2019
DOI: 10.1002/jcp.29241
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SENP1‐mediated NEMO de‐SUMOylation inhibits intermittent hypoxia induced inflammatory response of microglia in vitro

Abstract: Among the seven small ubiquitin-like modifier (SUMO)-specific proteases (SENPs), our previous work showed that SENP1 suppressed nuclear factor kappa B (NF-κB) activation and alleviates the inflammatory response in microglia. However, the mechanism is still largely unknown. In this study, western blot analysis and enzymelinked immunosorbent assay were utilized for evaluating the extent of NF-κB activation and expression of proinflammatory cytokines. qPCR and western blot analysis were performed to detect SENP1 … Show more

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Cited by 17 publications
(10 citation statements)
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References 55 publications
(64 reference statements)
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“…To explore the mechanism by which propofol affects hypoxia-induced inflammation in microglia, further experiments were carried out. NF-κB is a key transcription factor that is associated with hypoxia-induced inflammation [29,[48][49][50]. Propofol can inhibit NF-κB activation, thereby playing an anti-inflammatory role.…”
Section: Discussionmentioning
confidence: 99%
“…To explore the mechanism by which propofol affects hypoxia-induced inflammation in microglia, further experiments were carried out. NF-κB is a key transcription factor that is associated with hypoxia-induced inflammation [29,[48][49][50]. Propofol can inhibit NF-κB activation, thereby playing an anti-inflammatory role.…”
Section: Discussionmentioning
confidence: 99%
“…SUMO can bind IκB and inhibit its phosphorylation, hence inhibiting NF-κB in the nucleus to initiate transcription of target genes ( 56 ). Thus, SUMOylation and de-SUMOylation play an important role in regulating NF-κB activation and NF-κB-dependent transcription ( 57 , 58 ). Our results confirm that GA promoted the phosphorylation of NF-κB p65 and its translocation from the cytoplasm to the nucleus, which was speculated to be associated with SUMOylation.…”
Section: Discussionmentioning
confidence: 99%
“…[ 118 ] SENP1 mediates IKK γ deSUMOylation at Lys 277/309, and the loss of SENP1 leads to increased NF‐ κ B activity and cytokine production, and induces the inflammatory response. [ 119 , 120 ] Vesicular stomatitis virus (VSV) infection induces the SUMOylation of IRF3 and IRF7 conjugated by SUMO1, SUMO2, and SUMO3. [ 8 ] The mutant K152R of IRF3 and the mutant K406R of IRF7 have lost their SUMO modifications, and result in higher levels of IFN mRNA induction after viral infection.…”
Section: Sumoylation Is a Vital Regulator Of Antiviral Innate And Int...mentioning
confidence: 99%