IndraLab

Statements

OTULIN inhibits IL1B. 3 / 3
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"Consistent with the finding that OTULIN overexpression was shown to delay NF-kappaB activation of TNF, whereas its knockdown was reported to increase the output of NF-kappaB signaling [XREF_BIBR, XREF_BIBR, XREF_BIBR], we found that OTULIN overexpression strongly depressed NF-kappaB activity and reduced the release of TNF-alpha, IL-1beta, and IL-6, which are the primary pro inflammatory cytokines that aggravate brain injury."
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"Our findings suggest that IL-1β overproduction caused by a deficiency of otulin, an upstream triggering factor, could be a promising diagnostic and therapeutic target for NA."
38599290
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"OTULIN overexpression significantly suppressed the production of TNF-alpha, IL-1beta, and IL-6 in PM and N9 cells via inhibiting the nuclear translocation of NF-kappaB p65 but had no effect on the pro inflammatory cytokines secreted by un activated microglia, which directly indicates that OTULIN suppressed microglia mediated neuroinflammation by inhibiting the NF-kappaB pathway and attenuated the release of inflammatory mediators under the in vitro ischemic condition."
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