IndraLab

Statements

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"Our findings indicate that USP18 inhibition induces inflammation by increasing the STAT signaling and exacerbates IFN induced beta cell apoptosis by the mitochondrial pathway of cell death."
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"A partial form of inherited human USP18 deficiency underlies infection and inflammation."
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"The upregulation of USP18 ameliorated hind limbs ' motor function , inhibiting inflammation and apoptosis after SCII in rats ."
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"From the transcriptomic analysis we selected USP18, previously shown to decrease inflammation and insulin-resistance."
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"Through IFNAR1/2 receptors and the JAK/STAT signaling pathway, IFN-I has a further impact on the next important component of the development of the inflammatory response: the ISG15/USP18 axis, which regulates the activity of the immune system [36] and reduces the inflammatory response intensity by inhibiting the JAK/STAT signaling pathway, indicating that there possibly exists a negative feedback loop between USP18, IFN-I, and, therefore, TNF-α [43, 44]."
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"USP18 silencing enhanced basal inflammation and senescence."
31971958
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"USP18 reduced basal inflammation, senescence and insulin resistance in coronary endothelial cells."
31971958
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"Previous studies indicated that USP18 inhibited inflammation by negatively regulating NF-κB signaling pathway [31,32], and GSDMD-N terminal fragments form transmembrane pores to enable the release of IL-1β [33–35]."
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"Suppression of USP18 promotes inflammation by STAT signaling and aggravates β-cell apoptosis induced by IFN through the cell death in mitochondria (114)."
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"While upregulation of interferon-responsive genes suggests some form of long-lasting intrinsic inflammation response, ISG15 and USP18 in fact act to limit inflammation by controlling the NF-kB pathway[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"USP18 can also reduce intracellular inflammation and stress signaling by inhibiting the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway, which predisposes cells to ER stress and potentially affects CHOP expression ."
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"USP18 knockdown can promote the inflammatory response and apoptosis of pancreatic β cells induced by IFN, indicating that USP18 may be a suppressor gene in type 1 diabetes [165]."
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