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Cystathionine gamma lyase-H2S was a dominant H2S generating system in osteoclasts, while cystathionine beta-synthase did not generate H2S.
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ZYZ-803 stimulated the expression of cystathionine gamma-lyase (CSE) for H2S generation and the activity of endothelial NO synthase (eNOS) for NO production.Blocking CSE and/or eNOS suppressed ZYZ-803-induced H2S and NO production and cardioprotection.
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Golgi stress response elicited by monensin stimulates CSE by acting via ATF4 with characteristics distinguishable from the endoplasmic reticulum stress response
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The results of this study show that deletion of the cystathionine-gamma-lyase gene has no effects on hypoxia-induced changes in TASK K(+) channel activity.
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CSE is critical for the progression of kidney fibrosis.
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renal expression of CTH and other H2S-producing enzymes was markedly suppressed after IRI, which could be an integrated adaptive response for renal cell protection
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This study suggests that the CSE/H2S system is involved in the pathogenesis of obesity in mice.
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Data show that CSE plays an important role as an inhibitor of inflammation in the liver by producing H2S from L-cysteine.
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Study shows maintaining CSE expression is critically important for stress adaptation during posttraumatic acute lung injury and CS-induced COPD, most likely in a gender-dependent manner.
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CSE-derived H2S contributes to mouse uterus homeostasis. Sildenafil reduces uterus contractility and its effect involves CSE-derived H2S.
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The antiatherosclerotic effect of estrogen is mediated by CSE-generated H2S
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Cystathionine-Gamma-Lyase Gene Deletion is associated with reduced inflammation and liver damage.
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this study reveals the molecular basis for the differential expression of Cth in mouse models of essential hypertension under basal and pathophysiological conditions.
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the findings of this study indicate that a deficiency in 3MST does not significantly affect endotoxemia, while a deficiency in CBS or CSE slightly ameliorates the outcome of LPS-induced endotoxemia in vivo.
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lung MPO activity increased following induction of sepsis with CLP while siRNA treatment significantly reduced MPO activity. Liver and lung cytokine and chemokine levels in CLP-induced sepsis reduced following treatment with siRNA. These findings show a crucial pro-inflammatory role for H2S synthesized by CSE in macrophages in sepsis and suggest CSE gene silencing with siRNA as a potential therapeutic approach for this co
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H2S augmented the S-sulfhydration of the rate-limiting gluconeogenic enzymes and PGC-1alpha and increased their activities, which were lower in untreated : To investigate the regulation of hepatic glucose production by cystathionine gamma-lyase KO hepatocytes
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Endogenous cystathionine gamma-lyase/Hydrogen sulfide regulates ischaemic vascular remodelling mediated during hind limb ischaemia through NO-dependent monocyte recruitment
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The results of this study suggest that CSE is not critically involved in chronic pain signaling in mice and that sources different from CSE mediate the pain relevant effects of H2S.
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CSE-H2S increased PPARgamma activity by direct sulfhydration at the C139 site, thereby changing glucose into triglyceride storage in adipocytes.
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Therefore, our data suggest that DNA hypermethylation of CpG rich region in cse promoter might contribute to the decrease of cse transcription and H2S production in macrophages, and thus contribute to atherosclerosis development.
