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High NEMO expression is associated with hepatitis and hepatocarcinogenesis.
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NEMO deficiency hampered activation of IKK complex in osteoclast precursors, causing arrest of osteoclastogenesis and apoptosis. Interestingly, inhibiting apoptosis by genetic ablation of TNFr1 significantly increased cell survival, but failed to rescue osteoclastogenesis or reverse osteopetrosis.
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NEMO was critically involved in the cGAS-STING pathway.
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This study provides evidence for a protective function of canonical IKK/NF-kappaB signalling in the arenchymal compartment during pancreatitis. In the absence of the regulatory IKK subunit NEMO, a combination of a fibrogenic gene signature, enhanced acinar-ductal metaplasia and a lack of regeneration contribute to the exacerbation of pancreatitis.
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E+P treatment of breast cancer cells increased ER binding to the NEMO promoter, thereby increasing NEMO expression.
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robust caspase activation in NEMO-deficient cells is concomitant with RIPK3 recruitment to the apoptosis-mediating complex.
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lymphocyte-specific deletion of IKK2 or NEMO aggravated kidney injury after ischemia-reperfusion injury, and, in both conditions, the percentage of Th17 cells was increased.
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Whereas Parkin has been reported to positively regulate the expression of OPA1 through NEMO, herein we found that PARK2 overexpression did not modify the expression of OPA1.
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prevents colon inflammation by NF-kappaB-independent functions
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Thyrocyte-specific NEMO knock-out mice gradually develop hypothyroidism after birth, which leads to reduced body weight and shortened life span.
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SENP1 deletion in adipocytes causes Type 1 diabetes mellitus via enhanced SUMOylation of NEMO, leading to increased NF-kappaB activity, cytokine production and pancreatic inflammation.
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Crucial functions of inflammatory TAK1-NEMO signaling in protecting the brain endothelium and maintaining normal brain function.
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Data show that NEMO protein prevents hepatocarcinogenesis by inhibiting receptor (TNFRSF)-interacting serine-threonine kinase 1 (RIPK1) kinase activity-driven hepatocyte apoptosis.
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Data show that the in utero death of NF-NF-kappaB essential modulator (NEMO) and cylindromatosis protein double mutant mice is mediated by TNF receptor 1 (TNFR1) signaling and can be rescued by TNFR1 deficiency.
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signaling through NEMO might not only be involved in the production of NF-kappaB proinflammatory chemokines but also regulates podocyte dynamics independently of NF-kappaB
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The stability of the NEMO coiled coil is maintained by strong interhelix interactions in the region centered on residue 54.
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NEMO deficiency results in apoptosis, the development of liver fibrosis and hepatocellular carcinoma, all of which are substantially alleviated by allogeneic hepatocyte transplantation.
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Mass spectrometric analysis demonstrated that WA covalently modifies NEMO on a cysteine residue within the C-terminal zinc finger (ZF) domain. Point mutations to the ZF can reverse the WA-induced Lys-48-polyubiquitin binding phenotype
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Authors propose a model in murine cytomegalovirus virion-associated protein M45 delivered by viral particles activates NF-kappaB, presumably involving an interaction with RIP1 and NEMO.
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NEMO ubiquitination is required for optimal innate immune signaling responses. These findings suggest that NEMO ubiquitination is crucial for NF-kappaB activity in response to innate immune agonists.
