PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33146353-11 2020 PTX-2 concentrations were correlated with serum albumin (r=0.30, p=0.016), and were negatively correlated with serum creatinine levels (rho=-0.42, p=0.01) and body mass index (r=-0.32, p=0.011). Creatinine 117-127 amyloid P component, serum Homo sapiens 0-5 24831018-14 2014 Supplementation with exogenous H2S sources can regulate the expression of relevant genes in OA pathogenesis and progression, counteracting IL1beta pro-inflammatory signals that lead to cartilage destruction in part by reducing NFkappaB activation. Hydrogen Sulfide 31-34 interleukin 1 beta Homo sapiens 139-146 24114174-9 2014 These receptors co-precipitated, co-localized with the NCX1, and induced apoptosis in the presence of H2S. Hydrogen Sulfide 102-105 solute carrier family 8 member A1 Homo sapiens 55-59 24318675-10 2014 However, when the endogenous H2O2 level was inhibited by DPI or DMTU, the effect of H2S on the PM Na(+)/H(+) antiporter system was removed. Hydrogen Sulfide 84-87 Na+/H+ exchanger 1 Arabidopsis thaliana 98-119 24746521-1 2014 Hydrogen sulfide (H2S) is a well known toxic gas that is synthesized from the amino acids: cysteine (Cys) and homocysteine (Hcy) by three enzymes: cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE) and mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 209-212 24746521-1 2014 Hydrogen sulfide (H2S) is a well known toxic gas that is synthesized from the amino acids: cysteine (Cys) and homocysteine (Hcy) by three enzymes: cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE) and mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 18-21 cystathionine beta-synthase Homo sapiens 147-174 24746521-1 2014 Hydrogen sulfide (H2S) is a well known toxic gas that is synthesized from the amino acids: cysteine (Cys) and homocysteine (Hcy) by three enzymes: cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE) and mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 18-21 cystathionine beta-synthase Homo sapiens 176-179 24746521-1 2014 Hydrogen sulfide (H2S) is a well known toxic gas that is synthesized from the amino acids: cysteine (Cys) and homocysteine (Hcy) by three enzymes: cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE) and mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 18-21 cystathionine gamma-lyase Homo sapiens 182-207 24746521-1 2014 Hydrogen sulfide (H2S) is a well known toxic gas that is synthesized from the amino acids: cysteine (Cys) and homocysteine (Hcy) by three enzymes: cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE) and mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 18-21 cystathionine gamma-lyase Homo sapiens 209-212 24964843-17 2014 These results suggest that exogenous H2S can ameliorate the age-related changes of aortic morphology, decrease the concentration of AngII in plasma, down-regulate the expression of AT1R in vascular tissue, and mitigate the level of oxidative stress. Hydrogen Sulfide 37-40 angiotensinogen Rattus norvegicus 132-137 24964843-17 2014 These results suggest that exogenous H2S can ameliorate the age-related changes of aortic morphology, decrease the concentration of AngII in plasma, down-regulate the expression of AT1R in vascular tissue, and mitigate the level of oxidative stress. Hydrogen Sulfide 37-40 angiotensin II receptor, type 1b Rattus norvegicus 181-185 24949720-0 2014 mTORC2 phosphorylation of Akt1: a possible mechanism for hydrogen sulfide-induced cardioprotection. Hydrogen Sulfide 57-73 AKT serine/threonine kinase 1 Rattus norvegicus 26-30 24949720-1 2014 Hydrogen sulfide (H2S) is known to have cardiac protective effects through Akt activation. Hydrogen Sulfide 0-16 AKT serine/threonine kinase 1 Rattus norvegicus 75-78 24949720-1 2014 Hydrogen sulfide (H2S) is known to have cardiac protective effects through Akt activation. Hydrogen Sulfide 18-21 AKT serine/threonine kinase 1 Rattus norvegicus 75-78 24949720-3 2014 Based on the previous finding that PI3K inhibitor LY294002 abolishes H2S-induced Akt phosphorylation and cardioprotection, it is accepted that PI3K is the mediator of H2S-induced Akt phosphorylation. Hydrogen Sulfide 69-72 AKT serine/threonine kinase 1 Rattus norvegicus 81-84 24949720-3 2014 Based on the previous finding that PI3K inhibitor LY294002 abolishes H2S-induced Akt phosphorylation and cardioprotection, it is accepted that PI3K is the mediator of H2S-induced Akt phosphorylation. Hydrogen Sulfide 69-72 AKT serine/threonine kinase 1 Rattus norvegicus 179-182 24949720-3 2014 Based on the previous finding that PI3K inhibitor LY294002 abolishes H2S-induced Akt phosphorylation and cardioprotection, it is accepted that PI3K is the mediator of H2S-induced Akt phosphorylation. Hydrogen Sulfide 167-170 AKT serine/threonine kinase 1 Rattus norvegicus 81-84 24949720-3 2014 Based on the previous finding that PI3K inhibitor LY294002 abolishes H2S-induced Akt phosphorylation and cardioprotection, it is accepted that PI3K is the mediator of H2S-induced Akt phosphorylation. Hydrogen Sulfide 167-170 AKT serine/threonine kinase 1 Rattus norvegicus 179-182 24949720-5 2014 We undertook a series of experiments to further evaluate the role of mTORC2, PDK1, PTEN, PP2A and PHLPPL in H2S-induced Akt phosphorylation and cardioprotection, which, we believe, has not been investigated before. Hydrogen Sulfide 108-111 CREB regulated transcription coactivator 2 Mus musculus 69-75 24949720-5 2014 We undertook a series of experiments to further evaluate the role of mTORC2, PDK1, PTEN, PP2A and PHLPPL in H2S-induced Akt phosphorylation and cardioprotection, which, we believe, has not been investigated before. Hydrogen Sulfide 108-111 pyruvate dehydrogenase kinase 1 Rattus norvegicus 77-81 24949720-5 2014 We undertook a series of experiments to further evaluate the role of mTORC2, PDK1, PTEN, PP2A and PHLPPL in H2S-induced Akt phosphorylation and cardioprotection, which, we believe, has not been investigated before. Hydrogen Sulfide 108-111 phosphatase and tensin homolog Rattus norvegicus 83-87 24949720-5 2014 We undertook a series of experiments to further evaluate the role of mTORC2, PDK1, PTEN, PP2A and PHLPPL in H2S-induced Akt phosphorylation and cardioprotection, which, we believe, has not been investigated before. Hydrogen Sulfide 108-111 PH domain and leucine rich repeat protein phosphatase 2 Rattus norvegicus 98-104 24949720-5 2014 We undertook a series of experiments to further evaluate the role of mTORC2, PDK1, PTEN, PP2A and PHLPPL in H2S-induced Akt phosphorylation and cardioprotection, which, we believe, has not been investigated before. Hydrogen Sulfide 108-111 AKT serine/threonine kinase 1 Rattus norvegicus 120-123 24949720-14 2014 These data suggest mTORC2 phosphorylation of Akt is a key mediator of H2S-induced cardioprotection in I/R. Hydrogen Sulfide 70-73 CREB regulated transcription coactivator 2 Mus musculus 19-25 24949720-14 2014 These data suggest mTORC2 phosphorylation of Akt is a key mediator of H2S-induced cardioprotection in I/R. Hydrogen Sulfide 70-73 AKT serine/threonine kinase 1 Rattus norvegicus 45-48 24914509-2 2014 Hydrogen sulphide (H2S) is a gaseotransmitter produced mainly by cystathionine-gamma-lyase and cystathionine-beta-synthase. Hydrogen Sulfide 0-17 cystathionine gamma-lyase Homo sapiens 65-90 24707893-0 2014 The cystathionine gamma-lyase/hydrogen sulfide system maintains cellular glutathione status. Hydrogen Sulfide 30-46 cystathionine gamma-lyase Homo sapiens 4-29 24707893-2 2014 CSE (cystathionine gamma-lyase) is an important enzyme responsible for endogenous H2S production in mammalian systems, but little is known about the modulation of endogenous H2S production and its antioxidative activity. Hydrogen Sulfide 82-85 cystathionine gamma-lyase Homo sapiens 0-3 24707893-2 2014 CSE (cystathionine gamma-lyase) is an important enzyme responsible for endogenous H2S production in mammalian systems, but little is known about the modulation of endogenous H2S production and its antioxidative activity. Hydrogen Sulfide 82-85 cystathionine gamma-lyase Homo sapiens 5-30 24707893-2 2014 CSE (cystathionine gamma-lyase) is an important enzyme responsible for endogenous H2S production in mammalian systems, but little is known about the modulation of endogenous H2S production and its antioxidative activity. Hydrogen Sulfide 174-177 cystathionine gamma-lyase Homo sapiens 0-3 24707893-9 2014 Taken together, the results of the present study provide molecular insights into the antioxidative activity of CSE and highlights the importance of the CSE/H2S system in maintaining cellular glutathione status. Hydrogen Sulfide 156-159 cystathionine gamma-lyase Homo sapiens 111-114 24914509-2 2014 Hydrogen sulphide (H2S) is a gaseotransmitter produced mainly by cystathionine-gamma-lyase and cystathionine-beta-synthase. Hydrogen Sulfide 0-17 cystathionine beta-synthase Homo sapiens 95-122 24914509-2 2014 Hydrogen sulphide (H2S) is a gaseotransmitter produced mainly by cystathionine-gamma-lyase and cystathionine-beta-synthase. Hydrogen Sulfide 19-22 cystathionine gamma-lyase Homo sapiens 65-90 24914509-2 2014 Hydrogen sulphide (H2S) is a gaseotransmitter produced mainly by cystathionine-gamma-lyase and cystathionine-beta-synthase. Hydrogen Sulfide 19-22 cystathionine beta-synthase Homo sapiens 95-122 24914509-3 2014 Here we show that cystathionine-gamma-lyase and cystathionine -beta-synthase are ubiquitously distributed in human fallopian tube epithelium and that H2S signalling relaxes the spontaneous contraction of the human oviduct. Hydrogen Sulfide 150-153 cystathionine gamma-lyase Homo sapiens 18-43 24914509-3 2014 Here we show that cystathionine-gamma-lyase and cystathionine -beta-synthase are ubiquitously distributed in human fallopian tube epithelium and that H2S signalling relaxes the spontaneous contraction of the human oviduct. Hydrogen Sulfide 150-153 cystathionine beta-synthase Homo sapiens 48-76 24658667-6 2014 H2S was found to exert anti-apoptotic effects in the myocardium of smoking rats by inhibiting JNK and P38 mitogen-activated protein kinases pathways and activating PI3K/Akt signaling. Hydrogen Sulfide 0-3 mitogen-activated protein kinase 8 Rattus norvegicus 94-97 24891629-0 2014 Letter by Tsikas and Cooper regarding article, "dysregulation of hydrogen sulfide (H2S) producing enzyme cystathionine gamma-lyase (CSE) contributes to maternal hypertension and placental abnormalities in preeclampsia". Hydrogen Sulfide 65-81 cystathionine gamma-lyase Homo sapiens 105-130 24891629-0 2014 Letter by Tsikas and Cooper regarding article, "dysregulation of hydrogen sulfide (H2S) producing enzyme cystathionine gamma-lyase (CSE) contributes to maternal hypertension and placental abnormalities in preeclampsia". Hydrogen Sulfide 65-81 cystathionine gamma-lyase Homo sapiens 132-135 24891629-0 2014 Letter by Tsikas and Cooper regarding article, "dysregulation of hydrogen sulfide (H2S) producing enzyme cystathionine gamma-lyase (CSE) contributes to maternal hypertension and placental abnormalities in preeclampsia". Hydrogen Sulfide 83-86 cystathionine gamma-lyase Homo sapiens 105-130 24891629-0 2014 Letter by Tsikas and Cooper regarding article, "dysregulation of hydrogen sulfide (H2S) producing enzyme cystathionine gamma-lyase (CSE) contributes to maternal hypertension and placental abnormalities in preeclampsia". Hydrogen Sulfide 83-86 cystathionine gamma-lyase Homo sapiens 132-135 24891630-0 2014 Response to letter regarding article, "dysregulation of hydrogen sulfide (H2S) producing enzyme cystathionine gamma-lyase (CSE) contributes to maternal hypertension and placental abnormalities in preeclampsia". Hydrogen Sulfide 56-72 cystathionine gamma-lyase Homo sapiens 96-121 24891630-0 2014 Response to letter regarding article, "dysregulation of hydrogen sulfide (H2S) producing enzyme cystathionine gamma-lyase (CSE) contributes to maternal hypertension and placental abnormalities in preeclampsia". Hydrogen Sulfide 56-72 cystathionine gamma-lyase Homo sapiens 123-126 24891630-0 2014 Response to letter regarding article, "dysregulation of hydrogen sulfide (H2S) producing enzyme cystathionine gamma-lyase (CSE) contributes to maternal hypertension and placental abnormalities in preeclampsia". Hydrogen Sulfide 74-77 cystathionine gamma-lyase Homo sapiens 96-121 24891630-0 2014 Response to letter regarding article, "dysregulation of hydrogen sulfide (H2S) producing enzyme cystathionine gamma-lyase (CSE) contributes to maternal hypertension and placental abnormalities in preeclampsia". Hydrogen Sulfide 74-77 cystathionine gamma-lyase Homo sapiens 123-126 24961850-9 2014 Increased H2S would alleviate lung injury and the effect is at least partially depend on the adjustment of TLR4-Myd88-NF-kappaB pathway and AQP1/AQP5 expression to reduce inflammatory reaction and lessen pulmonary edema. Hydrogen Sulfide 10-13 toll-like receptor 4 Rattus norvegicus 107-111 24747165-0 2014 Hydrogen sulfide inhibits homocysteine-induced endoplasmic reticulum stress and neuronal apoptosis in rat hippocampus via upregulation of the BDNF-TrkB pathway. Hydrogen Sulfide 0-16 brain-derived neurotrophic factor Rattus norvegicus 142-146 24747165-0 2014 Hydrogen sulfide inhibits homocysteine-induced endoplasmic reticulum stress and neuronal apoptosis in rat hippocampus via upregulation of the BDNF-TrkB pathway. Hydrogen Sulfide 0-16 neurotrophic receptor tyrosine kinase 2 Rattus norvegicus 147-151 24747165-8 2014 Treatment with the H2S donor NaHS increased the endogenous H2S production and BDNF expression in a dose-dependent manner, and significantly reduced Hcy-induced neuronal apoptosis and ER stress responses in the hippocampus. Hydrogen Sulfide 19-22 brain derived neurotrophic factor Homo sapiens 78-82 24747165-10 2014 CONCLUSION: H2S attenuates ER stress and neuronal apoptosis in the hippocampus of Hcy-treated rats via upregulating the BDNF-TrkB pathway. Hydrogen Sulfide 12-15 brain-derived neurotrophic factor Rattus norvegicus 120-124 24747165-10 2014 CONCLUSION: H2S attenuates ER stress and neuronal apoptosis in the hippocampus of Hcy-treated rats via upregulating the BDNF-TrkB pathway. Hydrogen Sulfide 12-15 neurotrophic receptor tyrosine kinase 2 Rattus norvegicus 125-129 24961850-9 2014 Increased H2S would alleviate lung injury and the effect is at least partially depend on the adjustment of TLR4-Myd88-NF-kappaB pathway and AQP1/AQP5 expression to reduce inflammatory reaction and lessen pulmonary edema. Hydrogen Sulfide 10-13 MYD88, innate immune signal transduction adaptor Rattus norvegicus 112-117 24961850-9 2014 Increased H2S would alleviate lung injury and the effect is at least partially depend on the adjustment of TLR4-Myd88-NF-kappaB pathway and AQP1/AQP5 expression to reduce inflammatory reaction and lessen pulmonary edema. Hydrogen Sulfide 10-13 aquaporin 1 Rattus norvegicus 140-144 24961850-9 2014 Increased H2S would alleviate lung injury and the effect is at least partially depend on the adjustment of TLR4-Myd88-NF-kappaB pathway and AQP1/AQP5 expression to reduce inflammatory reaction and lessen pulmonary edema. Hydrogen Sulfide 10-13 aquaporin 5 Rattus norvegicus 145-149 24896355-0 2014 Regulation of cystathionine gamma-lyase/H2S system and its pathological implication. Hydrogen Sulfide 40-43 cystathionine gamma-lyase Homo sapiens 14-39 24825878-0 2014 Induction of microRNA-21 with exogenous hydrogen sulfide attenuates myocardial ischemic and inflammatory injury in mice. Hydrogen Sulfide 40-56 microRNA 21a Mus musculus 13-24 24825878-2 2014 Because of the anti-inflammatory effects of hydrogen sulfide, we proposed that the hydrogen sulfide donor, sodium sulfide (Na2S), would attenuate myocardial injury through upregulation of protective microRNA-21 (miR-21) and suppression of the inflammasome, a macromolecular structure that amplifies inflammation and mediates further injury. Hydrogen Sulfide 83-99 microRNA 21 Homo sapiens 199-210 24825878-2 2014 Because of the anti-inflammatory effects of hydrogen sulfide, we proposed that the hydrogen sulfide donor, sodium sulfide (Na2S), would attenuate myocardial injury through upregulation of protective microRNA-21 (miR-21) and suppression of the inflammasome, a macromolecular structure that amplifies inflammation and mediates further injury. Hydrogen Sulfide 83-99 microRNA 21 Homo sapiens 212-218 24896355-2 2014 Cystathionine gamma-lyase (CSE) is one major H2S-producing enzyme with L-cysteine as the main substrate in mammalian cells. Hydrogen Sulfide 45-48 cystathionine gamma-lyase Homo sapiens 0-25 24896355-2 2014 Cystathionine gamma-lyase (CSE) is one major H2S-producing enzyme with L-cysteine as the main substrate in mammalian cells. Hydrogen Sulfide 45-48 cystathionine gamma-lyase Homo sapiens 27-30 24896355-3 2014 Since the discovery of endogenously-produced H2S as a biological mediator, there has been an explosion of interest in CSE expression and regulation. Hydrogen Sulfide 45-48 cystathionine gamma-lyase Homo sapiens 118-121 24896355-5 2014 Considering the key role that CSE/H 2 S system plays in both health and diseases, a better understanding of the regulation of CSE/H 2 S system will help us to develop novel and more effective strategies to target CSE and alter H2S production inside cells. Hydrogen Sulfide 227-230 cystathionine gamma-lyase Homo sapiens 30-33 24896355-5 2014 Considering the key role that CSE/H 2 S system plays in both health and diseases, a better understanding of the regulation of CSE/H 2 S system will help us to develop novel and more effective strategies to target CSE and alter H2S production inside cells. Hydrogen Sulfide 227-230 cystathionine gamma-lyase Homo sapiens 126-129 24896355-5 2014 Considering the key role that CSE/H 2 S system plays in both health and diseases, a better understanding of the regulation of CSE/H 2 S system will help us to develop novel and more effective strategies to target CSE and alter H2S production inside cells. Hydrogen Sulfide 227-230 cystathionine gamma-lyase Homo sapiens 126-129 24629044-9 2014 H2 S was found to induce the nuclear accumulation of Nrf2 in lung tissue and consequently up-regulate the expression of antioxidant genes HO-1 and Trx-1 in the smoking rats. Hydrogen Sulfide 0-4 NFE2 like bZIP transcription factor 2 Rattus norvegicus 53-57 24284510-4 2014 Cystathionine-beta-synthase, a hydrogen sulfide-producing enzyme, was dramatically reduced in the ureteral obstructed kidney, but another enzyme cystathionine-gamma-lyase was increased. Hydrogen Sulfide 31-47 cystathionine beta-synthase Homo sapiens 0-27 24284510-7 2014 In cultured kidney fibroblasts, a hydrogen sulfide donor inhibited the cell proliferation by reducing DNA synthesis and downregulating the expressions of proliferation-related proteins including proliferating cell nuclear antigen and c-Myc. Hydrogen Sulfide 34-50 proliferating cell nuclear antigen Homo sapiens 195-229 24284510-7 2014 In cultured kidney fibroblasts, a hydrogen sulfide donor inhibited the cell proliferation by reducing DNA synthesis and downregulating the expressions of proliferation-related proteins including proliferating cell nuclear antigen and c-Myc. Hydrogen Sulfide 34-50 MYC proto-oncogene, bHLH transcription factor Homo sapiens 234-239 24665821-6 2014 H2S significantly (P<0.05) upregulated expression of GCLC and GCLM, and formation of GSH, and inhibited IL-1beta secretion in controls and HG-treated monocytes. Hydrogen Sulfide 0-3 glutamate-cysteine ligase catalytic subunit Homo sapiens 56-60 24665821-0 2014 Hydrogen sulfide upregulates glutamate-cysteine ligase catalytic subunit, glutamate-cysteine ligase modifier subunit, and glutathione and inhibits interleukin-1beta secretion in monocytes exposed to high glucose levels. Hydrogen Sulfide 0-16 glutamate-cysteine ligase catalytic subunit Homo sapiens 29-72 24665821-0 2014 Hydrogen sulfide upregulates glutamate-cysteine ligase catalytic subunit, glutamate-cysteine ligase modifier