IndraLab

Statements

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"In contrast, impaired OTUB1-deficient DC activation and cytokine production by OTUB1-deficient DCs protected mice from lipopolysaccharide-induced immunopathology."
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"In addition, engagement of TLR2, TLR7, and TLR9, which all signal via MyD88, and TLR3, which signals in a MyD88-independent manner through TRIF, resulted in significantly reduced IL-12, TNF, and IL-6 production by OTUB1-deficient BMDCs (Supplementary Fig. 2c), illustrating the stimulatory role of OTUB1 in proinflammatory TLR signaling.To understand how OTUB1 promotes cytokine production in DCs, we stimulated FLT3L-expanded BMDCs with TLA (Fig. 2c), TgPFN (Fig. 2d), and LPS (Fig. 2e) and analyzed signaling molecules by WB analysis."
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"Mechanistically, OTUB1 promoted cytokine production in DCs by downregulating K48-linked ubiquitination and increasing the stability of UBC13, an E2-conjugating enzyme critical for the activation of canonical NF-κB and MAPK signaling."
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