IndraLab

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Lipopolysaccharide inhibits RIPK1. 6 / 6
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"Further studies demonstrated that LPS stimulation of RIPK1-deficient monocytes resulted in increased necroptosis (inflammatory cell death) and IL-1β release; this has also been observed in animal models.As with RELA haploinsufficiency, the proinflammatory clinical features of RIPK1 deficiency result from reduced cell viability; however, there is additional release of a potent inflammatory mediator."
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"In the BV2 and N9 microglia cell lines, miR-335 strongly counteracted LPS induced proinflammatory gene expression, and downregulated receptor interacting protein 1 (RIP1) and RIP3, two important players of necroptotic and inflammatory signaling pathways."
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"As shown in Figures 1C, D , we found that LPS-induced morphological changes and heme release from erythrocytes were suppressed following an LPS-induced decrease in O-GlcNAcylation of RIPK1 that was blocked by TMG administration."
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"The LPS or bacterial induced necroptosis in wild type BMDMs was also inhibited by Necrostatin-1 (Nec-1), indicating a RIPK1 kinase dependency (XREF_SUPPLEMENTARY)."
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"The altered IL-1beta release has been associated with increased NLPR3 activity and MLKL dependent necroptosis, based on evidence that inhibitors of NLRP3 or MLKL can reduce IL-1beta secretion in LPS stimulated RIPK1 deficient cell lines (BLaER1 and THP1 cells)."
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"Importantly, due to the attenuation of HBP pathway LPS was shown to decrease O-GlcNAcylation of RIPK1 [ 89 ]."
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