subunit, and glutathione and inhibits interleukin-1beta secretion in monocytes exposed to high glucose levels. Hydrogen Sulfide 0-16 glutamate-cysteine ligase modifier subunit Homo sapiens 74-116 24665821-0 2014 Hydrogen sulfide upregulates glutamate-cysteine ligase catalytic subunit, glutamate-cysteine ligase modifier subunit, and glutathione and inhibits interleukin-1beta secretion in monocytes exposed to high glucose levels. Hydrogen Sulfide 0-16 interleukin 1 beta Homo sapiens 147-164 24665821-3 2014 This study examined the hypothesis that hydrogen sulfide (H2S) upregulates the glutamate-cysteine ligase catalytic subunit (GCLC) and GSH and inhibits IL-1beta in a monocyte cell model. Hydrogen Sulfide 40-56 glutamate-cysteine ligase catalytic subunit Homo sapiens 79-122 24665821-3 2014 This study examined the hypothesis that hydrogen sulfide (H2S) upregulates the glutamate-cysteine ligase catalytic subunit (GCLC) and GSH and inhibits IL-1beta in a monocyte cell model. Hydrogen Sulfide 40-56 glutamate-cysteine ligase catalytic subunit Homo sapiens 124-128 24665821-3 2014 This study examined the hypothesis that hydrogen sulfide (H2S) upregulates the glutamate-cysteine ligase catalytic subunit (GCLC) and GSH and inhibits IL-1beta in a monocyte cell model. Hydrogen Sulfide 40-56 interleukin 1 beta Homo sapiens 151-159 24665821-3 2014 This study examined the hypothesis that hydrogen sulfide (H2S) upregulates the glutamate-cysteine ligase catalytic subunit (GCLC) and GSH and inhibits IL-1beta in a monocyte cell model. Hydrogen Sulfide 58-61 glutamate-cysteine ligase catalytic subunit Homo sapiens 79-122 24665821-3 2014 This study examined the hypothesis that hydrogen sulfide (H2S) upregulates the glutamate-cysteine ligase catalytic subunit (GCLC) and GSH and inhibits IL-1beta in a monocyte cell model. Hydrogen Sulfide 58-61 glutamate-cysteine ligase catalytic subunit Homo sapiens 124-128 24665821-3 2014 This study examined the hypothesis that hydrogen sulfide (H2S) upregulates the glutamate-cysteine ligase catalytic subunit (GCLC) and GSH and inhibits IL-1beta in a monocyte cell model. Hydrogen Sulfide 58-61 interleukin 1 beta Homo sapiens 151-159 24699897-0 2014 Inhibition of the endogenous CSE/H2S system contributes to hypoxia and serum deprivation-induced apoptosis in mesenchymal stem cells. Hydrogen Sulfide 33-36 cystathionine gamma-lyase Homo sapiens 29-32 24699897-7 2014 Overexpression of CSE not only markedly prevented hypoxia/SD-induced decreases in endogenous H2S generation but also protected MSCs from apoptosis, while inhibition of CSE by its potent inhibitors significantly deteriorated the effect of hypoxia/SD in MSCs. Hydrogen Sulfide 93-96 cystathionine gamma-lyase Homo sapiens 18-21 24699897-8 2014 These data indicate that the H2S generation pathway exists in MSCs and the inhibition of the endogenous CSE/H2S system contributes to hypoxia/SD-induced apoptosis in MSCs. Hydrogen Sulfide 108-111 cystathionine gamma-lyase Homo sapiens 104-107 24699897-9 2014 Our findings suggest that modulation of the CSE/H2S system is a potential therapeutic avenue for promoting the viability of transplanted MSCs. Hydrogen Sulfide 48-51 cystathionine gamma-lyase Homo sapiens 44-47 25203706-0 2014 [Role of PI3K/Akt signaling in hydrogen sulfide-induced alteration in expression of collagen I and III in hepatic stellate cells]. Hydrogen Sulfide 31-47 AKT serine/threonine kinase 1 Rattus norvegicus 14-17 25203706-1 2014 OBJECTIVE: To investigate the role of the PI3K/Akt signaling pathway in hydrogen sulfide-induced alterations in expression of collagen I and collagen III in hepatic stellate cells. Hydrogen Sulfide 72-88 AKT serine/threonine kinase 1 Rattus norvegicus 47-50 25203706-5 2014 RESULTS: Compared with the untreated control cells, the hydrogen sulfide treated cells showed elevated expression of collagen I mRNA (F =14.635, P less than 0.05), collagen III mRNA (F =14.620, P less than 0.05), PI3K protein (F =26.672, P less than 0.05), and p-Akt (F =23.522, P less than 0.05). Hydrogen Sulfide 56-72 AKT serine/threonine kinase 1 Rattus norvegicus 263-266 25203706-7 2014 CONCLUSION: Hydrogen sulfide can activate the PI3K/Akt pathway and elevate the expression of collagen I and collagen III in rat hepatic stellate cells. Hydrogen Sulfide 12-28 AKT serine/threonine kinase 1 Rattus norvegicus 51-54 24180631-0 2014 S-propargyl-cysteine, a novel water-soluble modulator of endogenous hydrogen sulfide, promotes angiogenesis through activation of signal transducer and activator of transcription 3. Hydrogen Sulfide 68-84 signal transducer and activator of transcription 3 Rattus norvegicus 130-180 24622975-0 2014 Hydrogen sulfide alleviates cardiac contractile dysfunction in an Akt2-knockout murine model of insulin resistance: role of mitochondrial injury and apoptosis. Hydrogen Sulfide 0-16 thymoma viral proto-oncogene 2 Mus musculus 66-70 24622975-6 2014 Our results revealed that Akt2 ablation led to overtly enlarged ventricular end-systolic diameter, reduced myocardial and cardiomyocyte contractile function, and disrupted intracellular Ca(2+) homeostasis and apoptosis, the effects of which were ameliorated by H2S. Hydrogen Sulfide 261-264 thymoma viral proto-oncogene 2 Mus musculus 26-30 24746521-1 2014 Hydrogen sulfide (H2S) is a well known toxic gas that is synthesized from the amino acids: cysteine (Cys) and homocysteine (Hcy) by three enzymes: cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE) and mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 147-174 24746521-1 2014 Hydrogen sulfide (H2S) is a well known toxic gas that is synthesized from the amino acids: cysteine (Cys) and homocysteine (Hcy) by three enzymes: cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE) and mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 176-179 24746521-1 2014 Hydrogen sulfide (H2S) is a well known toxic gas that is synthesized from the amino acids: cysteine (Cys) and homocysteine (Hcy) by three enzymes: cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE) and mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 182-207 24687304-1 2014 Hydrogen sulfide (H2S) protects cardiomyoblasts against high glucose (HG)-induced injury by inhibiting the activation of p38 mitogen-activated protein kinase (MAPK). Hydrogen Sulfide 0-16 mitogen activated protein kinase 14 Rattus norvegicus 121-157 24687304-1 2014 Hydrogen sulfide (H2S) protects cardiomyoblasts against high glucose (HG)-induced injury by inhibiting the activation of p38 mitogen-activated protein kinase (MAPK). Hydrogen Sulfide 18-21 mitogen activated protein kinase 14 Rattus norvegicus 121-157 24556961-3 2014 In this report, we observed that the exogenously applied H2S donor sodium hydrosulfide (NaHS) and the HO-1 inducer hemin induce LR formation in tomato seedlings by triggering intracellular signaling events involving the induction of tomato HO-1 (SlHO-1), and the modulation of cell cycle regulatory genes, including the up-regulation of SlCDKA;1 and SlCYCA2;1, and simultaneous down-regulation of SlKRP2. Hydrogen Sulfide 57-60 heme oxygenase 1 Solanum lycopersicum 240-244 24556961-3 2014 In this report, we observed that the exogenously applied H2S donor sodium hydrosulfide (NaHS) and the HO-1 inducer hemin induce LR formation in tomato seedlings by triggering intracellular signaling events involving the induction of tomato HO-1 (SlHO-1), and the modulation of cell cycle regulatory genes, including the up-regulation of SlCDKA;1 and SlCYCA2;1, and simultaneous down-regulation of SlKRP2. Hydrogen Sulfide 57-60 p27KIP1-related-protein 2 Solanum lycopersicum 397-403 24556961-6 2014 The impairment of LR density and length as well as lateral root primordia number, the decreased tomato HO-1 gene expression and HO activity caused by an H2S scavenger hypotaurine were partially rescued by the addition of NaHS, hemin and CO (in particular). Hydrogen Sulfide 153-156 heme oxygenase 1 Solanum lycopersicum 103-107 24665821-6 2014 H2S significantly (P<0.05) upregulated expression of GCLC and GCLM, and formation of GSH, and inhibited IL-1beta secretion in controls and HG-treated monocytes. Hydrogen Sulfide 0-3 glutamate-cysteine ligase modifier subunit Homo sapiens 65-69 24665821-6 2014 H2S significantly (P<0.05) upregulated expression of GCLC and GCLM, and formation of GSH, and inhibited IL-1beta secretion in controls and HG-treated monocytes. Hydrogen Sulfide 0-3 interleukin 1 beta Homo sapiens 107-115 24665821-7 2014 This is the first demonstration of H2S upregulation of GCLC and GSH and inhibition of IL-1beta levels, which may be what mediates the beneficial effects of H2S-rich compounds in mitigating the pathogenesis of metabolic syndrome and atherosclerosis. Hydrogen Sulfide 35-38 glutamate-cysteine ligase catalytic subunit Homo sapiens 55-59 24665821-7 2014 This is the first demonstration of H2S upregulation of GCLC and GSH and inhibition of IL-1beta levels, which may be what mediates the beneficial effects of H2S-rich compounds in mitigating the pathogenesis of metabolic syndrome and atherosclerosis. Hydrogen Sulfide 156-159 glutamate-cysteine ligase catalytic subunit Homo sapiens 55-59 24665821-7 2014 This is the first demonstration of H2S upregulation of GCLC and GSH and inhibition of IL-1beta levels, which may be what mediates the beneficial effects of H2S-rich compounds in mitigating the pathogenesis of metabolic syndrome and atherosclerosis. Hydrogen Sulfide 156-159 interleukin 1 beta Homo sapiens 86-94 24832131-5 2014 Interestingly, during the initiation of lateral root primordia, IAA is a potent inducer of endogenous H 2S and CO, which is produced by L-cysteine desulfhydrase (LCD) and heme oxygenase-1 (HO-1), respectively. Hydrogen Sulfide 102-106 heme oxygenase 1 Homo sapiens 171-187 24622975-7 2014 Furthermore, Akt2 knockout displayed upregulated apoptotic protein markers (Bax, caspase-3, caspase-9, and caspace-12) and mitochondrial damage (reduced aconitase activity and NAD(+), elevated cytochrome-c release from mitochondria) along with reduced phosphorylation of PTEN, Akt, and GSK3beta in the absence of changes in pan protein expression, the effects of which were abolished or significantly ameliorated by H2S treatment. Hydrogen Sulfide 416-419 thymoma viral proto-oncogene 2 Mus musculus 13-17 24622975-7 2014 Furthermore, Akt2 knockout displayed upregulated apoptotic protein markers (Bax, caspase-3, caspase-9, and caspace-12) and mitochondrial damage (reduced aconitase activity and NAD(+), elevated cytochrome-c release from mitochondria) along with reduced phosphorylation of PTEN, Akt, and GSK3beta in the absence of changes in pan protein expression, the effects of which were abolished or significantly ameliorated by H2S treatment. Hydrogen Sulfide 416-419 thymoma viral proto-oncogene 1 Mus musculus 13-16 24622975-8 2014 In vitro data revealed that H2S-induced beneficial effect against Akt2 ablation was obliterated by mitochondrial uncoupling. Hydrogen Sulfide 28-31 thymoma viral proto-oncogene 2 Mus musculus 66-70 24622975-9 2014 Taken together, our findings suggest the H2S may reconcile Akt2 knockout-induced myocardial contractile defect and intracellular Ca(2+) mishandling, possibly via attenuation of mitochondrial injury and apoptosis. Hydrogen Sulfide 41-44 thymoma viral proto-oncogene 2 Mus musculus 59-63 24742186-5 2014 Moreover, this N-Cdot-TiO2 nanowire photoanode has been demonstrated for direct growth and interfacing of H9c2 cardiac myoblasts, with the capability of interrogating H2S cellular generation pathways by vascular endothelial growth factor stimulation as well as inhibition. Hydrogen Sulfide 167-170 vascular endothelial growth factor A Homo sapiens 203-237 24486403-8 2014 This process upregulates A2AR expression and enhances cAMP production and PKA activation, resulting in adenosinergic T-cell immunosuppression that can be modulated via H2S. Hydrogen Sulfide 168-171 adenosine A2a receptor Homo sapiens 25-29 25024795-9 2014 H2S treatment decreased the expression of pro-inflammatory markers TLR-4, TNF-alpha, IFNgamma, IL-2 and ICAM-1, increased the expression of pro-survival molecule Bcl-2 and decreased the expression of pro-apoptotic marker BID at postoperative day 1. Hydrogen Sulfide 0-3 toll-like receptor 4 Rattus norvegicus 67-72 25024795-9 2014 H2S treatment decreased the expression of pro-inflammatory markers TLR-4, TNF-alpha, IFNgamma, IL-2 and ICAM-1, increased the expression of pro-survival molecule Bcl-2 and decreased the expression of pro-apoptotic marker BID at postoperative day 1. Hydrogen Sulfide 0-3 tumor necrosis factor Rattus norvegicus 74-83 25024795-9 2014 H2S treatment decreased the expression of pro-inflammatory markers TLR-4, TNF-alpha, IFNgamma, IL-2 and ICAM-1, increased the expression of pro-survival molecule Bcl-2 and decreased the expression of pro-apoptotic marker BID at postoperative day 1. Hydrogen Sulfide 0-3 interleukin 18 Rattus norvegicus 85-93 25024795-9 2014 H2S treatment decreased the expression of pro-inflammatory markers TLR-4, TNF-alpha, IFNgamma, IL-2 and ICAM-1, increased the expression of pro-survival molecule Bcl-2 and decreased the expression of pro-apoptotic marker BID at postoperative day 1. Hydrogen Sulfide 0-3 interleukin 2 Rattus norvegicus 95-99 25024795-9 2014 H2S treatment decreased the expression of pro-inflammatory markers TLR-4, TNF-alpha, IFNgamma, IL-2 and ICAM-1, increased the expression of pro-survival molecule Bcl-2 and decreased the expression of pro-apoptotic marker BID at postoperative day 1. Hydrogen Sulfide 0-3 intercellular adhesion molecule 1 Rattus norvegicus 104-110 25024795-9 2014 H2S treatment decreased the expression of pro-inflammatory markers TLR-4, TNF-alpha, IFNgamma, IL-2 and ICAM-1, increased the expression of pro-survival molecule Bcl-2 and decreased the expression of pro-apoptotic marker BID at postoperative day 1. Hydrogen Sulfide 0-3 BCL2, apoptosis regulator Rattus norvegicus 162-167 24657251-1 2014 Hydrogen sulfide (H2S)/cystathionine gamma-lyase (CSE) pathway has been demonstrated to play vital roles in physiology and pathophysiology. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 23-48 24657251-1 2014 Hydrogen sulfide (H2S)/cystathionine gamma-lyase (CSE) pathway has been demonstrated to play vital roles in physiology and pathophysiology. Hydrogen Sulfide 18-21 cystathionine gamma-lyase Homo sapiens 23-48 24657251-4 2014 Inhibition of endogenous H2S/CSE pathway drastically decreased the proliferation of HepG2 and PLC/PRF/5 cells, and it also enhanced ROS production and mitochondrial disruption, pronounced DNA damage and increased apoptosis. Hydrogen Sulfide 25-28 heparan sulfate proteoglycan 2 Homo sapiens 94-97 24657251-6 2014 In addition, the negative regulation of cell proliferation by inhibition of H2S/CSE system correlated with the blockage of cell mitogenic and survival signal transduction of epidermal growth factor receptor (EGFR) via down-regulating the extracellular-signal-regulated kinase 1/2 (ERK1/2) activation. Hydrogen Sulfide 76-79 epidermal growth factor receptor Homo sapiens 174-206 24657251-6 2014 In addition, the negative regulation of cell proliferation by inhibition of H2S/CSE system correlated with the blockage of cell mitogenic and survival signal transduction of epidermal growth factor receptor (EGFR) via down-regulating the extracellular-signal-regulated kinase 1/2 (ERK1/2) activation. Hydrogen Sulfide 76-79 epidermal growth factor receptor Homo sapiens 208-212 24657251-6 2014 In addition, the negative regulation of cell proliferation by inhibition of H2S/CSE system correlated with the blockage of cell mitogenic and survival signal transduction of epidermal growth factor receptor (EGFR) via down-regulating the extracellular-signal-regulated kinase 1/2 (ERK1/2) activation. Hydrogen Sulfide 76-79 mitogen-activated protein kinase 1 Homo sapiens 238-279 24657251-6 2014 In addition, the negative regulation of cell proliferation by inhibition of H2S/CSE system correlated with the blockage of cell mitogenic and survival signal transduction of epidermal growth factor receptor (EGFR) via down-regulating the extracellular-signal-regulated kinase 1/2 (ERK1/2) activation. Hydrogen Sulfide 76-79 mitogen-activated protein kinase 3 Homo sapiens 281-287 24610811-3 2014 This study investigated the activities of cystathionine-gamma-lyase (CSE, the enzyme that catalyzes H2S formation) in livers of type 1 diabetic (T1D) animals and in peripheral blood mononuclear cells (PBMC) isolated from T1D patients. Hydrogen Sulfide 100-103 cystathionine gamma-lyase Homo sapiens 42-67 24610811-3 2014 This study investigated the activities of cystathionine-gamma-lyase (CSE, the enzyme that catalyzes H2S formation) in livers of type 1 diabetic (T1D) animals and in peripheral blood mononuclear cells (PBMC) isolated from T1D patients. Hydrogen Sulfide 100-103 cystathionine gamma-lyase Homo sapiens 69-72 24610811-10 2014 Studies with CSE siRNA provide evidence for a relationship between impaired CSE expression and reduced H2S levels. Hydrogen Sulfide 103-106 cystathionine gamma-lyase Homo sapiens 13-16 24610811-10 2014 Studies with CSE siRNA provide evidence for a relationship between impaired CSE expression and reduced H2S levels. Hydrogen Sulfide 103-106 cystathionine gamma-lyase Homo sapiens 76-79 24610811-11 2014 This study demonstrates for the first time that both hyperglycemia and hyperketonemia mediate a reduction in CSE expression and activity, which can contribute to the impaired H2S signaling associated with diabetes. Hydrogen Sulfide 175-178 cystathionine gamma-lyase Homo sapiens 109-112 24487028-0 2014 Hydrogen sulfide improves wound healing via restoration of endothelial progenitor cell functions and activation of angiopoietin-1 in type 2 diabetes. Hydrogen Sulfide 0-16 angiopoietin 1 Mus musculus 115-129 24487028-13 2014 Taken together, these results show that H2S improves wound healing by restoration of EPC functions and activation of Ang-1 in type 2 diabetic mice. Hydrogen Sulfide 40-43 angiopoietin 1 Mus musculus 117-122 24849440-6 2014 CONCLUSIONS: H2S can promote proliferation and migration of SW480 cells in vitro, the mechanism of which may involve up-regulated expression of SIRT1. Hydrogen Sulfide 13-16 sirtuin 1 Homo sapiens 144-149 25033556-2 2014 In the process of aging the levels of H2S and activities of H2S-producing enzymes (cysteine aminotransferase, cystathionine-gamma-lyase) are reduced in the myocardium; the pro-/antioxidant balance is destabilized (NADPH-oxidase activity is increased and thioredoxin reductase activity is decreased). Hydrogen Sulfide 38-41 peroxiredoxin 5 Rattus norvegicus 254-275 25033556-2 2014 In the process of aging the levels of H2S and activities of H2S-producing enzymes (cysteine aminotransferase, cystathionine-gamma-lyase) are reduced in the myocardium; the pro-/antioxidant balance is destabilized (NADPH-oxidase activity is increased and thioredoxin reductase activity is decreased). Hydrogen Sulfide 60-63 peroxiredoxin 5 Rattus norvegicus 254-275 24832131-5 2014 Interestingly, during the initiation of lateral root primordia, IAA is a potent inducer of endogenous H 2S and CO, which is produced by L-cysteine desulfhydrase (LCD) and heme oxygenase-1 (HO-1), respectively. Hydrogen Sulfide 102-106 heme oxygenase 1 Homo sapiens 189-193 24722316-0 2014 Dexamethasone ameliorates H2S-induced acute lung injury by alleviating matrix metalloproteinase-2 and -9 expression. Hydrogen Sulfide 26-29 matrix metallopeptidase 2 Rattus norvegicus 71-104 24722316-1 2014 Acute lung injury (ALI) is one of the fatal outcomes after exposure to high levels of hydrogen sulfide (H2S), and the matrix metalloproteinases (MMPs) especially MMP-2 and MMP-9 are believed to be involved in the development of ALI by degrading the extracellular matrix (ECM) of blood-air barrier. Hydrogen Sulfide 86-102 matrix metallopeptidase 2 Rattus norvegicus 145-149 24722316-1 2014 Acute lung