shown to inhibit the development of MASH by counteracting the hyperactivation of ASK1, the activation of which is known to increase hepatic lipid accumulation and inflammatory responses, mainly by promoting the activation of its downstream JNK‒p38 signaling pathway [179]."
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"A20 signaling in APAP necrosis is through the MAPK cascade Since A20 is known to degrade ASK1 , thus abrogating JNK activation ( 26 ) , we examined JNK expression in A20HepCKO mice after APAP ."
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"A20 reduces the stability and promotes the degradation of ASK1 through the ubiquitination process A20 restricts TNF-induced NF-kappaB signaling through its ubiquitin editing activity on RIP1 ,14,15 it is thus of interest to test whether A20 would be affecting the stability of ASK1 through a similar mechanism ."
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"The results from this study reveal a novel anti-apoptotic mechanism of A20 in TNF signaling pathway : A20 binds to apoptosis signal-regulating kinase1 ( ASK1 ) and mediates ASK1 degradation , leading to suppression of JNK activation and eventually blockage of apoptosis ."
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"Upon TNFα signaling and ischemia–reperfusion, TNFAIP3 suppresses the ASK1 signaling [217]."
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"According to Wang et al. (2017), CFLAR inhibits ASK1 by preventing its dimerization, while Zhang et al. (2018) found that the endogenous suppressor TNFAIP3 inhibits ASK1 by preventing its deubiquitination xref ."
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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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"However, TNFAIP3 (A20), which has both ubiquitin ligase and deubiquitinase activities, inactivates ASK1 in fatty-acid-induced cells and ameliorates NASH [ xref ]."
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"Recent studies reported that TNFAIP3 could block the onset and progression of nonalcoholic steatohepatitis (NASH) by suppressing ASK1 hyperactivation (28) or inhibiting TAK1 activation and was also regarded as the promising therapeutic target of NASH (29)."
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