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OTUD4 decreases the amount of ADSL. 13 / 13
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"These data indicate that OTUD4 restricts the expression of AMPs through MyD88 after bacterial infection.It should be noted that the basal phosphorylation of TAK1, p65, and p38 was higher in Vil-Cre;Otud4 IECs than in Otud4 IECs (Fig. 5C)."
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"In in vitro generated intestinal organoids, the basal expression of AMPs was also higher in Vil-Cre;Otud4 organoids than in Otud4 organoids, which was impaired by ST2825 (Fig. 5D and E and Fig. S6D), indicating that OTUD4 constitutively interacts with MyD88 and inhibits MyD88-dependent signaling and expression of AMPs."
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"Here in this study, we have demonstrated that OTUD4 inhibits the expression of AMPs in Paneth cells and supports intestinal inflammation and bacterial infection through deubiquitinating MyD88."
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"Here, we report that the ovarian tumor family deubiquitinase 4 (OTUD4) in Paneth cells restricts the expression of AMPs and thereby promotes experimental colitis and bacterial infection."
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"Knockout of OTUD4 promotes the expression of AMPs in intestinal organoids after stimulation with lipopolysaccharide (LPS) or peptidoglycan (PGN) and in the intestinal epithelial cells (IECs) of mice after DSS treatment or Salmonella typhimurium (S.t."
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"Mechanistically, knockout of OTUD4 results in hyper K63-linked ubiquitination of MyD88 and increases the activation of NF-kappaB and MAPKs to promote the expression of AMPs."
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"We further show that OTUD4 negatively regulates the expression of AMPs in IECs after DSS treatment or bacterial infection in a MyD88-dependent manner."
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"These results imply that the loss of OTUD4 in IECs does not inhibit the progression of colon cancer in the AOM/DSS and AOM/VP models.2.3 OTUD4 deficiency in IECs promotes the expression of AMPs and alters the microbiota after DSS treatment."
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"These data suggest that OTUD4 in IECs negatively regulates the expression of AMPs after DSS treatment.Because dysbiosis and alterations in the intestinal microbiota are associated with the progress of IBD and AMPs play an important role in restricting the invasion of the microbes in gut (Muniz et al., 2012), we collected feces from the Vil-Cre;Otud4 and the Otud4 mice which were given 2.5% DSS in drinking water for 0 or 5 days, and analyzed the microbial composition in the feces by 16S rRNA sequencing assays."
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"Results from qRT-PCR assays suggested that OTUD4 deficiency in Paneth cells promoted the expression of AMPs in the intestinal epithelium after DSS treatment (Fig. 4E), suggesting that OTUD4 in Paneth cells promotes intestinal inflammation.We next infected Def-Cre;Otud4 and Otud4 mice with S.t."
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"Expectedly, results from qRT-PCR analysis suggested that knockout of OTUD4 in Paneth cells promoted the expression of AMPs after S.t."
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"Collectively, these data demonstrate that OTUD4 in Paneth cells negatively regulates the expression of AMPs and promotes intestinal inflammation and bacterial infection.2.6 OTUD4 inhibits the expression of AMPs in a MyD88-dependent manner."
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"It has been demonstrated that OTUD4 negatively regulates MyD88-mediated pathways by deconjugating K63-linked polyubiquitin chains from MyD88 (Zhao, et al., 2018), we hypothesized that OTUD4 might inhibit the expression of AMPs by targeting MyD88 in IECs."
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