injury (ALI) is one of the fatal outcomes after exposure to high levels of hydrogen sulfide (H2S), and the matrix metalloproteinases (MMPs) especially MMP-2 and MMP-9 are believed to be involved in the development of ALI by degrading the extracellular matrix (ECM) of blood-air barrier. Hydrogen Sulfide 86-102 matrix metallopeptidase 2 Rattus norvegicus 162-167 24722316-1 2014 Acute lung injury (ALI) is one of the fatal outcomes after exposure to high levels of hydrogen sulfide (H2S), and the matrix metalloproteinases (MMPs) especially MMP-2 and MMP-9 are believed to be involved in the development of ALI by degrading the extracellular matrix (ECM) of blood-air barrier. Hydrogen Sulfide 86-102 matrix metallopeptidase 9 Rattus norvegicus 172-177 24722316-1 2014 Acute lung injury (ALI) is one of the fatal outcomes after exposure to high levels of hydrogen sulfide (H2S), and the matrix metalloproteinases (MMPs) especially MMP-2 and MMP-9 are believed to be involved in the development of ALI by degrading the extracellular matrix (ECM) of blood-air barrier. Hydrogen Sulfide 104-107 matrix metallopeptidase 2 Rattus norvegicus 162-167 24722316-1 2014 Acute lung injury (ALI) is one of the fatal outcomes after exposure to high levels of hydrogen sulfide (H2S), and the matrix metalloproteinases (MMPs) especially MMP-2 and MMP-9 are believed to be involved in the development of ALI by degrading the extracellular matrix (ECM) of blood-air barrier. Hydrogen Sulfide 104-107 matrix metallopeptidase 9 Rattus norvegicus 172-177 24722316-3 2014 The present work was aimed to investigate the roles of MMP-2 and MMP-9 in H2S-induced ALI and the protective effects of DXM. Hydrogen Sulfide 74-77 matrix metallopeptidase 2 Rattus norvegicus 55-60 24722316-3 2014 The present work was aimed to investigate the roles of MMP-2 and MMP-9 in H2S-induced ALI and the protective effects of DXM. Hydrogen Sulfide 74-77 matrix metallopeptidase 9 Rattus norvegicus 65-70 24722316-6 2014 Our results revealed that MMP-2 and MMP-9 were obviously increased in both mRNA and protein level after H2S exposure, and they could be inhibited by MMP inhibitor doxycycline (DOX) in rat model. Hydrogen Sulfide 104-107 matrix metallopeptidase 2 Rattus norvegicus 26-31 24722316-6 2014 Our results revealed that MMP-2 and MMP-9 were obviously increased in both mRNA and protein level after H2S exposure, and they could be inhibited by MMP inhibitor doxycycline (DOX) in rat model. Hydrogen Sulfide 104-107 matrix metallopeptidase 9 Rattus norvegicus 36-41 24722316-7 2014 Moreover, DXM significantly ameliorated the symptoms of H2S-induced ALI including alveolar edema, infiltration of inflammatory cells and the protein leakage in BAFL via up-regulating glucocorticoid receptor(GR) to mediate the suppression of MMP-2 and MMP-9. Hydrogen Sulfide 56-59 nuclear receptor subfamily 3, group C, member 1 Rattus norvegicus 183-206 24722316-7 2014 Moreover, DXM significantly ameliorated the symptoms of H2S-induced ALI including alveolar edema, infiltration of inflammatory cells and the protein leakage in BAFL via up-regulating glucocorticoid receptor(GR) to mediate the suppression of MMP-2 and MMP-9. Hydrogen Sulfide 56-59 matrix metallopeptidase 2 Rattus norvegicus 241-246 24722316-7 2014 Moreover, DXM significantly ameliorated the symptoms of H2S-induced ALI including alveolar edema, infiltration of inflammatory cells and the protein leakage in BAFL via up-regulating glucocorticoid receptor(GR) to mediate the suppression of MMP-2 and MMP-9. Hydrogen Sulfide 56-59 matrix metallopeptidase 9 Rattus norvegicus 251-256 24722316-9 2014 Our results, taken together, demonstrated that MMP-2 and MMP-9 were involved in the development of H2S-induced ALI and DXM exerted protective effects by alleviating the expression of MMP-2 and MMP-9. Hydrogen Sulfide 99-102 matrix metallopeptidase 2 Rattus norvegicus 47-52 24722316-9 2014 Our results, taken together, demonstrated that MMP-2 and MMP-9 were involved in the development of H2S-induced ALI and DXM exerted protective effects by alleviating the expression of MMP-2 and MMP-9. Hydrogen Sulfide 99-102 matrix metallopeptidase 9 Rattus norvegicus 57-62 24722316-9 2014 Our results, taken together, demonstrated that MMP-2 and MMP-9 were involved in the development of H2S-induced ALI and DXM exerted protective effects by alleviating the expression of MMP-2 and MMP-9. Hydrogen Sulfide 99-102 matrix metallopeptidase 2 Rattus norvegicus 183-188 24722316-9 2014 Our results, taken together, demonstrated that MMP-2 and MMP-9 were involved in the development of H2S-induced ALI and DXM exerted protective effects by alleviating the expression of MMP-2 and MMP-9. Hydrogen Sulfide 99-102 matrix metallopeptidase 9 Rattus norvegicus 193-198 24722316-10 2014 Therefore, MMP-2 and MMP-9 might represent novel pharmacological targets for the treatment of H2S and other hazard gases induced ALI. Hydrogen Sulfide 94-97 matrix metallopeptidase 2 Rattus norvegicus 11-16 24722316-10 2014 Therefore, MMP-2 and MMP-9 might represent novel pharmacological targets for the treatment of H2S and other hazard gases induced ALI. Hydrogen Sulfide 94-97 matrix metallopeptidase 9 Rattus norvegicus 21-26 24550391-0 2014 Hydrogen sulfide suppresses oxidized low-density lipoprotein (ox-LDL)-stimulated monocyte chemoattractant protein 1 generation from macrophages via the nuclear factor kappaB (NF-kappaB) pathway. Hydrogen Sulfide 0-16 C-C motif chemokine ligand 2 Homo sapiens 81-115 24550391-0 2014 Hydrogen sulfide suppresses oxidized low-density lipoprotein (ox-LDL)-stimulated monocyte chemoattractant protein 1 generation from macrophages via the nuclear factor kappaB (NF-kappaB) pathway. Hydrogen Sulfide 0-16 nuclear factor kappa B subunit 1 Homo sapiens 167-173 24550391-0 2014 Hydrogen sulfide suppresses oxidized low-density lipoprotein (ox-LDL)-stimulated monocyte chemoattractant protein 1 generation from macrophages via the nuclear factor kappaB (NF-kappaB) pathway. Hydrogen Sulfide 0-16 nuclear factor kappa B subunit 1 Homo sapiens 175-184 24550391-1 2014 This study was designed to examine the role of hydrogen sulfide (H2S) in the generation of oxidized low-density lipoprotein (ox-LDL)-stimulated monocyte chemoattractant protein 1 (MCP-1) from macrophages and possible mechanisms. Hydrogen Sulfide 47-63 C-C motif chemokine ligand 2 Homo sapiens 144-178 24550391-1 2014 This study was designed to examine the role of hydrogen sulfide (H2S) in the generation of oxidized low-density lipoprotein (ox-LDL)-stimulated monocyte chemoattractant protein 1 (MCP-1) from macrophages and possible mechanisms. Hydrogen Sulfide 47-63 C-C motif chemokine ligand 2 Homo sapiens 180-185 24550391-1 2014 This study was designed to examine the role of hydrogen sulfide (H2S) in the generation of oxidized low-density lipoprotein (ox-LDL)-stimulated monocyte chemoattractant protein 1 (MCP-1) from macrophages and possible mechanisms. Hydrogen Sulfide 65-68 C-C motif chemokine ligand 2 Homo sapiens 144-178 24550391-1 2014 This study was designed to examine the role of hydrogen sulfide (H2S) in the generation of oxidized low-density lipoprotein (ox-LDL)-stimulated monocyte chemoattractant protein 1 (MCP-1) from macrophages and possible mechanisms. Hydrogen Sulfide 65-68 C-C motif chemokine ligand 2 Homo sapiens 180-185 24550391-6 2014 Furthermore, NaHS decreased the ratio of free thiol groups in p65, whereas the thiol reductant DTT reversed the inhibiting effect of H2S on the p65 DNA binding activity. Hydrogen Sulfide 133-136 RELA proto-oncogene, NF-kB subunit Homo sapiens 144-147 24550391-7 2014 Most importantly, site-specific mutation of cysteine 38 to serine in p65 abolished the effect of H2S on the sulfhydration of NF-kappaB and ox-LDL-induced NF-kappaB activation. Hydrogen Sulfide 97-100 RELA proto-oncogene, NF-kB subunit Homo sapiens 69-72 24550391-7 2014 Most importantly, site-specific mutation of cysteine 38 to serine in p65 abolished the effect of H2S on the sulfhydration of NF-kappaB and ox-LDL-induced NF-kappaB activation. Hydrogen Sulfide 97-100 nuclear factor kappa B subunit 1 Homo sapiens 125-134 24550391-7 2014 Most importantly, site-specific mutation of cysteine 38 to serine in p65 abolished the effect of H2S on the sulfhydration of NF-kappaB and ox-LDL-induced NF-kappaB activation. Hydrogen Sulfide 97-100 nuclear factor kappa B subunit 1 Homo sapiens 154-163 24550391-8 2014 These results suggested that endogenous H2S inhibited ox-LDL-induced macrophage inflammation by suppressing NF-kappaB p65 phosphorylation, nuclear translocation, DNA binding activity, and recruitment to the MCP-1 promoter. Hydrogen Sulfide 40-43 nuclear factor kappa B subunit 1 Homo sapiens 108-117 24550391-8 2014 These results suggested that endogenous H2S inhibited ox-LDL-induced macrophage inflammation by suppressing NF-kappaB p65 phosphorylation, nuclear translocation, DNA binding activity, and recruitment to the MCP-1 promoter. Hydrogen Sulfide 40-43 RELA proto-oncogene, NF-kB subunit Homo sapiens 118-121 24550391-8 2014 These results suggested that endogenous H2S inhibited ox-LDL-induced macrophage inflammation by suppressing NF-kappaB p65 phosphorylation, nuclear translocation, DNA binding activity, and recruitment to the MCP-1 promoter. Hydrogen Sulfide 40-43 C-C motif chemokine ligand 2 Homo sapiens 207-212 24550391-9 2014 The sulfhydration of free thiol group on cysteine 38 in p65 served as a molecular mechanism by which H2S inhibited NF-kappaB pathway activation in ox-LDL-induced macrophage inflammation. Hydrogen Sulfide 101-104 RELA proto-oncogene, NF-kB subunit Homo sapiens 56-59 24550391-9 2014 The sulfhydration of free thiol group on cysteine 38 in p65 served as a molecular mechanism by which H2S inhibited NF-kappaB pathway activation in ox-LDL-induced macrophage inflammation. Hydrogen Sulfide 101-104 nuclear factor kappa B subunit 1 Homo sapiens 115-124 24508731-5 2014 Although without impact on lung oxidative status, systemic H2S blunted leukocyte infiltration into alveolar air spaces provoked by hyperoxia, and restored normal lung interleukin 10 levels that were otherwise depressed by 85% O2. Hydrogen Sulfide 59-62 interleukin 10 Mus musculus 167-181 24758901-5 2014 These observations suggest that the novel mechanism underlying the cardioprotective function of H2S is secondary to a combination of attenuation the recruitment of CD11b(+)Gr-1(+) myeloid cells and regulation of the Bax/Bcl-2 apoptotic signaling. Hydrogen Sulfide 96-99 integrin subunit alpha M Homo sapiens 164-169 24758901-5 2014 These observations suggest that the novel mechanism underlying the cardioprotective function of H2S is secondary to a combination of attenuation the recruitment of CD11b(+)Gr-1(+) myeloid cells and regulation of the Bax/Bcl-2 apoptotic signaling. Hydrogen Sulfide 96-99 BCL2 associated X, apoptosis regulator Homo sapiens 216-219 24758901-5 2014 These observations suggest that the novel mechanism underlying the cardioprotective function of H2S is secondary to a combination of attenuation the recruitment of CD11b(+)Gr-1(+) myeloid cells and regulation of the Bax/Bcl-2 apoptotic signaling. Hydrogen Sulfide 96-99 BCL2 apoptosis regulator Homo sapiens 220-225 24423987-5 2014 We found that intracerebroventricular injection of Hcy in rats leads to learning and memory dysfunctions in the Morris water maze and novel of object recognition test and decreases in the expression of cystathionine-beta-synthase, the major enzyme responsible for endogenous H2S generation, and the generation of endogenous H2S in the hippocampus of rats. Hydrogen Sulfide 275-278 cystathionine beta synthase Rattus norvegicus 202-229 24423987-5 2014 We found that intracerebroventricular injection of Hcy in rats leads to learning and memory dysfunctions in the Morris water maze and novel of object recognition test and decreases in the expression of cystathionine-beta-synthase, the major enzyme responsible for endogenous H2S generation, and the generation of endogenous H2S in the hippocampus of rats. Hydrogen Sulfide 324-327 cystathionine beta synthase Rattus norvegicus 202-229 23991830-4 2014 H2 S is produced by cystathionine gamma-lyase (CSE), cystathionine beta-synthase (CBS) and 3-mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 0-4 cystathionine gamma-lyase Homo sapiens 20-45 23991830-4 2014 H2 S is produced by cystathionine gamma-lyase (CSE), cystathionine beta-synthase (CBS) and 3-mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 0-4 cystathionine gamma-lyase Homo sapiens 47-50 23991830-4 2014 H2 S is produced by cystathionine gamma-lyase (CSE), cystathionine beta-synthase (CBS) and 3-mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 0-4 cystathionine beta-synthase Homo sapiens 53-80 23991830-4 2014 H2 S is produced by cystathionine gamma-lyase (CSE), cystathionine beta-synthase (CBS) and 3-mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 0-4 cystathionine beta-synthase Homo sapiens 82-85 23991830-4 2014 H2 S is produced by cystathionine gamma-lyase (CSE), cystathionine beta-synthase (CBS) and 3-mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 0-4 mercaptopyruvate sulfurtransferase Homo sapiens 91-127 23991830-7 2014 In specialized conditions (calcium overload in vascular smooth muscle, colon cancer cells), CSE and CBS can also associate with the mitochondria; H2 S produced by these enzymes, serves as an endogenous stimulator of cellular bioenergetics. Hydrogen Sulfide 146-150 cystathionine gamma-lyase Homo sapiens 92-95 23991830-7 2014 In specialized conditions (calcium overload in vascular smooth muscle, colon cancer cells), CSE and CBS can also associate with the mitochondria; H2 S produced by these enzymes, serves as an endogenous stimulator of cellular bioenergetics. Hydrogen Sulfide 146-150 cystathionine beta-synthase Homo sapiens 100-103 24508731-8 2014 The impact of NaHS on ATII cell migration was attenuated by glibenclamide, implicating ion channels, and was accompanied by activation of Akt, hinting at two possible mechanisms of H2S action. Hydrogen Sulfide 181-184 thymoma viral proto-oncogene 1 Mus musculus 138-141 24587076-0 2014 Hydrogen sulfide inhibits formaldehyde-induced endoplasmic reticulum stress in PC12 cells by upregulation of SIRT-1. Hydrogen Sulfide 0-16 sirtuin 1 Rattus norvegicus 109-115 24501330-13 2014 This novel mechanism, unrelated to ACE inhibition and based on H2S release, could explain the beneficial effects of sulfhydrylated ACE inhibitors reported in the clinical literature. Hydrogen Sulfide 63-66 angiotensin I converting enzyme Rattus norvegicus 131-134 24535538-0 2014 GYY4137, a hydrogen sulfide (H2S) donor, shows potent anti-hepatocellular carcinoma activity through blocking the STAT3 pathway. Hydrogen Sulfide 11-27 signal transducer and activator of transcription 3 Homo sapiens 114-119 24535538-0 2014 GYY4137, a hydrogen sulfide (H2S) donor, shows potent anti-hepatocellular carcinoma activity through blocking the STAT3 pathway. Hydrogen Sulfide 29-32 signal transducer and activator of transcription 3 Homo sapiens 114-119 24335973-0 2014 Hydrogen sulfide attenuates sFlt1-induced hypertension and renal damage by upregulating vascular endothelial growth factor. Hydrogen Sulfide 0-16 vascular endothelial growth factor A Rattus norvegicus 88-122 24335973-11 2014 These results suggest that hydrogen sulfide ameliorates sFlt1-induced hypertension, proteinuria, and glomerular endotheliosis in rats by increasing VEGF expression. Hydrogen Sulfide 27-43 vascular endothelial growth factor A Rattus norvegicus 148-152 24754330-13 2014 In pig, rolipram-induced response is produced through the PKA pathway involving BKCa and IKCa channel activation and [Ca2+]i desensitization-dependent mechanisms, this relaxation also being due to neuronal NO and H2S release. Hydrogen Sulfide 213-216 protein kinase cAMP-activated catalytic subunit alpha Sus scrofa 58-61 24374752-3 2014 The present study was designed to determine whether GYY4137, a novel H2S-releasing molecule, protected H9c2 cells against high glucose (HG)-induced cytotoxicity by activation of the AMPK/mTOR signal pathway. Hydrogen Sulfide 69-72 mechanistic target of rapamycin kinase Rattus norvegicus 187-191 24752097-0 2014 [Effect of exogenous hydrogen sulfide on BACE-1 enzyme expression and beta-amyloid peptide metabolism in high-glucose primary neuronal culture]. Hydrogen Sulfide 21-37 beta-secretase 1 Homo sapiens 41-47 24752097-1 2014 OBJECTIVE: To investigate the effects of exogenous hydrogen sulfide (H2S) on beta-site APP cleaving enzyme 1 (BACE-1) and beta-amyloid peptide (Abeta) metabolism in primary culture of neurons under high-glucose condition. Hydrogen Sulfide 51-67 beta-secretase 1 Homo sapiens 110-116 24752097-1 2014 OBJECTIVE: To investigate the effects of exogenous hydrogen sulfide (H2S) on beta-site APP cleaving enzyme 1 (BACE-1) and beta-amyloid peptide (Abeta) metabolism in primary culture of neurons under high-glucose condition. Hydrogen Sulfide 69-72 beta-secretase 1 Homo sapiens 77-108 24752097-1 2014 OBJECTIVE: To investigate the effects of exogenous hydrogen sulfide (H2S) on beta-site APP cleaving enzyme 1 (BACE-1) and beta-amyloid peptide (Abeta) metabolism in primary culture of neurons under high-glucose condition. Hydrogen Sulfide 69-72 beta-secretase 1 Homo sapiens 110-116 24873153-8 2014 CONCLUSION: The reduced concentration of H2S and decreased expressions of CBS and CSE in the penile corpus cavernosum of the diabetic rats suggested that the H2S signaling pathway might be involved in hyperglycemia-induced erectile dysfunction. Hydrogen Sulfide 158-161 cystathionine gamma-lyase Rattus norvegicus 82-85 24515102-1 2014 The hexa-coordinate heme in the H2S-generating human enzyme cystathionine beta-synthase (CBS) acts as a redox-sensitive regulator that impairs CBS activity upon binding of NO( ) or CO at the reduced iron. Hydrogen Sulfide 32-35 hexosaminidase subunit alpha Homo sapiens 4-8 24515102-1 2014 The hexa-coordinate heme in the H2S-generating human enzyme cystathionine beta-synthase (CBS) acts as a redox-sensitive regulator that impairs CBS activity upon binding of NO( ) or CO at the reduced iron. Hydrogen Sulfide 32-35 cystathionine beta-synthase Homo sapiens 60-87 24515102-1 2014 The hexa-coordinate heme in the H2S-generating human enzyme cystathionine beta-synthase (CBS) acts as a redox-sensitive regulator that impairs CBS activity upon binding of NO( ) or CO at the reduced iron. Hydrogen Sulfide 32-35 cystathionine beta-synthase Homo sapiens 89-92 24515102-1 2014 The hexa-coordinate heme in the H2S-generating human enzyme cystathionine beta-synthase (CBS) acts as a redox-sensitive regulator that impairs CBS activity upon binding of NO( ) or CO at the reduced iron. Hydrogen Sulfide 32-35 cystathionine beta-synthase Homo sapiens 143-146 24515102-7 2014 The novel findings reported here shed new light on CBS regulation by NO( ) and its possible (patho)physiological relevance, enforcing the growing evidence for an interplay among the gasotransmitters NO( ), CO, and H2S in cell signaling. Hydrogen Sulfide 214-217 cystathionine beta-synthase Homo sapiens 51-54 24491430-1 2014 Cystathionine beta synthase (CBS) is the main contributor to the production of hydrogen sulfide (H2S) in the brain. Hydrogen Sulfide 79-95 cystathionine beta-synthase Mus musculus 29-32 24491430-1 2014 Cystathionine beta synthase (CBS) is the main contributor to the production of hydrogen sulfide (H2S) in the brain. Hydrogen Sulfide 79-95 cystathionine beta-synthase Mus musculus 0-27 24491430-1 2014 Cystathionine beta synthase (CBS) is the main contributor to the production of hydrogen sulfide (H2S) in the brain. Hydrogen Sulfide 97-100 cystathionine beta-synthase Mus musculus 0-27 24491430-1 2014 Cystathionine beta synthase (CBS) is the main contributor to the production of hydrogen sulfide (H2S) in the brain. Hydrogen Sulfide 97-100 cystathionine beta-synthase Mus musculus 29-32 24491430-5 