IndraLab

Statements



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"Interestingly, while loss of OTULIN in myeloid cells triggers aberrant inflammation and cytokine release (Damgaard et al., 2016), some cell types, such as fibroblasts, compensate for the loss of OTULIN by downregulating LUBAC, and as a trade-off, these cells are unable to appropriately respond to cytokine signals and undergo apoptosis (Damgaard et al., 2019)."

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"Finally, the numerous other upregulated cytokines in LysMCre-OtulinLacZ and flox mice, which includes anti-inflammatory IL-10, will generate a delicate balance of responses, enabling these mice to deal with inflammation induced by loss of OTULIN."

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"OTULIN also prevents liver inflammation and HCC by inhibiting FADD and RIPK1 kinase-mediated hepatocyte apoptosis [122]."

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"The protease OTULIN, revealed by Dixit and colleagues to limit cell death and inflammation via ubiquitin (regulatory protein) modification (22), is another potential therapeutic target."

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"While loss of OTULIN leads to excessive inflammation through accumulation of linear-Ub, germline deficiencies of LUBAC also result in autoinflammation."

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"Deletion of Otulin in Mouse Immune Cells Drives Acute Systemic Inflammation."

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"OTULIN overexpression attenuated microglia activation in LPS induced brain inflammation."

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"Interestingly, conditional deletion of otulin in myeloid cells, but not T or B cells, causes systemic inflammation, neutrophil infiltration, and multi-organ inflammation in mouse models."

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"The deficiency of OTULIN reportedly induces autoinflammatory syndrome, and anti -TNF-α neutralizing antibodies suppressed the inflammation induced by OTULIN deficiency [21,22] ."

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"Recent work suggested that OTULIN can limit inflammation by deubiquitinating LUBAC [9]."

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"In an acute model, induced loss of OTULIN in immune cells leads to multi-organ inflammation and deterioration of animals within a few days; this can be ameliorated by anti-TNF, but not by neutralization of other upregulated cytokines."

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"OTULIN inhibits RIPK1-mediated keratinocyte necroptosis to prevent skin inflammation in mice."

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"64 Specific OTULIN deficiency can cause chronic liver inflammation and cancer in mice."

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"Another DUB, OTULIN, also suppresses inflammation."

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"OTULIN deficiency also increases intestinal pathology in mice genetically engineered to secrete excess TNF, confirming that chronic exposure to TNF promotes epithelial cell death and inflammation in OTULIN deficient mice."

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"OTULIN limits cell death and inflammation by deubiquitinating LUBAC."

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"OTULIN prevents liver inflammation and hepatocellular carcinoma by inhibiting FADD- and RIPK1 kinase-mediated apoptosis in hepatocytes [55]."

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"40 TNFs play a crucial role in OTULIN deficiency‐related inflammation, with anti‐TNF antibodies effectively treating inflammation induced by OTULIN deficiency."