IndraLab

Statements



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"These results suggested that USP8 may mediate attenuation of the inflammatory response via the MAPK pathway."

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"In conclusion, USP8 inhibited lipopolysaccharide-triggered inflammation and pyroptosis in human bronchial epithelial cells by activating PI3K/AKT signaling and inhibiting NF-κB signaling pathway."

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"Overexpression of USP8 inhibits inflammation and ferroptosis in chronic obstructive pulmonary disease by regulating the OTUB1/SLC7A11 signaling pathway."

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"An earlier study by Zhang et al. showed that USP8, through deubiquitination and inactivation of TAK1, suppressed intermittent hypoxia/reoxygenation-induced inflammation in renal tubular epithelial cells [16]."

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"USP8 treatment improved cognitive dysfunction and inhibited inflammation and oxidative stress in CLP mice."

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"In liver fibrosis models and activated Kupffer cells (KCs), the elevated expression of METTL3 enhances metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) levels via m6A methylation and facilitates the degradation of ubiquitin-specific peptidase 8 (USP8) mRNA, subsequently reduces transforming growth factor β-activated kinase 1 (TAK1) regulation, enhances cell pyroptosis markers (NLRP3, caspase-1, GSDMD-N) and NF-κB p-p65 levels, thereby promoting macrophage pyroptosis and inflammation [58]."

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"The mechanism by which USP8 inhibits inflammation in vivo remains unclear."

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"Overexpression of USP8 suppressed inflammation in COPD mice."