2014 We hypothesize that CBS/H2S pathway plays an important role in the protection of learning and memory functions in the brain at the level of the hippocampus. Hydrogen Sulfide 24-27 cystathionine beta-synthase Mus musculus 20-23 24758901-0 2014 Hydrogen sulfide attenuates the recruitment of CD11b+Gr-1+ myeloid cells and regulates Bax/Bcl-2 signaling in myocardial ischemia injury. Hydrogen Sulfide 0-16 integrin subunit alpha M Homo sapiens 47-52 24758901-0 2014 Hydrogen sulfide attenuates the recruitment of CD11b+Gr-1+ myeloid cells and regulates Bax/Bcl-2 signaling in myocardial ischemia injury. Hydrogen Sulfide 0-16 BCL2 associated X, apoptosis regulator Homo sapiens 87-90 24758901-0 2014 Hydrogen sulfide attenuates the recruitment of CD11b+Gr-1+ myeloid cells and regulates Bax/Bcl-2 signaling in myocardial ischemia injury. Hydrogen Sulfide 0-16 BCL2 apoptosis regulator Homo sapiens 91-96 24491853-4 2014 In the human body, H2S production is predominantly catalyzed by cystathionine-beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 19-22 cystathionine beta-synthase Homo sapiens 64-91 24491853-4 2014 In the human body, H2S production is predominantly catalyzed by cystathionine-beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 19-22 cystathionine gamma-lyase Homo sapiens 102-127 24491853-4 2014 In the human body, H2S production is predominantly catalyzed by cystathionine-beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 19-22 cystathionine gamma-lyase Homo sapiens 129-132 24491853-5 2014 CSE is the primary H2S-producing enzyme in the vasculature. Hydrogen Sulfide 19-22 cystathionine gamma-lyase Homo sapiens 0-3 24491853-9 2014 2013; 127: 2523-2534) demonstrates that decreased endogenous H2S production by CSE genetic deletion accelerates atherosclerosis in athero-prone ApoE-/- mice, pinpointing that endogenously produced H2S by CSE activation may be of benefit in the prevention and treatment of atherosclerosis. Hydrogen Sulfide 61-64 cystathionine gamma-lyase Homo sapiens 79-82 24366262-12 2014 Our results suggest that endogenously generated H2S acts as a stealth hyperpolarizing factor on smooth muscle cells to maintain the CO-dependent transwall gradient and inhibits NO production from nNOS. Hydrogen Sulfide 48-51 nitric oxide synthase 1, neuronal Mus musculus 196-200 24508566-6 2014 H2S production was detected when glomeruli were incubated with AMPS or GMPS and ionotropic purinergic P2X7 receptor/channel agonist, BzATP. Hydrogen Sulfide 0-3 purinergic receptor P2X 7 Homo sapiens 102-115 24508802-0 2014 Endogenous and exogenous hydrogen sulfide facilitates T-type calcium channel currents in Cav3.2-expressing HEK293 cells. Hydrogen Sulfide 25-41 calcium voltage-gated channel subunit alpha1 H Homo sapiens 89-95 24508802-1 2014 Hydrogen sulfide (H2S), a gasotransmitter, is formed from l-cysteine by multiple enzymes including cystathionine-gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 99-124 24508802-1 2014 Hydrogen sulfide (H2S), a gasotransmitter, is formed from l-cysteine by multiple enzymes including cystathionine-gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 126-129 24508802-1 2014 Hydrogen sulfide (H2S), a gasotransmitter, is formed from l-cysteine by multiple enzymes including cystathionine-gamma-lyase (CSE). Hydrogen Sulfide 18-21 cystathionine gamma-lyase Homo sapiens 99-124 24508802-1 2014 Hydrogen sulfide (H2S), a gasotransmitter, is formed from l-cysteine by multiple enzymes including cystathionine-gamma-lyase (CSE). Hydrogen Sulfide 18-21 cystathionine gamma-lyase Homo sapiens 126-129 24508802-2 2014 We have shown that an H2S donor, NaHS, causes hyperalgesia in rodents, an effect inhibited by knockdown of Cav3.2 T-type Ca(2+) channels (T-channels), and that NaHS facilitates T-channel-dependent currents (T-currents) in NG108-15 cells that naturally express Cav3.2. Hydrogen Sulfide 22-25 calcium voltage-gated channel subunit alpha1 H Homo sapiens 107-113 24508802-2 2014 We have shown that an H2S donor, NaHS, causes hyperalgesia in rodents, an effect inhibited by knockdown of Cav3.2 T-type Ca(2+) channels (T-channels), and that NaHS facilitates T-channel-dependent currents (T-currents) in NG108-15 cells that naturally express Cav3.2. Hydrogen Sulfide 22-25 calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus 260-266 24508802-3 2014 In the present study, we asked if endogenous and exogenous H2S participates in regulation of the channel functions in Cav3.2-transfected HEK293 (Cav3.2-HEK293) cells. Hydrogen Sulfide 59-62 calcium voltage-gated channel subunit alpha1 H Homo sapiens 118-124 24508802-3 2014 In the present study, we asked if endogenous and exogenous H2S participates in regulation of the channel functions in Cav3.2-transfected HEK293 (Cav3.2-HEK293) cells. Hydrogen Sulfide 59-62 calcium voltage-gated channel subunit alpha1 H Homo sapiens 145-151 24508802-7 2014 Similarly, Na2S, another H2S donor, at 0.1-0.3mM significantly increased T-currents in the presence, but not absence, of PPG in Cav3.2-HEK293 cells. Hydrogen Sulfide 25-28 calcium voltage-gated channel subunit alpha1 H Homo sapiens 128-134 24508802-11 2014 These results suggest that the function of Cav3.2 T-channels is tonically enhanced by endogenous H2S synthesized by CSE in Cav3.2-HEK293 cells, and that exogenous H2S is capable of enhancing Cav3.2 function when endogenous H2S production by CSE is inhibited. Hydrogen Sulfide 97-100 calcium voltage-gated channel subunit alpha1 H Homo sapiens 43-49 24508802-11 2014 These results suggest that the function of Cav3.2 T-channels is tonically enhanced by endogenous H2S synthesized by CSE in Cav3.2-HEK293 cells, and that exogenous H2S is capable of enhancing Cav3.2 function when endogenous H2S production by CSE is inhibited. Hydrogen Sulfide 97-100 cystathionine gamma-lyase Homo sapiens 116-119 24508802-11 2014 These results suggest that the function of Cav3.2 T-channels is tonically enhanced by endogenous H2S synthesized by CSE in Cav3.2-HEK293 cells, and that exogenous H2S is capable of enhancing Cav3.2 function when endogenous H2S production by CSE is inhibited. Hydrogen Sulfide 97-100 calcium voltage-gated channel subunit alpha1 H Homo sapiens 123-129 24508802-11 2014 These results suggest that the function of Cav3.2 T-channels is tonically enhanced by endogenous H2S synthesized by CSE in Cav3.2-HEK293 cells, and that exogenous H2S is capable of enhancing Cav3.2 function when endogenous H2S production by CSE is inhibited. Hydrogen Sulfide 97-100 calcium voltage-gated channel subunit alpha1 H Homo sapiens 123-129 24508802-11 2014 These results suggest that the function of Cav3.2 T-channels is tonically enhanced by endogenous H2S synthesized by CSE in Cav3.2-HEK293 cells, and that exogenous H2S is capable of enhancing Cav3.2 function when endogenous H2S production by CSE is inhibited. Hydrogen Sulfide 163-166 calcium voltage-gated channel subunit alpha1 H Homo sapiens 43-49 24508802-11 2014 These results suggest that the function of Cav3.2 T-channels is tonically enhanced by endogenous H2S synthesized by CSE in Cav3.2-HEK293 cells, and that exogenous H2S is capable of enhancing Cav3.2 function when endogenous H2S production by CSE is inhibited. Hydrogen Sulfide 163-166 cystathionine gamma-lyase Homo sapiens 241-244 24508802-11 2014 These results suggest that the function of Cav3.2 T-channels is tonically enhanced by endogenous H2S synthesized by CSE in Cav3.2-HEK293 cells, and that exogenous H2S is capable of enhancing Cav3.2 function when endogenous H2S production by CSE is inhibited. Hydrogen Sulfide 163-166 calcium voltage-gated channel subunit alpha1 H Homo sapiens 43-49 24508802-11 2014 These results suggest that the function of Cav3.2 T-channels is tonically enhanced by endogenous H2S synthesized by CSE in Cav3.2-HEK293 cells, and that exogenous H2S is capable of enhancing Cav3.2 function when endogenous H2S production by CSE is inhibited. Hydrogen Sulfide 163-166 cystathionine gamma-lyase Homo sapiens 241-244 24587333-8 2014 The stimulatory effect of SNP on Ca(2+) accumulation and CaM1 (calmodulin 1) expression could be abolished by inhibiting H2S synthesis. Hydrogen Sulfide 121-124 calmodulin 1 Homo sapiens 57-61 24587333-8 2014 The stimulatory effect of SNP on Ca(2+) accumulation and CaM1 (calmodulin 1) expression could be abolished by inhibiting H2S synthesis. Hydrogen Sulfide 121-124 calmodulin 1 Homo sapiens 63-75 24587076-6 2014 OBJECTIVE: We hypothesize that the protection of H2S against FA-induced neurotoxicity involves in inhibiting ER stress by upregulation of SIRT-1. Hydrogen Sulfide 49-52 sirtuin 1 Rattus norvegicus 138-144 24587076-7 2014 The present study attempted to investigate the protective effect of H2S on FA-induced ER stress in PC12 cells and the contribution of SIRT-1 to the protection of H2S against FA-induced injuries, including ER stress, cytotoxicity and apoptosis. Hydrogen Sulfide 162-165 sirtuin 1 Rattus norvegicus 134-140 24587076-10 2014 Moreover, the protective effects of H2S on FA-elicited ER stress, cytotoxicity and apoptosis were reversed by Sirtinol, a specific inhibitor of SIRT-1. Hydrogen Sulfide 36-39 sirtuin 1 Rattus norvegicus 144-150 24587076-11 2014 CONCLUSION/SIGNIFICANCE: These data indicate that H2S exerts its protection against the neurotoxicity of FA through overcoming ER stress via upregulation of SIRT-1. Hydrogen Sulfide 50-53 sirtuin 1 Rattus norvegicus 157-163 24451084-3 2014 Under externally applied compressive force, the piezoelectric output of CdS nanorod arrays is very sensitive to H2S. Hydrogen Sulfide 112-115 CDP-diacylglycerol synthase 1 Homo sapiens 72-75 24451084-0 2014 Synthesis of CdS nanorod arrays and their applications in flexible piezo-driven active H2S sensors. Hydrogen Sulfide 87-90 CDP-diacylglycerol synthase 1 Homo sapiens 13-16 24451084-1 2014 A flexible piezo-driven active H2S sensor has been fabricated from CdS nanorod arrays. Hydrogen Sulfide 31-34 CDP-diacylglycerol synthase 1 Homo sapiens 67-70 24451084-2 2014 By coupling the piezoelectric and gas sensing properties of CdS nanorods, the piezoelectric output generated by CdS nanorod arrays acts not only as a power source, but also as a response signal to H2S. Hydrogen Sulfide 197-200 CDP-diacylglycerol synthase 1 Homo sapiens 60-63 24451084-2 2014 By coupling the piezoelectric and gas sensing properties of CdS nanorods, the piezoelectric output generated by CdS nanorod arrays acts not only as a power source, but also as a response signal to H2S. Hydrogen Sulfide 197-200 CDP-diacylglycerol synthase 1 Homo sapiens 112-115 24444438-0 2014 Hydrogen sulfide protected gastric epithelial cell from ischemia/reperfusion injury by Keap1 s-sulfhydration, MAPK dependent anti-apoptosis and NF-kappaB dependent anti-inflammation pathway. Hydrogen Sulfide 0-16 kelch like ECH associated protein 1 Homo sapiens 87-92 24444438-0 2014 Hydrogen sulfide protected gastric epithelial cell from ischemia/reperfusion injury by Keap1 s-sulfhydration, MAPK dependent anti-apoptosis and NF-kappaB dependent anti-inflammation pathway. Hydrogen Sulfide 0-16 nuclear factor kappa B subunit 1 Homo sapiens 144-153 24444438-7 2014 H2S also induced Keap1 s-sulfhydration, and further Keap1/Nrf2 disassociation and Nrf2 activation. Hydrogen Sulfide 0-3 kelch like ECH associated protein 1 Homo sapiens 17-22 24444438-7 2014 H2S also induced Keap1 s-sulfhydration, and further Keap1/Nrf2 disassociation and Nrf2 activation. Hydrogen Sulfide 0-3 kelch like ECH associated protein 1 Homo sapiens 52-57 24444438-7 2014 H2S also induced Keap1 s-sulfhydration, and further Keap1/Nrf2 disassociation and Nrf2 activation. Hydrogen Sulfide 0-3 NFE2 like bZIP transcription factor 2 Homo sapiens 58-62 24444438-7 2014 H2S also induced Keap1 s-sulfhydration, and further Keap1/Nrf2 disassociation and Nrf2 activation. Hydrogen Sulfide 0-3 NFE2 like bZIP transcription factor 2 Homo sapiens 82-86 24444438-8 2014 H2S exerted its protective effect through reactive oxygen species clearance, inhibition of p38 and JNK dependent cell apoptosis and NF-kappaB dependent inflammation pathway. Hydrogen Sulfide 0-3 mitogen-activated protein kinase 14 Homo sapiens 91-94 24444438-8 2014 H2S exerted its protective effect through reactive oxygen species clearance, inhibition of p38 and JNK dependent cell apoptosis and NF-kappaB dependent inflammation pathway. Hydrogen Sulfide 0-3 mitogen-activated protein kinase 8 Homo sapiens 99-102 24444438-8 2014 H2S exerted its protective effect through reactive oxygen species clearance, inhibition of p38 and JNK dependent cell apoptosis and NF-kappaB dependent inflammation pathway. Hydrogen Sulfide 0-3 nuclear factor kappa B subunit 1 Homo sapiens 132-141 24403532-0 2014 Hydrogen sulfide [corrected] increases survival during sepsis: protective effect of CHOP inhibition. Hydrogen Sulfide 0-16 DNA-damage inducible transcript 3 Mus musculus 84-88 24403532-5 2014 We found that C/EBP homologous protein 10 (CHOP), a mediator of the endoplasmic reticulum stress response, was elevated in several organs after CLP, and its expression was inhibited by H2S treatment. Hydrogen Sulfide 185-188 DNA-damage inducible transcript 3 Mus musculus 14-41 24403532-5 2014 We found that C/EBP homologous protein 10 (CHOP), a mediator of the endoplasmic reticulum stress response, was elevated in several organs after CLP, and its expression was inhibited by H2S treatment. Hydrogen Sulfide 185-188 DNA-damage inducible transcript 3 Mus musculus 43-47 24403532-9 2014 Finally, we showed that H2S inhibited CHOP expression in macrophages by a mechanism involving Nrf2 activation. Hydrogen Sulfide 24-27 DNA-damage inducible transcript 3 Mus musculus 38-42 24403532-9 2014 Finally, we showed that H2S inhibited CHOP expression in macrophages by a mechanism involving Nrf2 activation. Hydrogen Sulfide 24-27 nuclear factor, erythroid derived 2, like 2 Mus musculus 94-98 24403532-10 2014 In conclusion, our findings show a protective effect of H2S treatment afforded, at least partially, by inhibition of CHOP expression. Hydrogen Sulfide 56-59 DNA-damage inducible transcript 3 Mus musculus 117-121 23581627-0 2014 Hydrogen sulfide prevents heart failure development via inhibition of renin release from mast cells in isoproterenol-treated rats. Hydrogen Sulfide 0-16 renin Rattus norvegicus 70-75 23581627-2 2014 We previously reported that hydrogen sulfide (H2S), an endogenous gaseous mediator, regulates renin synthesis and release in juxtaglomerular cells. Hydrogen Sulfide 28-44 renin Rattus norvegicus 94-99 23581627-2 2014 We previously reported that hydrogen sulfide (H2S), an endogenous gaseous mediator, regulates renin synthesis and release in juxtaglomerular cells. Hydrogen Sulfide 46-49 renin Rattus norvegicus 94-99 23581627-3 2014 The present study was designed to investigate whether H2S can protect against isoproterenol (ISO)-induced heart failure via inhibition of local renin activity in rat hearts. Hydrogen Sulfide 54-57 renin Rattus norvegicus 144-149 23581627-12 2014 CONCLUSIONS: For the first time, we demonstrated that H2S might protect heart during heart failure by suppression of local renin level through inhibition of both mast cell infiltration and renin degranulation. Hydrogen Sulfide 54-57 renin Rattus norvegicus 123-128 23581627-12 2014 CONCLUSIONS: For the first time, we demonstrated that H2S might protect heart during heart failure by suppression of local renin level through inhibition of both mast cell infiltration and renin degranulation. Hydrogen Sulfide 54-57 renin Rattus norvegicus 189-194 23581969-3 2014 RECENT ADVANCES: In addition to cystathionine beta-synthase and cystathionine gamma-lyase, 3-mercaptopyruvate sulfurtransferase along with cysteine aminotransferase was recently demonstrated to produce H2S. Hydrogen Sulfide 202-205 cystathionine gamma-lyase Homo sapiens 64-89 23581969-3 2014 RECENT ADVANCES: In addition to cystathionine beta-synthase and cystathionine gamma-lyase, 3-mercaptopyruvate sulfurtransferase along with cysteine aminotransferase was recently demonstrated to produce H2S. Hydrogen Sulfide 202-205 mercaptopyruvate sulfurtransferase Homo sapiens 91-127 23682865-3 2014 RECENT ADVANCES: The activity of BKCa channels is regulated by O2, carbon monoxide (CO), and hydrogen sulfide (H2S), suggesting that integration of these signals may be crucial to the physiological response of this tissue. Hydrogen Sulfide 93-109 potassium calcium-activated channel subfamily M alpha 1 Rattus norvegicus 33-37 23682865-3 2014 RECENT ADVANCES: The activity of BKCa channels is regulated by O2, carbon monoxide (CO), and hydrogen sulfide (H2S), suggesting that integration of these signals may be crucial to the physiological response of this tissue. Hydrogen Sulfide 111-114 potassium calcium-activated channel subfamily M alpha 1 Rattus norvegicus 33-37 23682865-6 2014 Conversely, H2S is a potent BKCa inhibitor. Hydrogen Sulfide 12-15 potassium calcium-activated channel subfamily M alpha 1 Rattus norvegicus 28-32 23682865-7 2014 H2S is produced endogenously by cystathionine-beta-synthase and cystathionine-gamma-lyase in the rat carotid body, and its intracellular concentration is dependent upon the balance between its enzymatic generation and its mitochondrial breakdown. Hydrogen Sulfide 0-3 cystathionine beta synthase Rattus norvegicus 32-59 23682865-7 2014 H2S is produced endogenously by cystathionine-beta-synthase and cystathionine-gamma-lyase in the rat carotid body, and its intracellular concentration is dependent upon the balance between its enzymatic generation and its mitochondrial breakdown. Hydrogen Sulfide 0-3 cystathionine gamma-lyase Rattus norvegicus 64-89 24138560-8 2014 CONCLUSION: We conclude that H2S affects [Ca(2+)]i homeostasis that is mediated by H2S-evoked NO production via an endothelial nitric oxide synthase (eNOS)-NO-sGC-cyclic guanosine monophosphate-PKG-Gq-protein-PLC-IP3 pathway to induce Ca(2+) release, and this pathway is identical to the one we recently proposed for a sole effect of NO and the two gaseous molecules synergistically function to regulate Ca(2+) homeostasis. Hydrogen Sulfide 29-32 nitric oxide synthase 3 Homo sapiens 115-148 24138560-8 2014 CONCLUSION: We conclude that H2S affects [Ca(2+)]i homeostasis that is mediated by H2S-evoked NO production via an endothelial nitric oxide synthase (eNOS)-NO-sGC-cyclic guanosine monophosphate-PKG-Gq-protein-PLC-IP3 pathway to induce Ca(2+) release, and this pathway is identical to the one we recently proposed for a sole effect of NO and the two gaseous molecules synergistically function to regulate Ca(2+) homeostasis. Hydrogen Sulfide 29-32 protein kinase cGMP-dependent 1 Homo sapiens 194-197 24138560-8 2014 CONCLUSION: We conclude that H2S affects [Ca(2+)]i homeostasis that is mediated by H2S-evoked NO production via an endothelial nitric oxide synthase (eNOS)-NO-sGC-cyclic guanosine monophosphate-PKG-Gq-protein-PLC-IP3 pathway to induce Ca(2+) release, and this pathway is identical to the one we recently proposed for a sole effect of NO and the two gaseous molecules synergistically function to regulate Ca(2+) homeostasis. Hydrogen Sulfide 83-86 nitric oxide synthase 3 Homo sapiens 115-148 24138560-8 2014 CONCLUSION: We conclude that H2S affects [Ca(2+)]i homeostasis that is mediated by H2S-evoked NO production via an endothelial nitric oxide synthase (eNOS)-NO-sGC-cyclic guanosine monophosphate-PKG-Gq-protein-PLC-IP3 pathway to induce Ca(2+) release, and this pathway is identical to the one we recently proposed for a sole effect of NO and the two gaseous molecules synergistically function to regulate Ca(2+) homeostasis. Hydrogen Sulfide 83-86 protein kinase cGMP-dependent 1 Homo sapiens 194-197 24422501-4 2014 Further investigations showed that H2S sustained higher activities of guaiacol peroxidase, ascorbate peroxidase, catalase, and glutathione reductase and lower activities of lipoxygenase, polyphenol oxidase, phenylalanine ammonia