IndraLab

Statements

USP16 binds SKIL. 28 / 28
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"These findings suggest that SNO-USP16 at the C731 site is involved in CME-induced GSH imbalance."
41339351
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"Therefore, SNO-USP16 could facilitate the ubiquitination and degradation of KDM1A in CME."
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"Moreover, the enhanced SNO-USP16 levels in the CME model were lowered by infection with AAV9-USP16-WT, which was more apparent in the AAV9-USP16-C731A infection group (Fig.  xref )."
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"SNO-USP16 at the C731 site facilitates KDM1A ubiquitination."
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"Therefore, SNO-USP16 was predicted to play a role in the pathogenesis of CME."
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"In the present study, we provide evidence that iNOS contributes to SNO-USP16 at the C731 site and subsequently results in KDM1A protein ubiquitination, thus leading to a GSH imbalance under hypoxic conditions."
41339351
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"Given that SNO-USP16 contributed to GSH imbalance during CME, we further elucidated whether SNO-USP16 could affect KDM1A protein ubiquitination."
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"These findings prove that iNOS-mediated SNO-USP16 promotes CME progression."
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"In conclusion, our results confirmed that iNOS-mediated SNO-USP16 served as a driver of ubiquitination and degradation of KDM1A protein, which disrupted GSH homeostasis and exacerbated CME-induced myocardial injury (Fig.  xref )."
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"Thus, inhibition of SNO-USP16 at the C731 site suppresses the ubiquitination and degradation of KDM1A."
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"iNOS-mediated SNO-USP16 contributes to CME-induced GSH imbalance and KDM1A downregulation."
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"Inhibition of SNO-USP16 at the C731 site represses ubiquitination and degradation of KDM1A protein to epigenetically activate GCLM and GLS, which maintains GSH homeostasis and relieves CME-induced myocardial injury."
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"Therefore, we further explored the regulation of iNOS by SNO-USP16 in the context of CME."
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"As shown in Fig.  xref , treatment with the iNOS inhibitor 1400 W effectively reversed the hypoxia-induced upregulation of SNO-USP16."
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"The enhanced SNO-USP16 levels in the CME group were partially reduced by 1400 W irradiation (Fig.  xref )."
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"Altogether, SNO-USP16 inhibition stabilizes the KDM1A protein to epigenetically activate GCLM and GLS, thus maintaining GSH homeostasis and relieving CME-induced myocardial injury."
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"Taken together, iNOS facilitated SNO-USP16 to impair GSH homeostasis in the CME by reducing KDM1A expression."
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"Inhibition of SNO-USP16 at the C731 site improves GSH homeostasis in CME models."
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"Mounting evidence indicates that SNO may affect cardiac function under both physiological and pathological conditions by regulating oxidative stress xref , xref SNO-USP16 levels were markedly increased by CME treatment in this study."
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"Therefore, we measured SNO-USP16 levels using a biotin-switch assay."
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"This study demonstrates the contribution of SNO-USP16 to GSH imbalance in CME."
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"As shown in Fig.  xref , SNO-USP16 levels in the myocardial tissues of CME rats were markedly higher than those in sham rats."
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"Consistently, SNO-USP16 levels were elevated in hypoxia-challenged cardiomyocytes (Fig.  xref )."
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"Furthermore, inhibition of SNO-USP16 at the C731 site restrained the overproduction of ROS and restored GSH homeostasis, thus mitigating CME-induced myocardial injury."
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"Given that USP16 can deubiquitinate KDM1A, we further evaluated the effect of SNO-USP16 on KDM1A ubiquitination."
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"Additionally, hypoxia led to elevated SNO-USP16 levels in USP16-WT-transfected cardiomyocytes, which were abrogated by the C731 mutation (Fig.  xref )."
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"Next, we validated the role of SNO-USP16 in CME in vivo."
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"In this study, hypoxia-induced ubiquitination and degradation of the KDM1A protein were abolished by mutation of SNO-USP16 at C731."
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