lyase, and protease than those of water control. Hydrogen Sulfide 35-38 glutathione-disulfide reductase Homo sapiens 127-148 23852531-0 2014 Hydrogen sulfide induces heme oxygenase-1 in human kidney cells. Hydrogen Sulfide 0-16 heme oxygenase 1 Homo sapiens 25-41 23852531-2 2014 The aim of this study was to investigate if H2S effects the expression of the antioxidant enzyme heme oxygenase-1 (HO-1) in human kidney cells. Hydrogen Sulfide 44-47 heme oxygenase 1 Homo sapiens 97-113 23852531-2 2014 The aim of this study was to investigate if H2S effects the expression of the antioxidant enzyme heme oxygenase-1 (HO-1) in human kidney cells. Hydrogen Sulfide 44-47 heme oxygenase 1 Homo sapiens 115-119 23852531-5 2014 There was a significant increase in HO-1 expression after treatment with the H2S donors in both mesangial and podocyte cells. Hydrogen Sulfide 77-80 heme oxygenase 1 Homo sapiens 36-40 23852531-6 2014 These results suggest that H2S has a role in the regulation of HO-1 expression, and the ability to upregulate this antioxidant enzyme maybe a potential mechanism by which H2S exerts its protective effects. Hydrogen Sulfide 27-30 heme oxygenase 1 Homo sapiens 63-67 23852531-6 2014 These results suggest that H2S has a role in the regulation of HO-1 expression, and the ability to upregulate this antioxidant enzyme maybe a potential mechanism by which H2S exerts its protective effects. Hydrogen Sulfide 171-174 heme oxygenase 1 Homo sapiens 63-67 23852134-2 2014 Cystathionine gamma-lyase (CSE) is a key enzyme in the trans-sulfuration pathway responsible for the production of endogenous H2S. Hydrogen Sulfide 126-129 cystathionine gamma-lyase Homo sapiens 0-25 23852134-2 2014 Cystathionine gamma-lyase (CSE) is a key enzyme in the trans-sulfuration pathway responsible for the production of endogenous H2S. Hydrogen Sulfide 126-129 cystathionine gamma-lyase Homo sapiens 27-30 23852134-7 2014 Therefore, the up-regulation of CSE expression during hypoxia may be useful for increasing the production and concentration of H2S in mammalian cells and indirectly protecting cells from hypoxia. Hydrogen Sulfide 127-130 cystathionine gamma-lyase Homo sapiens 32-35 24337227-0 2014 H2S inhibition of chemical hypoxia-induced proliferation of HPASMCs is mediated by the upregulation of COX-2/PGI2. Hydrogen Sulfide 0-3 mitochondrially encoded cytochrome c oxidase II Homo sapiens 103-108 24337227-10 2014 Importantly, the exposure of the cells to H(2)S suppressed the CoCl(2)-induced downregulation in COX-2 expression and PGI(2) secretion from the HPASMCs. Hydrogen Sulfide 42-47 mitochondrially encoded cytochrome c oxidase II Homo sapiens 97-102 24337227-11 2014 In conclusion, the results from the current study suggest that H(2)S enhances hypoxia-induced cell proliferation through the upregulation of COX-2/PGI(2), as opposed to ROS. Hydrogen Sulfide 63-68 mitochondrially encoded cytochrome c oxidase II Homo sapiens 141-146 24467431-5 2014 The active channels were functionally competent with demonstrated modulatory response to H2 S and transforming growth factor (TGF)-beta1 whereby H2S significantly inhibited the stimulatory effect of TGF-beta1 on current density of both BKCa and IK(ir). Hydrogen Sulfide 145-148 transforming growth factor beta 1 Homo sapiens 199-208 24467431-6 2014 Furthermore, H2S attenuated TGF-beta1-stimulated KCa1.1/Kv1.1 (encode BK(Ca)) and Kir2.1 (encode IK(ir)) expression in TCs. Hydrogen Sulfide 13-16 transforming growth factor beta 1 Homo sapiens 28-37 24467431-6 2014 Furthermore, H2S attenuated TGF-beta1-stimulated KCa1.1/Kv1.1 (encode BK(Ca)) and Kir2.1 (encode IK(ir)) expression in TCs. Hydrogen Sulfide 13-16 potassium calcium-activated channel subfamily M alpha 1 Homo sapiens 49-55 24467431-6 2014 Furthermore, H2S attenuated TGF-beta1-stimulated KCa1.1/Kv1.1 (encode BK(Ca)) and Kir2.1 (encode IK(ir)) expression in TCs. Hydrogen Sulfide 13-16 potassium voltage-gated channel subfamily A member 1 Homo sapiens 56-61 24467431-6 2014 Furthermore, H2S attenuated TGF-beta1-stimulated KCa1.1/Kv1.1 (encode BK(Ca)) and Kir2.1 (encode IK(ir)) expression in TCs. Hydrogen Sulfide 13-16 potassium inwardly rectifying channel subfamily J member 2 Homo sapiens 82-88 24412510-0 2014 Hydrogen sulfide improves spatial memory impairment and decreases production of Abeta in APP/PS1 transgenic mice. Hydrogen Sulfide 0-16 amyloid beta (A4) precursor protein Mus musculus 80-85 24412510-0 2014 Hydrogen sulfide improves spatial memory impairment and decreases production of Abeta in APP/PS1 transgenic mice. Hydrogen Sulfide 0-16 presenilin 1 Mus musculus 93-96 24412510-8 2014 administration of an H2S donor (NaHS) into APP/PS1 mice, application of exogenous H2S resulted in improved spatial learning and memory acquisition in APP/PS1 mice. Hydrogen Sulfide 21-24 amyloid beta precursor protein Homo sapiens 43-50 24412510-8 2014 administration of an H2S donor (NaHS) into APP/PS1 mice, application of exogenous H2S resulted in improved spatial learning and memory acquisition in APP/PS1 mice. Hydrogen Sulfide 21-24 presenilin 1 Mus musculus 47-50 24412510-8 2014 administration of an H2S donor (NaHS) into APP/PS1 mice, application of exogenous H2S resulted in improved spatial learning and memory acquisition in APP/PS1 mice. Hydrogen Sulfide 82-85 presenilin 1 Mus musculus 47-50 24412510-9 2014 H2S administration also led to significant decrease in extracellular levels of Abeta40 and Abeta42, the expression of BACE1 and PS1, and a significant increase of ADAM17 expression. Hydrogen Sulfide 0-3 beta-site APP cleaving enzyme 1 Mus musculus 118-123 24412510-9 2014 H2S administration also led to significant decrease in extracellular levels of Abeta40 and Abeta42, the expression of BACE1 and PS1, and a significant increase of ADAM17 expression. Hydrogen Sulfide 0-3 presenilin 1 Mus musculus 128-131 24412510-9 2014 H2S administration also led to significant decrease in extracellular levels of Abeta40 and Abeta42, the expression of BACE1 and PS1, and a significant increase of ADAM17 expression. Hydrogen Sulfide 0-3 a disintegrin and metallopeptidase domain 17 Mus musculus 163-169 24269241-10 2014 The findings reveal the therapeutic potential of H2S for BLM-induced pulmonary fibrosis in male rats, which were at least partly due to inhibition NF-kappaB p65 expression and regulation of Th1/Th2 balance. Hydrogen Sulfide 49-52 synaptotagmin 1 Rattus norvegicus 157-160 24475175-0 2014 Leptin-induced endothelium-dependent vasorelaxation of peripheral arteries in lean and obese rats: role of nitric oxide and hydrogen sulfide. Hydrogen Sulfide 124-140 leptin Rattus norvegicus 0-6 24475175-8 2014 The EDHF-dependent vasodilatory effect of leptin was blocked by either the inhibitor of cystathionine gamma-lyase, propargylglycine, or a hydrogen sulfide (H2S) scavenger, bismuth (III) subsalicylate. Hydrogen Sulfide 138-154 leptin Rattus norvegicus 42-48 24475175-8 2014 The EDHF-dependent vasodilatory effect of leptin was blocked by either the inhibitor of cystathionine gamma-lyase, propargylglycine, or a hydrogen sulfide (H2S) scavenger, bismuth (III) subsalicylate. Hydrogen Sulfide 156-159 leptin Rattus norvegicus 42-48 24475175-10 2014 The EDHF-dependent component of leptin-induced vasorelaxation is mediated, at least partially, by H2S. Hydrogen Sulfide 98-101 leptin Rattus norvegicus 32-38 24466346-5 2014 Immunoblotting results showed that H2S pretreatment reversed TBI-induced cleavage of caspase-3 and decline of Bcl-2, suppressed LC3-II, Beclin-1 and Vps34 activation and maintained p62 level in injured cortex and hippocampus post TBI. Hydrogen Sulfide 35-38 caspase 3 Mus musculus 85-94 24466346-5 2014 Immunoblotting results showed that H2S pretreatment reversed TBI-induced cleavage of caspase-3 and decline of Bcl-2, suppressed LC3-II, Beclin-1 and Vps34 activation and maintained p62 level in injured cortex and hippocampus post TBI. Hydrogen Sulfide 35-38 B cell leukemia/lymphoma 2 Mus musculus 110-115 24466346-5 2014 Immunoblotting results showed that H2S pretreatment reversed TBI-induced cleavage of caspase-3 and decline of Bcl-2, suppressed LC3-II, Beclin-1 and Vps34 activation and maintained p62 level in injured cortex and hippocampus post TBI. Hydrogen Sulfide 35-38 beclin 1, autophagy related Mus musculus 136-144 24466346-5 2014 Immunoblotting results showed that H2S pretreatment reversed TBI-induced cleavage of caspase-3 and decline of Bcl-2, suppressed LC3-II, Beclin-1 and Vps34 activation and maintained p62 level in injured cortex and hippocampus post TBI. Hydrogen Sulfide 35-38 phosphatidylinositol 3-kinase catalytic subunit type 3 Mus musculus 149-154 24466346-5 2014 Immunoblotting results showed that H2S pretreatment reversed TBI-induced cleavage of caspase-3 and decline of Bcl-2, suppressed LC3-II, Beclin-1 and Vps34 activation and maintained p62 level in injured cortex and hippocampus post TBI. Hydrogen Sulfide 35-38 nucleoporin 62 Mus musculus 181-184 24270013-0 2014 Differential susceptibility to hydrogen sulfide-induced apoptosis between PHLDA1-overexpressing oral cancer cell lines and oral keratinocytes: role of PHLDA1 as an apoptosis suppressor. Hydrogen Sulfide 31-47 pleckstrin homology like domain family A member 1 Homo sapiens 74-80 24270013-7 2014 H2S exposure in Ca9-22 cells, but not keratinocytes, enhanced the expression of pleckstrin homology-like domain, family A, member 1 (PHLDA1), which was identified through a differential display method. Hydrogen Sulfide 0-3 pleckstrin homology like domain family A member 1 Homo sapiens 80-131 24270013-7 2014 H2S exposure in Ca9-22 cells, but not keratinocytes, enhanced the expression of pleckstrin homology-like domain, family A, member 1 (PHLDA1), which was identified through a differential display method. Hydrogen Sulfide 0-3 pleckstrin homology like domain family A member 1 Homo sapiens 133-139 24222380-1 2014 A general multiscale simulation procedure is proposed to accurately predict the uptakes of pollution gases such as CO2, SO2, H2S, and CO in one of the most investigated porous organic cages CC3 by using a sophisticated force field vdW3 fitted by double hybrid functional (B2PLYP) with a dispersion correction (D3) separately for gas-gas and CC3-gas interactions. Hydrogen Sulfide 125-128 C-C motif chemokine ligand 14 Homo sapiens 190-193 24331419-0 2014 Hydrogen sulfide delays GA-triggered programmed cell death in wheat aleurone layers by the modulation of glutathione homeostasis and heme oxygenase-1 expression. Hydrogen Sulfide 0-16 heme oxygenase 1, chloroplastic Triticum aestivum 133-149 24331419-11 2014 Together, the above results clearly suggested that the H2S-delayed PCD in GA-treated wheat aleurone cells was associated with the modulation of GSH homeostasis and HO-1 gene expression. Hydrogen Sulfide 55-58 heme oxygenase 1, chloroplastic Triticum aestivum 164-168 24491890-1 2014 gamma-Cystathionase (CTH, EC: 4.4.1.1), an enzyme widely distributed in the world of prokaryotic and eukaryotic organisms, catalyzes the formation and transformations of sulfane sulfur-containing compounds and plays a pivotal role in the L-cysteine desulfuration pathway. Hydrogen Sulfide 170-177 cystathionine gamma-lyase Homo sapiens 0-19 24491890-1 2014 gamma-Cystathionase (CTH, EC: 4.4.1.1), an enzyme widely distributed in the world of prokaryotic and eukaryotic organisms, catalyzes the formation and transformations of sulfane sulfur-containing compounds and plays a pivotal role in the L-cysteine desulfuration pathway. Hydrogen Sulfide 170-177 cystathionine gamma-lyase Homo sapiens 21-24 24491890-6 2014 A decrease of the expression of CTH entails a drop in the level of cysteine , glutathione (GSH), taurine and hydrogen sulfide (H2S) in the cells and, more importantly, leads to cystathioninuria. Hydrogen Sulfide 109-125 cystathionine gamma-lyase Homo sapiens 32-35 24491890-6 2014 A decrease of the expression of CTH entails a drop in the level of cysteine , glutathione (GSH), taurine and hydrogen sulfide (H2S) in the cells and, more importantly, leads to cystathioninuria. Hydrogen Sulfide 127-130 cystathionine gamma-lyase Homo sapiens 32-35 24491890-7 2014 H2S, endogenously formed by CTH, affects the vasodilation and regulation of blood pressure. Hydrogen Sulfide 0-3 cystathionine gamma-lyase Homo sapiens 28-31 24491890-8 2014 CTH knockout mice have decreased levels of H2S, hypertension, and reduced capacity for vascular endothelium relaxation. Hydrogen Sulfide 43-46 cystathionine gamma-lyase Homo sapiens 0-3 24491890-9 2014 Overexpression of the gene encoding CTH in the cells leads to increased production of H2S. Hydrogen Sulfide 86-89 cystathionine gamma-lyase Homo sapiens 36-39 24491890-10 2014 H2S plays a role in protection of neurons against oxidative stress, and stimulates an increase in gamma-glutamylcysteine synthetase and thereby an increase in the level of GSH. Hydrogen Sulfide 0-3 glutamate-cysteine ligase catalytic subunit Homo sapiens 98-131 24416422-3 2014 In this study, we have identified human cystathionine ss-synthase (CBS) as a new player in nitrite reduction with implications for the nitrite-dependent control of H2S production. Hydrogen Sulfide 164-167 cystathionine beta-synthase Homo sapiens 67-70 24416422-6 2014 Formation of Fe(II)-NO CBS via its nitrite reductase activity inhibits CBS, providing an avenue for regulating biogenesis of H2S and cysteine, the limiting reagent for synthesis of glutathione, a major antioxidant. Hydrogen Sulfide 125-128 cystathionine beta-synthase Homo sapiens 23-26 24416422-6 2014 Formation of Fe(II)-NO CBS via its nitrite reductase activity inhibits CBS, providing an avenue for regulating biogenesis of H2S and cysteine, the limiting reagent for synthesis of glutathione, a major antioxidant. Hydrogen Sulfide 125-128 cystathionine beta-synthase Homo sapiens 71-74 25215294-8 2014 These findings suggest that siRNA reduces the inflammatory effects of hydrogen sulfide through the ERK-NF-kappaB signalling pathway and hydrogen sulfide plays its inflammatory role through ERK-NF-kappaB pathway in these cells. Hydrogen Sulfide 70-86 mitogen-activated protein kinase 1 Mus musculus 99-102 25215294-8 2014 These findings suggest that siRNA reduces the inflammatory effects of hydrogen sulfide through the ERK-NF-kappaB signalling pathway and hydrogen sulfide plays its inflammatory role through ERK-NF-kappaB pathway in these cells. Hydrogen Sulfide 70-86 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 103-112 25215294-8 2014 These findings suggest that siRNA reduces the inflammatory effects of hydrogen sulfide through the ERK-NF-kappaB signalling pathway and hydrogen sulfide plays its inflammatory role through ERK-NF-kappaB pathway in these cells. Hydrogen Sulfide 70-86 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 193-202 25215294-8 2014 These findings suggest that siRNA reduces the inflammatory effects of hydrogen sulfide through the ERK-NF-kappaB signalling pathway and hydrogen sulfide plays its inflammatory role through ERK-NF-kappaB pathway in these cells. Hydrogen Sulfide 136-152 mitogen-activated protein kinase 1 Mus musculus 189-192 25215294-8 2014 These findings suggest that siRNA reduces the inflammatory effects of hydrogen sulfide through the ERK-NF-kappaB signalling pathway and hydrogen sulfide plays its inflammatory role through ERK-NF-kappaB pathway in these cells. Hydrogen Sulfide 136-152 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 193-202 24790991-3 2014 Cocktail method was used to evaluate the influences of acute H2S poisoning on the activities of cytochrome P450 isoforms CYP2B6, CYP2D6, CYP3A4, CYP1A2, CYP2C19, and CYP2C9, which were reflected by the changes of pharmacokinetic parameters of six specific probe drugs, bupropion, metoprolol, midazolam, phenacetin, omeprazole, and tolbutamide, respectively. Hydrogen Sulfide 61-64 cytochrome P450, family 2, subfamily b, polypeptide 3 Rattus norvegicus 121-127 24790991-3 2014 Cocktail method was used to evaluate the influences of acute H2S poisoning on the activities of cytochrome P450 isoforms CYP2B6, CYP2D6, CYP3A4, CYP1A2, CYP2C19, and CYP2C9, which were reflected by the changes of pharmacokinetic parameters of six specific probe drugs, bupropion, metoprolol, midazolam, phenacetin, omeprazole, and tolbutamide, respectively. Hydrogen Sulfide 61-64 cytochrome P450, family 2, subfamily d, polypeptide 4 Rattus norvegicus 129-135 24790991-3 2014 Cocktail method was used to evaluate the influences of acute H2S poisoning on the activities of cytochrome P450 isoforms CYP2B6, CYP2D6, CYP3A4, CYP1A2, CYP2C19, and CYP2C9, which were reflected by the changes of pharmacokinetic parameters of six specific probe drugs, bupropion, metoprolol, midazolam, phenacetin, omeprazole, and tolbutamide, respectively. Hydrogen Sulfide 61-64 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 145-151 25382321-12 2014 Moreover, changes of CSE protein contents of PBMCs were consistent with serum H2S contents, and there were significant correlation between H2S and certain cytokines based on stepwise regression analysis. Hydrogen Sulfide 78-81 cystathionine gamma-lyase Homo sapiens 21-24 25382321-12 2014 Moreover, changes of CSE protein contents of PBMCs were consistent with serum H2S contents, and there were significant correlation between H2S and certain cytokines based on stepwise regression analysis. Hydrogen Sulfide 139-142 cystathionine gamma-lyase Homo sapiens 21-24 25382321-13 2014 Furthermore, compared with those of PBMCs group, in vitro study indicated that Jurkat cells of H2S group expressed IFN-gamma, IL-10, IL-4 and IL-2 protein increased obviously (P < 0.05), while IL-4, IL-2 and CSE expression of PPG group decreased markedly (P < 0.05). Hydrogen Sulfide 95-98 interferon gamma Homo sapiens 115-124 25382321-13 2014 Furthermore, compared with those of PBMCs group, in vitro study indicated that Jurkat cells of H2S group expressed IFN-gamma, IL-10, IL-4 and IL-2 protein increased obviously (P < 0.05), while IL-4, IL-2 and CSE expression of PPG group decreased markedly (P < 0.05). Hydrogen Sulfide 95-98 interleukin 10 Homo sapiens 126-131 25382321-13 2014 Furthermore, compared with those of PBMCs group, in vitro study indicated that Jurkat cells of H2S group expressed IFN-gamma, IL-10, IL-4 and IL-2 protein increased obviously (P < 0.05), while IL-4, IL-2 and CSE expression of PPG group decreased markedly (P < 0.05). Hydrogen Sulfide 95-98 interleukin 4 Homo sapiens 133-137 25382321-13 2014 Furthermore, compared with those of PBMCs group, in vitro study indicated that Jurkat cells of H2S group expressed IFN-gamma, IL-10, IL-4 and IL-2 protein increased obviously (P < 0.05), while IL-4, IL-2 and CSE expression of PPG group decreased markedly (P < 0.05). Hydrogen Sulfide 95-98 interleukin 2 Homo sapiens 142-146 25382321-13 2014 Furthermore, compared with those of PBMCs group, in vitro study indicated that Jurkat cells of H2S group expressed IFN-gamma, IL-10, IL-4 and IL-2 protein increased obviously (P < 0.05), while IL-4, IL-2 and CSE expression of PPG group decreased markedly (P < 0.05). Hydrogen Sulfide 95-98 interleukin 4 Homo sapiens 196-200 25382321-13 2014 Furthermore, compared with those of PBMCs group, in vitro study indicated that Jurkat cells of H2S group expressed IFN-gamma, IL-10, IL-4 and IL-2 protein increased obviously (P < 0.05), while IL-4, IL-2 and CSE expression of PPG group decreased markedly (P < 0.05). Hydrogen Sulfide 95-98 interleukin 2 Homo sapiens 202-206 25382321-13 2014 Furthermore, compared with those of PBMCs group, in vitro study indicated that Jurkat cells of H2S group expressed IFN-gamma, IL-10, IL-4 and IL-2 protein increased obviously (P < 0.05), while IL-4, IL-2 and CSE expression of PPG group decreased markedly (P < 0.05). Hydrogen Sulfide 95-98 cystathionine gamma-lyase Homo sapiens 211-214 24516168-1 2014 Previous studies have demonstrated that hydrogen sulfide (H2S) protects against multiple cardiovascular disease states in a similar manner as nitric oxide (NO). Hydrogen Sulfide 40-56 histocompatibility 2, S region (C4, Slp, Bf, C2) Mus musculus 58-61 23758073-3 2014 Here, we examined the role of cystathionine gamma-lyase (CSE, an enzyme produces H2S) in ALF induced by D-Galactosamine (GalN) and lipopolysaccharide (LPS). Hydrogen Sulfide 81-84 cystathionase (cystathionine gamma-lyase) Mus musculus 30-55 23758073-3 2014 Here, we examined the role of cystathionine gamma-lyase (CSE, an enzyme produces H2S) in ALF induced by D-Galactosamine (GalN) and lipopolysaccharide (LPS). Hydrogen Sulfide 81-84 cystathionase (cystathionine gamma-lyase) Mus musculus 57-60 23682813-8 2014 Pretreatment with NaHS or stimulation of endogenous H2S production also significantly suppressed opioid withdrawal-induced ERK1/2 activation in mice striatum or SH-SY5Y cells. Hydrogen Sulfide 52-55 mitogen-activated protein kinase 3 Mus musculus 123-129 25215294-0 2014 Inhibition of hydrogen sulfide production by gene silencing attenuates inflammatory activity by downregulation of NF-kappaB and MAP kinase activity in LPS-activated RAW 264.7 cells. Hydrogen Sulfide 14-30 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 114-123 25215294-1 2014 Hydrogen sulfide is an endogenous inflammatory mediator produced by the activity of cystathionine gamma-lyase (CSE) in macrophages. Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 84-109 25215294-1 2014 Hydrogen sulfide is an endogenous inflammatory mediator produced by the activity of cystathionine gamma-lyase (CSE) in macrophages. Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 111-114 24790991-8 2014 Acute H2S poisoning could inhibit the activity of CYP2B6, CYP2D6, CYP1A2, and CYP2C9 in rats. Hydrogen Sulfide 6-9 cytochrome P450, family 2, subfamily b, polypeptide 3 Rattus norvegicus 50-56 24790991-8 2014 Acute H2S poisoning could inhibit the activity of CYP2B6, CYP2D6, CYP1A2, and CYP2C9 in rats. Hydrogen Sulfide 6-9 cytochrome P450, family 2, subfamily d, polypeptide 4 Rattus norvegicus 58-64 24790991-8 2014 Acute H2S poisoning could inhibit the activity of CYP2B6, CYP2D6, CYP1A2, and CYP2C9 in rats. Hydrogen Sulfide 6-9 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 66-72 25531647-5 2014 Plasma H2S was positively correlated with plasma TGF-beta1, and negatively correlated with MMP-12 in CHD/DN patients. Hydrogen Sulfide 7-10 transforming growth factor beta 1 Homo sapiens 49-58 25531647-5 2014 Plasma H2S was positively correlated with plasma TGF-beta1, and negatively correlated with MMP-12 in CHD/DN patients. Hydrogen Sulfide 7-10 matrix metallopeptidase 12 Homo sapiens 91-97 25531647-9 2014 CONCLUSIONS: These findings suggest possible linkage between H2S metabolism and TGF-beta/Smad signaling pathway modulation abnormalities that may contribute to the development of UAAS in CHD/DN patients. Hydrogen Sulfide 61-64 transforming growth factor beta 1 Homo sapiens 80-88 25335229-1 2014 In the study we investigated the effect of blockade cystathionine-gamma -lyase (CSE), an enzyme of hydrogen sulfide (H2S) (de novo) synthesis on the endothelium-dependent relaxation of aortic smooth muscle (SM) in old rats. Hydrogen Sulfide 99-115 cystathionine gamma-lyase Rattus norvegicus 52-78 25050128-2 2014 TFR (11~2700 mg/L) evoked dose-dependent vasodilation and hyperpolarization in MCA of both sham and CIR that were partially inhibited by 30 muM N-nitro-L-arginine-methyl-ester and 10 muM indomethacin and further attenuated by endogenous H2S synthese-CSE inhibitor PPG (100 muM) or Ca(2+)-activated potassium channel (Kca) inhibitor TEA (1 mM). Hydrogen Sulfide 237-240 transferrin receptor Rattus norvegicus 0-3 25050128-5 2014 We conclude that, in MCA of CIR rats, TFR induces non-NO and non-PGI2-mediated effects of vasodilatation and hyperpolarization involving Kca and increases CSE mRNA expression level in endothelial cells and H2S content in the cerebrum. Hydrogen Sulfide 206-209 transferrin receptor Rattus norvegicus 38-41 25050128-6 2014 These findings suggest that the response induced by TFR is potentially related to endothelium-derived hyperpolarizing factor mediated by the endogenous H2S and promote the use of TFR in protection of brain from ischemia-reperfusion injury. Hydrogen Sulfide 152-155 transferrin receptor Rattus norvegicus 52-55 25335229-1 2014 In the study we investigated the effect of blockade cystathionine-gamma -lyase (CSE), an enzyme of hydrogen sulfide (H2S) (de novo) synthesis on the endothelium-dependent relaxation of aortic smooth muscle (SM) in old rats. Hydrogen Sulfide 99-115 cystathionine gamma-lyase Rattus norvegicus 80-83 25335229-1 2014 In the study we investigated the effect of blockade cystathionine-gamma -lyase (CSE), an enzyme of hydrogen sulfide (H2S) (de novo) synthesis on the endothelium-dependent relaxation of aortic smooth muscle (SM) in old rats. Hydrogen Sulfide 117-120 cystathionine gamma-lyase Rattus norvegicus 52-78 25335229-1 2014 In the study we investigated the effect of blockade cystathionine-gamma -lyase (CSE), an enzyme of hydrogen sulfide (H2S) (de novo) synthesis on the endothelium-dependent relaxation of aortic smooth muscle (SM) in old rats. Hydrogen Sulfide 117-120 cystathionine gamma-lyase Rattus norvegicus 80-83 24961969-9 2014 TRPA1 also detects other gaseous molecules, such as hydrogen sulfide (H2S) and carbon dioxide (CO2). Hydrogen Sulfide 52-68 transient receptor potential cation channel subfamily A member 1 Homo sapiens 0-5 24961969-9 2014 TRPA1 also detects other gaseous molecules, such as hydrogen sulfide (H2S) and carbon dioxide (CO2). Hydrogen Sulfide 70-73 transient receptor potential cation channel subfamily A member 1 Homo sapiens 0-5 24117897-6 2014 Treatment with H2 S prevented MCD-diet-induced NASH, as evidenced by hematoxylin and eosin staining, reduced apoptosis and activities of alanine aminotransferase and aspartate aminotransferase, and attenuated hepatic fat accumulation in rats. Hydrogen Sulfide 15-19 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 166-192 24966472-9 2014 CONCLUSION: Our results indicate that H2S attenuates hepatic I/R injury, at least in part, by regulating apoptosis through inhibiting JNK1 signaling. Hydrogen Sulfide 38-41 mitogen-activated protein kinase 8 Homo sapiens 134-138 25005183-9 2014 Homocysteine is a precursor of hydrogen sulfide (H2S) which is formed by transulfuration process catalyzed by the enzymes, cystathionine beta-synthase and cystathionine gamma-lyase. Hydrogen Sulfide 31-47 cystathionine beta-synthase Homo sapiens 123-150 25005183-9 2014 Homocysteine is a precursor of hydrogen sulfide (H2S) which is formed by transulfuration process catalyzed by the enzymes, cystathionine beta-synthase and cystathionine gamma-lyase. Hydrogen Sulfide 31-47 cystathionine gamma-lyase Homo sapiens 155-180 25005183-9 2014 Homocysteine is a precursor of hydrogen sulfide (H2S) which is formed by transulfuration process catalyzed by the enzymes, cystathionine beta-synthase and cystathionine gamma-lyase. Hydrogen Sulfide 49-52 cystathionine beta-synthase Homo sapiens 123-150 25005183-9 2014 Homocysteine is a precursor of hydrogen sulfide (H2S) which is formed by transulfuration process catalyzed by the enzymes, cystathionine beta-synthase and cystathionine gamma-lyase. Hydrogen Sulfide 49-52 cystathionine gamma-lyase Homo sapiens 155-180 24863338-15 2014 H2S exhibits a potent anti-apoptotic ability by attenuating oxidative stress and inhibiting caspase-3 activation, which in turn restores peritoneal injury. Hydrogen Sulfide 0-3 caspase 3 Rattus norvegicus 92-101 24239876-3 2014 The endogenous level of H2S in the brain is significantly higher than that in peripheral tissues, and is mainly formed by cystathionine beta-synthase (CBS) in astrocytes and released in response to neuronal excitation. Hydrogen Sulfide 24-27 cystathionine beta-synthase Homo sapiens 122-149 25452233-4 2014 We also found that hydrogen sulfide-related reactive sulfur species (RSS) function as potent nucleophiles to eliminate electrophilic modification of H-Ras and suppress the onset of chronic heart failure after myocardial infarction. Hydrogen Sulfide 19-35 HRas proto-oncogene, GTPase Homo sapiens 149-154 25452234-1 2014 Hydrogen sulfide (H2S), the third known gaseous transmitter following nitric oxide and carbon monoxide, is generated by multiple enzymes including cystathionine-gamma-lyase (CSE) in vivo. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Rattus norvegicus 147-172 25452234-1 2014 Hydrogen sulfide (H2S), the third known gaseous transmitter following nitric oxide and carbon monoxide, is generated by multiple enzymes including cystathionine-gamma-lyase (CSE) in vivo. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Rattus norvegicus 174-177 25452234-1 2014 Hydrogen sulfide (H2S), the third known gaseous transmitter following nitric oxide and carbon monoxide, is generated by multiple enzymes including cystathionine-gamma-lyase (CSE) in vivo. Hydrogen Sulfide 18-21 cystathionine gamma-lyase Rattus norvegicus 147-172 24527529-8 2014 CONCLUSION: Hypertension inhibits endogenous H2S synthesis by suppressing the expressions of CSE and CBS in the corpus cavernosum, which might be related with hypertension-induced reduction of erectile function. Hydrogen Sulfide 45-48 cystathionine gamma-lyase Rattus norvegicus 93-96 24527529-8 2014 CONCLUSION: Hypertension inhibits endogenous H2S synthesis by suppressing the expressions of CSE and CBS in the corpus cavernosum, which might be related with hypertension-induced reduction of erectile function. Hydrogen Sulfide 45-48 cystathionine beta synthase Rattus norvegicus 101-104 25452234-1 2014 Hydrogen sulfide (H2S), the third known gaseous transmitter following nitric oxide and carbon monoxide, is generated by multiple enzymes including cystathionine-gamma-lyase (CSE) in vivo. Hydrogen Sulfide 18-21 cystathionine gamma-lyase Rattus norvegicus 174-177 25452234-6 2014 The pronociceptive effect of NaHS was abolished by inhibitors or knockdown of Cav3.2 and by an inhibitor of TRPA1, another target molecule of H2S. Hydrogen Sulfide 142-145 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 108-113 25452234-11 2014 Taken together, these findings suggest that inhibitors of the CSE/H2S/Cav3.2 or TRPA1 pathways might be useful for the treatment of colonic pain diseases such as irritable bowel syndrome, while H2S donors or Cav3.2 activators might be useful for the treatment of inflammatory bowel disease including Crohn"s disease. Hydrogen Sulfide 66-69 cystathionine gamma-lyase Rattus norvegicus 62-65 25452234-11 2014 Taken together, these findings suggest that inhibitors of the CSE/H2S/Cav3.2 or TRPA1 pathways might be useful for the treatment of colonic pain diseases such as irritable bowel syndrome, while H2S donors or Cav3.2 activators might be useful for the treatment of inflammatory bowel disease including Crohn"s disease. Hydrogen Sulfide 194-197 cystathionine gamma-lyase Rattus norvegicus 62-65 24336065-0 2013 The effects of H2S on the activities of CYP2B6, CYP2D6, CYP3A4, CYP2C19 and CYP2C9 in vivo in rat. Hydrogen Sulfide 15-18 cytochrome P450, family 2, subfamily b, polypeptide 3 Rattus norvegicus 40-46 24213681-2 2013 Screening of 21,599 agents identified several potent inhibitors of cystathionine beta-synthase and cystathionine gamma-lyase, the two key enzymes generating H2S in mammals, with IC50 values in the low two-digit micromolar range. Hydrogen Sulfide 157-160 cystathionine beta-synthase Homo sapiens 67-94 24213681-2 2013 Screening of 21,599 agents identified several potent inhibitors of cystathionine beta-synthase and cystathionine gamma-lyase, the two key enzymes generating H2S in mammals, with IC50 values in the low two-digit micromolar range. Hydrogen Sulfide 157-160 cystathionine gamma-lyase Homo sapiens 99-124 24246677-1 2013 Chronic exposure to high glucose induces the expression of cystathionine gamma-lyase (CSE), a hydrogen sulfide-producing enzyme, in pancreatic beta-cells, thereby suppressing apoptosis. Hydrogen Sulfide 94-110 cystathionase (cystathionine gamma-lyase) Mus musculus 59-84 24246677-1 2013 Chronic exposure to high glucose induces the expression of cystathionine gamma-lyase (CSE), a hydrogen sulfide-producing enzyme, in pancreatic beta-cells, thereby suppressing apoptosis. Hydrogen Sulfide 94-110 cystathionase (cystathionine gamma-lyase) Mus musculus 86-89 24246677-8 2013 Administration of NaHS, a hydrogen sulfide donor, reduced TBP-2 gene levels in isolated islets from CSE-KO mice. Hydrogen Sulfide 26-42 TATA-box binding protein like 2 Homo sapiens 58-63 24246677-10 2013 These results provide evidence that CSE-produced hydrogen sulfide protects beta-cells from glucotoxicity via regulation of TBP-2 expression levels and thus prevents the onset/development of type 2 diabetes. Hydrogen Sulfide 49-65 cystathionase (cystathionine gamma-lyase) Mus musculus 36-39 24246677-10 2013 These results provide evidence that CSE-produced hydrogen sulfide protects beta-cells from glucotoxicity via regulation of TBP-2 expression levels and thus prevents the onset/development of type 2 diabetes. Hydrogen Sulfide 49-65 thioredoxin interacting protein Mus musculus 123-128 24336065-0 2013 The effects of H2S on the activities of CYP2B6, CYP2D6, CYP3A4, CYP2C19 and CYP2C9 in vivo in rat. Hydrogen Sulfide 15-18 cytochrome P450, family 2, subfamily d, polypeptide 4 Rattus norvegicus 48-54 24349344-6 2013 H2S production rate in gallbladder tissue from each group was determined; immunohistochemistry and western blotting were used to determine expression levels of the H2S-producing enzymes cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) in gallbladder. Hydrogen Sulfide 164-167 cystathionine beta-synthase Cavia porcellus 186-213 24349344-6 2013 H2S production rate in gallbladder tissue from each group was determined; immunohistochemistry and western blotting were used to determine expression levels of the H2S-producing enzymes cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) in gallbladder. Hydrogen Sulfide 164-167 cystathionine beta-synthase Cavia porcellus 215-218 24140888-0 2013 Cardioprotection of H2S by downregulating iNOS and upregulating HO-1 expression in mice with CVB3-induced myocarditis. Hydrogen Sulfide 20-23 nitric oxide synthase 2, inducible Mus musculus 42-46 24140888-0 2013 Cardioprotection of H2S by downregulating iNOS and upregulating HO-1 expression in mice with CVB3-induced myocarditis. Hydrogen Sulfide 20-23 heme oxygenase 1 Mus musculus 64-68 24140888-12 2013 SIGNIFICANCE: Our data support that H2S can inhibit iNOS overexpression and induce HO-1 expression, both of which contribute to the cardioprotection of H2S in CVB3-induced mice myocarditis. Hydrogen Sulfide 36-39 nitric oxide synthase 2, inducible Mus musculus 52-56 24140888-12 2013 SIGNIFICANCE: Our data support that H2S can inhibit iNOS overexpression and induce HO-1 expression, both of which contribute to the cardioprotection of H2S in CVB3-induced mice myocarditis. Hydrogen Sulfide 36-39 heme oxygenase 1 Mus musculus 83-87 24140888-12 2013 SIGNIFICANCE: Our data support that H2S can inhibit iNOS overexpression and induce HO-1 expression, both of which contribute to the cardioprotection of H2S in CVB3-induced mice myocarditis. Hydrogen Sulfide 152-155 heme oxygenase 1 Mus musculus 83-87 23808525-6 2013 One of the mechanisms of H(2)S signalling discussed here is S-sulfhydration of catalytic cysteine residue of PTP1B, a negative regulator of insulin and leptin signalling. Hydrogen Sulfide 25-30 protein tyrosine phosphatase non-receptor type 1 Homo sapiens 109-114 23808525-6 2013 One of the mechanisms of H(2)S signalling discussed here is S-sulfhydration of catalytic cysteine residue of PTP1B, a negative regulator of insulin and leptin signalling. Hydrogen Sulfide 25-30 insulin Homo sapiens 140-147 23846016-1 2013 Hydrogen sulfide (H2S) produced by cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) in the transsulfuration pathway of homocysteine plays a number of pathophysiological roles. Hydrogen Sulfide 0-16 cystathionine beta-synthase Mus musculus 35-62 24200305-0 2013 Effect of hydrogen sulphide on the expression of osteoprotegerin and receptor activator of NF-kappaB ligand in human periodontal ligament cells induced by tension-force stimulation. Hydrogen Sulfide 10-27 TNF receptor superfamily member 11b Homo sapiens 49-64 24200305-9 2013 The expression of OPG was increased in a concentration-dependent manner by H2S treatment. Hydrogen Sulfide 75-78 TNF receptor superfamily member 11b Homo sapiens 18-21 24200305-10 2013 Importantly, the relative OPG/RANKL expression ratio was significantly increased upon induction by H2S, an effect that was enhanced by tension-force application. Hydrogen Sulfide 99-102 TNF receptor superfamily member 11b Homo sapiens 26-29 24200305-10 2013 Importantly, the relative OPG/RANKL expression ratio was significantly increased upon induction by H2S, an effect that was enhanced by tension-force application. Hydrogen Sulfide 99-102 TNF superfamily member 11 Homo sapiens 30-35 24200305-11 2013 CONCLUSIONS: H2S could promote osteogenic differentiation by regulating the relative OPG/RANKL expression ratio of hPDLCs, which is enhanced by tension force. Hydrogen Sulfide 13-16 TNF receptor superfamily member 11b Homo sapiens 85-88 24200305-11 2013 CONCLUSIONS: H2S could promote osteogenic differentiation by regulating the relative OPG/RANKL expression ratio of hPDLCs, which is enhanced by tension force. Hydrogen Sulfide 13-16 TNF superfamily member 11 Homo sapiens 89-94 23846016-1 2013 Hydrogen sulfide (H2S) produced by cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) in the transsulfuration pathway of homocysteine plays a number of pathophysiological roles. Hydrogen Sulfide 0-16 cystathionine beta-synthase Mus musculus 64-67 23846016-1 2013 Hydrogen sulfide (H2S) produced by cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) in the transsulfuration pathway of homocysteine plays a number of pathophysiological roles. Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 73-98 23846016-1 2013 Hydrogen sulfide (H2S) produced by cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) in the transsulfuration pathway of homocysteine plays a number of pathophysiological roles. Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 100-103 23846016-1 2013 Hydrogen sulfide (H2S) produced by cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) in the transsulfuration pathway of homocysteine plays a number of pathophysiological roles. Hydrogen Sulfide 18-21 cystathionine beta-synthase Mus musculus 35-62 23846016-1 2013 Hydrogen sulfide (H2S) produced by cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) in the transsulfuration pathway of homocysteine plays a number of pathophysiological roles. Hydrogen Sulfide 18-21 cystathionine beta-synthase Mus musculus 64-67 23846016-1 2013 Hydrogen sulfide (H2S) produced by cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) in the transsulfuration pathway of homocysteine plays a number of pathophysiological roles. Hydrogen Sulfide 18-21 cystathionase (cystathionine gamma-lyase) Mus musculus 73-98 23846016-1 2013 Hydrogen sulfide (H2S) produced by cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) in the transsulfuration pathway of homocysteine plays a number of pathophysiological roles. Hydrogen Sulfide 18-21 cystathionase (cystathionine gamma-lyase) Mus musculus 100-103 23846016-6 2013 Treatment with sodium hydrogen sulfide (NaHS, a H2S producer) during UO reduced UO-induced oxidative stress with preservations of catalase, copper-zinc superoxide dismutase (CuZnSOD), and manganese superoxide dismutase (MnSOD) expression, and glutathione level. Hydrogen Sulfide 48-51 superoxide dismutase 2, mitochondrial Mus musculus 188-218 23846016-6 2013 Treatment with sodium hydrogen sulfide (NaHS, a H2S producer) during UO reduced UO-induced oxidative stress with preservations of catalase, copper-zinc superoxide dismutase (CuZnSOD), and manganese superoxide dismutase (MnSOD) expression, and glutathione level. Hydrogen Sulfide 48-51 superoxide dismutase 2, mitochondrial Mus musculus 220-225 24100226-2 2013 Interestingly, the genome of the roundworm Caenorhabditis elegans contains three expressed genes predicted to encode OAS-TL orthologs (cysl-1-cysl-3), and a related pseudogene (cysl-4); these genes play different roles in resistance to hypoxia, hydrogen sulfide and cyanide. Hydrogen Sulfide 245-261 Cysteine synthase Caenorhabditis elegans 177-183 24100226-7 2013 Based on the available evidences we propose the following model: CYSL-1 interacts with EGL-9 and activates HIF-1 that upregulates expression of genes detoxifying sulfide and cyanide, the CYSL-2 acts as a cyanoalanine synthase in the cyanide detoxification pathway and simultaneously produces hydrogen sulfide, while the role of CYSL-3 remains unclear although it exhibits sulfhydrylase activity in vitro. Hydrogen Sulfide 292-308 Cysteine synthase 1 Caenorhabditis elegans 65-71 24100226-7 2013 Based on the available evidences we propose the following model: CYSL-1 interacts with EGL-9 and activates HIF-1 that upregulates expression of genes detoxifying sulfide and cyanide, the CYSL-2 acts as a cyanoalanine synthase in the cyanide detoxification pathway and simultaneously produces hydrogen sulfide, while the role of CYSL-3 remains unclear although it exhibits sulfhydrylase activity in vitro. Hydrogen Sulfide 292-308 Bifunctional L-3-cyanoalanine synthase/cysteine synthase Caenorhabditis elegans 187-193 23770272-0 2013 Hydrogen sulfide prevents OGD/R-induced apoptosis via improving mitochondrial dysfunction and suppressing an ROS-mediated caspase-3 pathway in cortical neurons. Hydrogen Sulfide 0-16 caspase 3 Mus musculus 122-131 23770272-1 2013 Hydrogen sulfide (H2S), an endogenous gaseous mediator, has been shown to have protective effects against neuronal damage caused by brain ischemia. Hydrogen Sulfide 0-16 histocompatibility 2, S region (C4, Slp, Bf, C2) Mus musculus 18-21 24008358-2 2013 In this study, we sought to determine whether endogenously synthesized H2S via cystathionine-gamma-lyase (CSE) plays a pro- or anti-inflammatory role in caerulein-induced pancreatitis. Hydrogen Sulfide 71-74 cystathionase (cystathionine gamma-lyase) Mus musculus 79-104 23646934-4 2013 RESULTS: Using the lipid phosphatase PTEN as a model protein, we find that the "H2S donor" sodium hydrosulfide (NaHS) leads to very rapid reversible oxidation of the enzyme in vitro. Hydrogen Sulfide 80-83 phosphatase and tensin homolog Homo sapiens 37-41 23646934-6 2013 Polysulfide-mediated oxidation of PTEN was induced by all "H2S donors" tested, including sodium sulfide (Na2S), gaseous H2S, and morpholin-4-ium 4-methoxyphenyl(morpholino) phosphinodithioate (GYY4137). Hydrogen Sulfide 59-62 phosphatase and tensin homolog Homo sapiens 34-38 23646934-6 2013 Polysulfide-mediated oxidation of PTEN was induced by all "H2S donors" tested, including sodium sulfide (Na2S), gaseous H2S, and morpholin-4-ium 4-methoxyphenyl(morpholino) phosphinodithioate (GYY4137). Hydrogen Sulfide 120-123 phosphatase and tensin homolog Homo sapiens 34-38 23646934-7 2013 Moreover, we show that polysulfides formed in H2S solutions readily modify PTEN inside intact cells. Hydrogen Sulfide 46-49 phosphatase and tensin homolog Homo sapiens 75-79 24008358-2 2013 In this study, we sought to determine whether endogenously synthesized H2S via cystathionine-gamma-lyase (CSE) plays a pro- or anti-inflammatory role in caerulein-induced pancreatitis. Hydrogen Sulfide 71-74 cystathionase (cystathionine gamma-lyase) Mus musculus 106-109 24008358-8 2013 When comparing the two saline-treated control groups, we noted that the CSE KO mice showed significantly less pancreatic H2S-synthesizing activity relative to the WT mice. Hydrogen Sulfide 121-124 cystathionase (cystathionine gamma-lyase) Mus musculus 72-75 24008358-9 2013 These results indicate that endogenous H2S generated by CSE plays a key proinflammatory role via NF-kappaB activation in caerulein-induced pancreatitis, and its genetic deletion affords significant protection against acute pancreatitis and associated lung injury. Hydrogen Sulfide 39-42 cystathionase (cystathionine gamma-lyase) Mus musculus 56-59 24236104-6 2013 The in vitro effects of CBS silencing can be reversed by exogenous supplementation with the GSH and H2S producing chemical Na2S. Hydrogen Sulfide 100-103 cystathionine beta-synthase Homo sapiens 24-27 24093945-8 2013 On the basis of its high selectivity for H2S, we used CLSS-2 to detect enzymatically produced H2S from isolated cystathionine gamma-lyase (CSE) enzymes (p < 0.001) and also from C6 cells expressing CSE (p < 0.001). Hydrogen Sulfide 41-44 cystathionine gamma-lyase Homo sapiens 112-137 23418650-7 2013 Supplementation of exogenous H2S hyperpolarized vascular SMCs and endothelial cells from wide-type and CSE-KO mice. Hydrogen Sulfide 29-32 cystathionase (cystathionine gamma-lyase) Mus musculus 103-106 23418650-10 2013 The expression of SK2.3 but not IK3.1 channel in vascular tissues was increased by H2S and decreased by CSE inhibitor or CSE gene KO. Hydrogen Sulfide 83-86 skin antigen 2 Mus musculus 18-21 24093945-8 2013 On the basis of its high selectivity for H2S, we used CLSS-2 to detect enzymatically produced H2S from isolated cystathionine gamma-lyase (CSE) enzymes (p < 0.001) and also from C6 cells expressing CSE (p < 0.001). Hydrogen Sulfide 41-44 cystathionine gamma-lyase Homo sapiens 139-142 24093945-8 2013 On the basis of its high selectivity for H2S, we used CLSS-2 to detect enzymatically produced H2S from isolated cystathionine gamma-lyase (CSE) enzymes (p < 0.001) and also from C6 cells expressing CSE (p < 0.001). Hydrogen Sulfide 94-97 cystathionine gamma-lyase Homo sapiens 112-137 24093945-8 2013 On the basis of its high selectivity for H2S, we used CLSS-2 to detect enzymatically produced H2S from isolated cystathionine gamma-lyase (CSE) enzymes (p < 0.001) and also from C6 cells expressing CSE (p < 0.001). Hydrogen Sulfide 94-97 cystathionine gamma-lyase Homo sapiens 139-142 24093945-8 2013 On the basis of its high selectivity for H2S, we used CLSS-2 to detect enzymatically produced H2S from isolated cystathionine gamma-lyase (CSE) enzymes (p < 0.001) and also from C6 cells expressing CSE (p < 0.001). Hydrogen Sulfide 94-97 cystathionine gamma-lyase Homo sapiens 201-204 24093945-9 2013 CLSS-2 can readily differentiate between H2S production in active CSE and CSE inhibited with beta-cyanoalanine (BCA) in both isolated CSE enzymes (p < 0.005) and in C6 cells (p < 0.005). Hydrogen Sulfide 41-44 cystathionine gamma-lyase Homo sapiens 66-69 23864610-0 2013 Transport of H2S and HS(-) across the human red blood cell membrane: rapid H2S diffusion and AE1-mediated Cl(-)/HS(-) exchange. Hydrogen Sulfide 13-16 solute carrier family 4 member 1 (Diego blood group) Homo sapiens 93-96 24012591-0 2013 Hydrogen sulfide-mediated stimulation of mitochondrial electron transport involves inhibition of the mitochondrial phosphodiesterase 2A, elevation of cAMP and activation of protein kinase A. Hydrogen Sulfide 0-16 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 173-189 24012591-3 2013 Other lines of recent studies demonstrated that one of the biological actions of H2S involves inhibition of cAMP and cGMP phosphodiesterases (PDEs). Hydrogen Sulfide 81-84 phosphodiesterase 2A Rattus norvegicus 142-146 23872072-0 2013 Dysregulation of cystathionine gamma-lyase (CSE)/hydrogen sulfide pathway contributes to ox-LDL-induced inflammation in macrophage. Hydrogen Sulfide 49-65 cystathionine gamma-lyase Homo sapiens 17-42 24117256-1 2013 Hydrogen sulfide (H2S) is synthesized from L-cysteine by cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE), and is enzymatically metabolized in mitochondria by sulfide:quinone oxidoreductase (SQR). Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 57-84 24117256-1 2013 Hydrogen sulfide (H2S) is synthesized from L-cysteine by cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE), and is enzymatically metabolized in mitochondria by sulfide:quinone oxidoreductase (SQR). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 94-119 24117256-1 2013 Hydrogen sulfide (H2S) is synthesized from L-cysteine by cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE), and is enzymatically metabolized in mitochondria by sulfide:quinone oxidoreductase (SQR). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 121-124 24117256-1 2013 Hydrogen sulfide (H2S) is synthesized from L-cysteine by cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE), and is enzymatically metabolized in mitochondria by sulfide:quinone oxidoreductase (SQR). Hydrogen Sulfide 0-16 crystallin zeta Homo sapiens 187-209 24117256-1 2013 Hydrogen sulfide (H2S) is synthesized from L-cysteine by cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE), and is enzymatically metabolized in mitochondria by sulfide:quinone oxidoreductase (SQR). Hydrogen Sulfide 18-21 cystathionine beta-synthase Homo sapiens 57-84 24117256-1 2013 Hydrogen sulfide (H2S) is synthesized from L-cysteine by cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE), and is enzymatically metabolized in mitochondria by sulfide:quinone oxidoreductase (SQR). Hydrogen Sulfide 18-21 cystathionine gamma-lyase Homo sapiens 94-119 24117256-1 2013 Hydrogen sulfide (H2S) is synthesized from L-cysteine by cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE), and is enzymatically metabolized in mitochondria by sulfide:quinone oxidoreductase (SQR). Hydrogen Sulfide 18-21 cystathionine gamma-lyase Homo sapiens 121-124 24117256-1 2013 Hydrogen sulfide (H2S) is synthesized from L-cysteine by cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE), and is enzymatically metabolized in mitochondria by sulfide:quinone oxidoreductase (SQR). Hydrogen Sulfide 18-21 crystallin zeta Homo sapiens 187-209 24117256-2 2013 Recent studies have indicated that H2S is synthesized by CSE in perivascular adipose tissue (PVAT), and is responsible for the anticontractile effect of PVAT on adjacent vessels. Hydrogen Sulfide 35-38 cystathionine gamma-lyase Homo sapiens 57-60 24117256-7 2013 In addition, cannabinoid CB1 receptor agonist administered for 2 weeks increases H2S by impairing mitochondria biogenesis. Hydrogen Sulfide 81-84 cannabinoid receptor 1 Homo sapiens 25-28 24117258-8 2013 Increased CBS and CSE expression also caused a significant elevation in H2S production in the liver. Hydrogen Sulfide 72-75 cystathionase (cystathionine gamma-lyase) Mus musculus 18-21 23872072-0 2013 Dysregulation of cystathionine gamma-lyase (CSE)/hydrogen sulfide pathway contributes to ox-LDL-induced inflammation in macrophage. Hydrogen Sulfide 49-65 cystathionine gamma-lyase Homo sapiens 44-47 23872072-1 2013 Hydrogen sulfide (H2S), mainly produced by cystathionine gamma-lyase (CSE) in vascular system, emerges as a novel gasotransmitter exerting anti-inflammatory and anti-atherosclerotic effects. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 43-68 23872072-1 2013 Hydrogen sulfide (H2S), mainly produced by cystathionine gamma-lyase (CSE) in vascular system, emerges as a novel gasotransmitter exerting anti-inflammatory and anti-atherosclerotic effects. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 70-73 23872072-1 2013 Hydrogen sulfide (H2S), mainly produced by cystathionine gamma-lyase (CSE) in vascular system, emerges as a novel gasotransmitter exerting anti-inflammatory and anti-atherosclerotic effects. Hydrogen Sulfide 18-21 cystathionine gamma-lyase Homo sapiens 43-68 23872072-1 2013 Hydrogen sulfide (H2S), mainly produced by cystathionine gamma-lyase (CSE) in vascular system, emerges as a novel gasotransmitter exerting anti-inflammatory and anti-atherosclerotic effects. Hydrogen Sulfide 18-21 cystathionine gamma-lyase Homo sapiens 70-73 23872072-2 2013 Alterations of CSE/H2S pathway may thus be involved in atherosclerosis pathogenesis. Hydrogen Sulfide 19-22 cystathionine gamma-lyase Homo sapiens 15-18 23872072-6 2013 Exogenous supplementation of H2S with NaHS and Na2S also decreased the production of TNF-alpha and intercellular adhesion molecule-1 (ICAM-1) in ox-LDL-stimulated macrophage, and alleviated the adhesion of macrophage to endothelial monolayer. Hydrogen Sulfide 29-32 tumor necrosis factor Homo sapiens 85-94 23872072-6 2013 Exogenous supplementation of H2S with NaHS and Na2S also decreased the production of TNF-alpha and intercellular adhesion molecule-1 (ICAM-1) in ox-LDL-stimulated macrophage, and alleviated the adhesion of macrophage to endothelial monolayer. Hydrogen Sulfide 29-32 intercellular adhesion molecule 1 Homo sapiens 99-132 23872072-6 2013 Exogenous supplementation of H2S with NaHS and Na2S also decreased the production of TNF-alpha and intercellular adhesion molecule-1 (ICAM-1) in ox-LDL-stimulated macrophage, and alleviated the adhesion of macrophage to endothelial monolayer. Hydrogen Sulfide 29-32 intercellular adhesion molecule 1 Homo sapiens 134-140 23872072-11 2013 Taken together, the findings demonstrate that ox-LDL may down-regulate the CSE/H2S pathway, which plays an anti-inflammatory role in ox-LDL-stimulated macrophage by suppressing JNK/NF-kappaB signaling. Hydrogen Sulfide 79-82 cystathionine gamma-lyase Homo sapiens 75-78 23872072-11 2013 Taken together, the findings demonstrate that ox-LDL may down-regulate the CSE/H2S pathway, which plays an anti-inflammatory role in ox-LDL-stimulated macrophage by suppressing JNK/NF-kappaB signaling. Hydrogen Sulfide 79-82 mitogen-activated protein kinase 8 Homo sapiens 177-180 23872072-12 2013 The study reveals new therapeutic strategies for atherosclerosis, based on modulating CSE/H2S pathway. Hydrogen Sulfide 90-93 cystathionine gamma-lyase Homo sapiens 86-89 23992829-1 2013 BACKGROUND: Hydrogen sulfide (H2S) is an endogenously generated gaseous transmitter known for its cytoprotective effect mediated by the PI3K-Akt signaling pathway. Hydrogen Sulfide 12-28 AKT serine/threonine kinase 1 Homo sapiens 141-144 23992829-1 2013 BACKGROUND: Hydrogen sulfide (H2S) is an endogenously generated gaseous transmitter known for its cytoprotective effect mediated by the PI3K-Akt signaling pathway. Hydrogen Sulfide 30-33 AKT serine/threonine kinase 1 Homo sapiens 141-144 23992829-13 2013 CONCLUSIONS: Our data confirmed that H2S arguments the proliferation and survival of hiPSC-MSCs through activation of the PI3K-Akt pathway and that such effects could be mediated through inhibition of BKCa. Hydrogen Sulfide 37-40 AKT serine/threonine kinase 1 Homo sapiens 127-130 24036365-3 2013 H2S is produced from L-cysteine by enzymes such as cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST) along with cysteine aminotransferase (CAT). Hydrogen Sulfide 0-3 cystathionine beta-synthase Homo sapiens 51-78 24036365-3 2013 H2S is produced from L-cysteine by enzymes such as cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST) along with cysteine aminotransferase (CAT). Hydrogen Sulfide 0-3 cystathionine gamma-lyase Homo sapiens 86-111 24036365-3 2013 H2S is produced from L-cysteine by enzymes such as cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST) along with cysteine aminotransferase (CAT). Hydrogen Sulfide 0-3 cystathionine gamma-lyase Homo sapiens 113-116 24036365-3 2013 H2S is produced from L-cysteine by enzymes such as cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST) along with cysteine aminotransferase (CAT). Hydrogen Sulfide 0-3 mercaptopyruvate sulfurtransferase Homo sapiens 123-159 24036365-4 2013 We recently identified a fourth pathway, where H2S is produced from D-cysteine by the enzyme D-amino acid oxidase (DAO) along with 3MST. Hydrogen Sulfide 47-50 D-amino acid oxidase Homo sapiens 93-113 24036365-4 2013 We recently identified a fourth pathway, where H2S is produced from D-cysteine by the enzyme D-amino acid oxidase (DAO) along with 3MST. Hydrogen Sulfide 47-50 D-amino acid oxidase Homo sapiens 115-118 24036365-12 2013 In addition, this review shows the recent findings that indicate that the H2S-derived polysulfides found in the brain activate TRPA1 channels more potently than parental H2S. Hydrogen Sulfide 74-77 transient receptor potential cation channel subfamily A member 1 Homo sapiens 127-132 24036365-12 2013 In addition, this review shows the recent findings that indicate that the H2S-derived polysulfides found in the brain activate TRPA1 channels more potently than parental H2S. Hydrogen Sulfide 170-173 transient receptor potential cation channel subfamily A member 1 Homo sapiens 127-132 23572589-7 2013 The Archean ocean is efficient in diluting primary atmospheric S MIF in the marine pools of sulfate and elemental sulfur with inputs from SO2 and H2S, respectively. Hydrogen Sulfide 146-149 macrophage migration inhibitory factor Homo sapiens 65-68 23350603-3 2013 CDO(-/-) mice had elevated urinary excretion of thiosulfate, high tissue and serum cystathionine and lanthionine levels, and evidence of inhibition and destabilization of cytochrome c oxidase, which is consistent with excess production of H2S/HS(-). Hydrogen Sulfide 239-242 cysteine dioxygenase 1, cytosolic Mus musculus 0-3 23350603-6 2013 INNOVATION: The CDO(-/-) mouse model provides new insights into tissue-specific cysteine metabolism, particularly the role of pancreas in metabolism of excess cysteine by CBS-catalyzed reactions, and will be a useful model for studying the effects of excess endogenous production of H2S/HS(-). Hydrogen Sulfide 283-286 cysteine dioxygenase 1, cytosolic Mus musculus 16-19 23350603-7 2013 CONCLUSION: The CDO(-/-) mouse clearly demonstrates that H2S/HS(-) production in tissues can exceed the capacity of the animal to oxidize sulfide to sulfate and demonstrates that pancreas and lung are more susceptible to toxicity from endogenous H2S/HS(-)production than are liver and kidney. Hydrogen Sulfide 57-60 cysteine dioxygenase 1, cytosolic Mus musculus 16-19 23350603-7 2013 CONCLUSION: The CDO(-/-) mouse clearly demonstrates that H2S/HS(-) production in tissues can exceed the capacity of the animal to oxidize sulfide to sulfate and demonstrates that pancreas and lung are more susceptible to toxicity from endogenous H2S/HS(-)production than are liver and kidney. Hydrogen Sulfide 246-249 cysteine dioxygenase 1, cytosolic Mus musculus 16-19 23830348-12 2013 CONCLUSIONS: The beneficial effect of H2S, at least in part, was associated with a decrease of Nox4-ROS-ERK1/2 signaling axis and an increase in HO-1 expression. Hydrogen Sulfide 38-41 NADPH oxidase 4 Rattus norvegicus 95-99 23830348-12 2013 CONCLUSIONS: The beneficial effect of H2S, at least in part, was associated with a decrease of Nox4-ROS-ERK1/2 signaling axis and an increase in HO-1 expression. Hydrogen Sulfide 38-41 mitogen activated protein kinase 3 Rattus norvegicus 104-110 23830348-12 2013 CONCLUSIONS: The beneficial effect of H2S, at least in part, was associated with a decrease of Nox4-ROS-ERK1/2 signaling axis and an increase in HO-1 expression. Hydrogen Sulfide 38-41 heme oxygenase 1 Rattus norvegicus 145-149 23830907-1 2013 Hydrogen sulfide (H2S) is a gasotransmitter endogenously generated from the metabolism of L-cysteine by action of two main enzymes called cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine beta synthase Rattus norvegicus 138-165 23830907-1 2013 Hydrogen sulfide (H2S) is a gasotransmitter endogenously generated from the metabolism of L-cysteine by action of two main enzymes called cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Rattus norvegicus 176-201 23830907-1 2013 Hydrogen sulfide (H2S) is a gasotransmitter endogenously generated from the metabolism of L-cysteine by action of two main enzymes called cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Rattus norvegicus 203-206 23830907-1 2013 Hydrogen sulfide (H2S) is a gasotransmitter endogenously generated from the metabolism of L-cysteine by action of two main enzymes called cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 18-21 cystathionine beta synthase Rattus norvegicus 138-165 23830907-1 2013 Hydrogen sulfide (H2S) is a gasotransmitter endogenously generated from the metabolism of L-cysteine by action of two main enzymes called cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 18-21 cystathionine gamma-lyase Rattus norvegicus 176-201 23830907-1 2013 Hydrogen sulfide (H2S) is a gasotransmitter endogenously generated from the metabolism of L-cysteine by action of two main enzymes called cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 18-21 cystathionine gamma-lyase Rattus norvegicus 203-206 23974514-0 2013 Hydrogen sulfide suppresses the expression of MMP-8, MMP-13, and TIMP-1 in left ventricles of rats with cardiac volume overload. Hydrogen Sulfide 0-16 matrix metallopeptidase 8 Rattus norvegicus 46-51 23974514-0 2013 Hydrogen sulfide suppresses the expression of MMP-8, MMP-13, and TIMP-1 in left ventricles of rats with cardiac volume overload. Hydrogen Sulfide 0-16 matrix metallopeptidase 13 Rattus norvegicus 53-59 23974514-0 2013 Hydrogen sulfide suppresses the expression of MMP-8, MMP-13, and TIMP-1 in left ventricles of rats with cardiac volume overload. Hydrogen Sulfide 0-16 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 65-71 23974514-1 2013 AIM: To study the effects of hydrogen sulfide (H2S) on the left ventricular expression of MMP-8, MMP-13, and TIMP-1 in a rat model of congenital heart disease. Hydrogen Sulfide 29-45 matrix metallopeptidase 8 Rattus norvegicus 90-95 23974514-1 2013 AIM: To study the effects of hydrogen sulfide (H2S) on the left ventricular expression of MMP-8, MMP-13, and TIMP-1 in a rat model of congenital heart disease. Hydrogen Sulfide 29-45 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 109-115 23974514-1 2013 AIM: To study the effects of hydrogen sulfide (H2S) on the left ventricular expression of MMP-8, MMP-13, and TIMP-1 in a rat model of congenital heart disease. Hydrogen Sulfide 47-50 matrix metallopeptidase 8 Rattus norvegicus 90-95 23974514-1 2013 AIM: To study the effects of hydrogen sulfide (H2S) on the left ventricular expression of MMP-8, MMP-13, and TIMP-1 in a rat model of congenital heart disease. Hydrogen Sulfide 47-50 matrix metallopeptidase 13 Rattus norvegicus 97-103 23974514-1 2013 AIM: To study the effects of hydrogen sulfide (H2S) on the left ventricular expression of MMP-8, MMP-13, and TIMP-1 in a rat model of congenital heart disease. Hydrogen Sulfide 47-50 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 109-115 23974514-10 2013 CONCLUSION: H2S suppresses protein and mRNA expression of MMP-8, MMP-13, and TIMP-1 in rats with cardiac volume overload, which may be contributed to the amelioration of ventricular structural remodeling and cardiac function. Hydrogen Sulfide 12-15 matrix metallopeptidase 8 Rattus norvegicus 58-63 23974514-10 2013 CONCLUSION: H2S suppresses protein and mRNA expression of MMP-8, MMP-13, and TIMP-1 in rats with cardiac volume overload, which may be contributed to the amelioration of ventricular structural remodeling and cardiac function. Hydrogen Sulfide 12-15 matrix metallopeptidase 13 Rattus norvegicus 65-71 23974514-10 2013 CONCLUSION: H2S suppresses protein and mRNA expression of MMP-8, MMP-13, and TIMP-1 in rats with cardiac volume overload, which may be contributed to the amelioration of ventricular structural remodeling and cardiac function. Hydrogen Sulfide 12-15 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 77-83 23834820-2 2013 We have previously reported that TTX-resistant (TTX-R) sodium channels in colon-specific dorsal root ganglion (DRG) neurons were sensitized and the expression of the endogenous hydrogen sulfide producing enzyme cystathionine beta-synthetase (CBS) was upregulated in a rat model of visceral hypersensitivity induced by neonatal maternal deprivation (NMD). Hydrogen Sulfide 177-193 cystathionine beta synthase Rattus norvegicus 211-240 23834820-2 2013 We have previously reported that TTX-resistant (TTX-R) sodium channels in colon-specific dorsal root ganglion (DRG) neurons were sensitized and the expression of the endogenous hydrogen sulfide producing enzyme cystathionine beta-synthetase (CBS) was upregulated in a rat model of visceral hypersensitivity induced by neonatal maternal deprivation (NMD). Hydrogen Sulfide 177-193 cystathionine beta synthase Rattus norvegicus 242-245 23834820-4 2013 This study was designed to examine roles for CBS-H2S signaling in sensitization of sodium channels in a previously validated rat model of IBS. Hydrogen Sulfide 49-52 cystathionine beta synthase Rattus norvegicus 45-48 23834820-7 2013 The endogenous H2S producing enzyme CBS antagonist was injected intraperitoneally. Hydrogen Sulfide 15-18 cystathionine beta synthase Rattus norvegicus 36-39 23834820-13 2013 CONCLUSION: These data suggest that sensitization of sodium channels of colon DRG neurons in NMD rats is most likely mediated by CBS-H2S signaling, thus identifying a potential target for treatment for chronic visceral pain in patients with IBS. Hydrogen Sulfide 133-136 cystathionine beta synthase Rattus norvegicus 129-132 23842678-0 2013 Hydrogen sulfide induces hypersensitivity of rat capsaicin-sensitive lung vagal neurons: role of TRPA1 receptors. Hydrogen Sulfide 0-16 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 97-102 23842678-2 2013 Hydrogen sulfide (H2S) is an endogenous mediator inducing hyperalgesia through transient receptor potential ankyrin 1 (TRPA1) receptors located on nociceptors. Hydrogen Sulfide 0-16 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 79-117 23842678-2 2013 Hydrogen sulfide (H2S) is an endogenous mediator inducing hyperalgesia through transient receptor potential ankyrin 1 (TRPA1) receptors located on nociceptors. Hydrogen Sulfide 0-16 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 119-124 23842678-2 2013 Hydrogen sulfide (H2S) is an endogenous mediator inducing hyperalgesia through transient receptor potential ankyrin 1 (TRPA1) receptors located on nociceptors. Hydrogen Sulfide 18-21 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 79-117 23842678-2 2013 Hydrogen sulfide (H2S) is an endogenous mediator inducing hyperalgesia through transient receptor potential ankyrin 1 (TRPA1) receptors located on nociceptors. Hydrogen Sulfide 18-21 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 119-124 23842678-11 2013 These results suggest that H2S induces a nonspecific sensitizing effect on CSLV fibers to both chemical and mechanical stimulation in rat lungs, which appears mediated through an action on the TRPA1 receptors expressed on the nerve endings of CSLV afferents. Hydrogen Sulfide 27-30 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 193-198 24059525-1 2013 Hydrogen sulfide (H2S), a classic cytochrome c oxidase inhibitor, is also an in vitro oxidase substrate and an in vivo candidate hormonal ("gasotransmitter") species affecting sleep and hibernation. Hydrogen Sulfide 0-16 cytochrome c, somatic Homo sapiens 34-46 24059525-1 2013 Hydrogen sulfide (H2S), a classic cytochrome c oxidase inhibitor, is also an in vitro oxidase substrate and an in vivo candidate hormonal ("gasotransmitter") species affecting sleep and hibernation. Hydrogen Sulfide 18-21 cytochrome c, somatic Homo sapiens 34-46 24043838-1 2013 Cystathionine beta-synthase (CBS) controls the flux of sulfur from methionine to cysteine, a precursor of glutathione, taurine, and H2S. Hydrogen Sulfide 132-135 cystathionine beta-synthase Homo sapiens 0-27 23877364-0 2013 Lipopolysaccharide regulates biosynthesis of cystathionine gamma-lyase and hydrogen sulfide through Toll-like receptor-4/p38 and Toll-like receptor-4/NF-kappaB pathways in macrophages. Hydrogen Sulfide 75-91 toll-like receptor 4 Mus musculus 100-120 23877364-0 2013 Lipopolysaccharide regulates biosynthesis of cystathionine gamma-lyase and hydrogen sulfide through Toll-like receptor-4/p38 and Toll-like receptor-4/NF-kappaB pathways in macrophages. Hydrogen Sulfide 75-91 mitogen-activated protein kinase 14 Mus musculus 121-124 23877364-0 2013 Lipopolysaccharide regulates biosynthesis of cystathionine gamma-lyase and hydrogen sulfide through Toll-like receptor-4/p38 and Toll-like receptor-4/NF-kappaB pathways in macrophages. Hydrogen Sulfide 75-91 toll-like receptor 4 Mus musculus 129-149 23877364-0 2013 Lipopolysaccharide regulates biosynthesis of cystathionine gamma-lyase and hydrogen sulfide through Toll-like receptor-4/p38 and Toll-like receptor-4/NF-kappaB pathways in macrophages. Hydrogen Sulfide 75-91 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 150-159 23877364-1 2013 Hydrogen sulfide (H2S), formed mainly by the enzyme cystathionine gamma-lyase (CSE) in macrophages, is emerging as a novel regulator in inflammation. Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 52-77 23877364-1 2013 Hydrogen sulfide (H2S), formed mainly by the enzyme cystathionine gamma-lyase (CSE) in macrophages, is emerging as a novel regulator in inflammation. Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 79-82 23877364-1 2013 Hydrogen sulfide (H2S), formed mainly by the enzyme cystathionine gamma-lyase (CSE) in macrophages, is emerging as a novel regulator in inflammation. Hydrogen Sulfide 18-21 cystathionase (cystathionine gamma-lyase) Mus musculus 52-77 23877364-1 2013 Hydrogen sulfide (H2S), formed mainly by the enzyme cystathionine gamma-lyase (CSE) in macrophages, is emerging as a novel regulator in inflammation. Hydrogen Sulfide 18-21 cystathionase (cystathionine gamma-lyase) Mus musculus 79-82 23877364-4 2013 It showed that LPS increased the expressions of CSE and biosynthesis of H2S in C57BL/6 mice both in vivo and in vitro. Hydrogen Sulfide 72-75 toll-like receptor 4 Mus musculus 15-18 23877364-5 2013 However, the effects of LPS were not present in TLR4(-/-) mice, indicating the crucial role of TLR4 in LPS-induced expression of CSE and biosynthesis of H2S. Hydrogen Sulfide 153-156 toll-like receptor 4 Mus musculus 95-99 23877364-5 2013 However, the effects of LPS were not present in TLR4(-/-) mice, indicating the crucial role of TLR4 in LPS-induced expression of CSE and biosynthesis of H2S. Hydrogen Sulfide 153-156 toll-like receptor 4 Mus musculus 103-106 23877364-6 2013 We subsequently used JNK inhibitor, P38 inhibitor, and ERK inhibitor to block the downstream MAPK pathways of TLR4 in macrophages, and found that LPS-induced CSE expression and H2S synthesizing activity were inhibited by pretreatment with the p38 inhibitor. Hydrogen Sulfide 177-180 mitogen-activated protein kinase 1 Mus musculus 55-58 23877364-6 2013 We subsequently used JNK inhibitor, P38 inhibitor, and ERK inhibitor to block the downstream MAPK pathways of TLR4 in macrophages, and found that LPS-induced CSE expression and H2S synthesizing activity were inhibited by pretreatment with the p38 inhibitor. Hydrogen Sulfide 177-180 mitogen-activated protein kinase 1 Mus musculus 93-97 23877364-6 2013 We subsequently used JNK inhibitor, P38 inhibitor, and ERK inhibitor to block the downstream MAPK pathways of TLR4 in macrophages, and found that LPS-induced CSE expression and H2S synthesizing activity were inhibited by pretreatment with the p38 inhibitor. Hydrogen Sulfide 177-180 toll-like receptor 4 Mus musculus 110-114 23877364-6 2013 We subsequently used JNK inhibitor, P38 inhibitor, and ERK inhibitor to block the downstream MAPK pathways of TLR4 in macrophages, and found that LPS-induced CSE expression and H2S synthesizing activity were inhibited by pretreatment with the p38 inhibitor. Hydrogen Sulfide 177-180 toll-like receptor 4 Mus musculus 146-149 23877364-6 2013 We subsequently used JNK inhibitor, P38 inhibitor, and ERK inhibitor to block the downstream MAPK pathways of TLR4 in macrophages, and found that LPS-induced CSE expression and H2S synthesizing activity were inhibited by pretreatment with the p38 inhibitor. Hydrogen Sulfide 177-180 mitogen-activated protein kinase 14 Mus musculus 243-246 23877364-8 2013 These results suggest that LPS increases the biosynthesis of CSE and H2S in macrophages mainly in a TLR4-p38-dependent and TLR-4-NF-kappaB-dependent manner. Hydrogen Sulfide 69-72 toll-like receptor 4 Mus musculus 27-30 23877364-8 2013 These results suggest that LPS increases the biosynthesis of CSE and H2S in macrophages mainly in a TLR4-p38-dependent and TLR-4-NF-kappaB-dependent manner. Hydrogen Sulfide 69-72 toll-like receptor 4 Mus musculus 100-104 23877364-8 2013 These results suggest that LPS increases the biosynthesis of CSE and H2S in macrophages mainly in a TLR4-p38-dependent and TLR-4-NF-kappaB-dependent manner. Hydrogen Sulfide 69-72 mitogen-activated protein kinase 14 Mus musculus 105-108 23877364-8 2013 These results suggest that LPS increases the biosynthesis of CSE and H2S in macrophages mainly in a TLR4-p38-dependent and TLR-4-NF-kappaB-dependent manner. Hydrogen Sulfide 69-72 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 129-138 23912965-0 2013 Exogenous hydrogen sulfide protects H9c2 cardiac cells against high glucose-induced injury by inhibiting the activities of the p38 MAPK and ERK1/2 pathways. Hydrogen Sulfide 10-26 mitogen activated protein kinase 3 Rattus norvegicus 140-146 23912965-2 2013 In this study, we demonstrate the inhibitory effects of exogenous hydrogen sulfide (H2S) on the activation of the MAPK pathway. Hydrogen Sulfide 66-82 mitogen activated protein kinase 3 Rattus norvegicus 114-118 23912965-2 2013 In this study, we demonstrate the inhibitory effects of exogenous hydrogen sulfide (H2S) on the activation of the MAPK pathway. Hydrogen Sulfide 84-87 mitogen activated protein kinase 3 Rattus norvegicus 114-118 23912965-3 2013 The aim of the present study was to determine whether exogenous H2S prevents high glucose (HG)-induced injury by inhibiting the activation of the p38 MAPK and extracellular signal-regulated kinase (ERK)1/2 (members of MAPK) pathways in cardiomyoblasts (H9c2 cells). Hydrogen Sulfide 64-67 mitogen activated protein kinase 3 Rattus norvegicus 159-205 23912965-3 2013 The aim of the present study was to determine whether exogenous H2S prevents high glucose (HG)-induced injury by inhibiting the activation of the p38 MAPK and extracellular signal-regulated kinase (ERK)1/2 (members of MAPK) pathways in cardiomyoblasts (H9c2 cells). Hydrogen Sulfide 64-67 mitogen activated protein kinase 3 Rattus norvegicus 150-154 23912965-5 2013 The increased expression levels of p-p38 MAPK and p-ERK1/2 were markedly reduced by pre-treatment of the H9c2 cells with 400 microM sodium hydrogen sulfide (NaHS; a donor of H2S) prior to exposure to 35 mM glucose. Hydrogen Sulfide 174-177 mitogen activated protein kinase 3 Rattus norvegicus 52-58 23912965-8 2013 Taken together, the data from the present study demonstrate for the first time, to our knowledge, that exogenous H2S exerts a protective effect against HG-induced injury by inhibiting the activation of the p38 MAPK and ERK1/2 pathways and preventing oxidative stress in H9c2 cells. Hydrogen Sulfide 113-116 mitogen activated protein kinase 3 Rattus norvegicus 219-225 23733596-0 2013 L-cysteine and hydrogen sulfide increase PIP3 and AMPK/PPARgamma expression and decrease ROS and vascular inflammation markers in high glucose treated human U937 monocytes. Hydrogen Sulfide 15-31 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 50-54 23733596-0 2013 L-cysteine and hydrogen sulfide increase PIP3 and AMPK/PPARgamma expression and decrease ROS and vascular inflammation markers in high glucose treated human U937 monocytes. Hydrogen Sulfide 15-31 peroxisome proliferator activated receptor gamma Homo sapiens 55-64 23733596-5 2013 The effect of LC on PIP3 was prevented by propargylglycine, an inhibitor of cystathionine-gamma-lyase (CSE) that catalyzes H2S formation from LC. Hydrogen Sulfide 123-126 cystathionine gamma-lyase Homo sapiens 76-101 23733596-5 2013 The effect of LC on PIP3 was prevented by propargylglycine, an inhibitor of cystathionine-gamma-lyase (CSE) that catalyzes H2S formation from LC. Hydrogen Sulfide 123-126 cystathionine gamma-lyase Homo sapiens 103-106 23733596-6 2013 Signal silencing studies with CSE siRNA also showed the inhibition of H2S formation and PIP3 upregulation in LC-supplemented CSE knockdown cells exposed to HG. Hydrogen Sulfide 70-73 cystathionine gamma-lyase Homo sapiens 30-33 23945069-10 2013 Furthermore, H2S significantly attenuated TGF-beta1-stimulated Kv4.3 and alpha-smooth muscle actin expression, which coincided with its inhibition of TGF-beta-induced myofibroblast transformation. Hydrogen Sulfide 13-16 transforming growth factor beta 1 Homo sapiens 42-51 23945069-10 2013 Furthermore, H2S significantly attenuated TGF-beta1-stimulated Kv4.3 and alpha-smooth muscle actin expression, which coincided with its inhibition of TGF-beta-induced myofibroblast transformation. Hydrogen Sulfide 13-16 potassium voltage-gated channel subfamily D member 3 Homo sapiens 63-68 23945069-10 2013 Furthermore, H2S significantly attenuated TGF-beta1-stimulated Kv4.3 and alpha-smooth muscle actin expression, which coincided with its inhibition of TGF-beta-induced myofibroblast transformation. Hydrogen Sulfide 13-16 transforming growth factor beta 1 Homo sapiens 42-50 23873754-0 2013 Inflammatory acidic pH enhances hydrogen sulfide-induced transient receptor potential ankyrin 1 activation in RIN-14B cells. Hydrogen Sulfide 32-48 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 57-95 23873754-10 2013 H2 S failed to increase the intracellular ROS level and only slightly decreased pHi . Hydrogen Sulfide 0-4 glucose-6-phosphate isomerase Rattus norvegicus 80-83 23873754-11 2013 These results suggest that H2 S directly activates TRPA1 and that its increment of diffusion into cells may be involved in the potentiation of TRPA1 activation under external acidic conditions. Hydrogen Sulfide 27-31 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 51-56 23873754-11 2013 These results suggest that H2 S directly activates TRPA1 and that its increment of diffusion into cells may be involved in the potentiation of TRPA1 activation under external acidic conditions. Hydrogen Sulfide 27-31 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 143-148 23896061-0 2013 Hydrogen sulfide-releasing aspirin inhibits the growth of leukemic Jurkat cells and modulates beta-catenin expression. Hydrogen Sulfide 0-16 catenin beta 1 Homo sapiens 94-106 23571523-1 2013 OBJECTIVE: Hydrogen sulfide (H2S), generated in the myocardium predominantly via cystathionine-gamma-lyase (CSE), is cardioprotective. Hydrogen Sulfide 11-27 cystathionine gamma-lyase Rattus norvegicus 81-106 23571523-1 2013 OBJECTIVE: Hydrogen sulfide (H2S), generated in the myocardium predominantly via cystathionine-gamma-lyase (CSE), is cardioprotective. Hydrogen Sulfide 11-27 cystathionine gamma-lyase Rattus norvegicus 108-111 23571523-1 2013 OBJECTIVE: Hydrogen sulfide (H2S), generated in the myocardium predominantly via cystathionine-gamma-lyase (CSE), is cardioprotective. Hydrogen Sulfide 29-32 cystathionine gamma-lyase Rattus norvegicus 81-106 23571523-1 2013 OBJECTIVE: Hydrogen sulfide (H2S), generated in the myocardium predominantly via cystathionine-gamma-lyase (CSE), is cardioprotective. Hydrogen Sulfide 29-32 cystathionine gamma-lyase Rattus norvegicus 108-111 23571523-9 2013 H2S generation rate was positively correlated with T-AOC and GSH/GSSG ratio, and inversely correlated with IL-6 and TNF-alpha levels. Hydrogen Sulfide 0-3 interleukin 6 Rattus norvegicus 107-111 23571523-9 2013 H2S generation rate was positively correlated with T-AOC and GSH/GSSG ratio, and inversely correlated with IL-6 and TNF-alpha levels. Hydrogen Sulfide 0-3 tumor necrosis factor Rattus norvegicus 116-125 23912155-9 2013 These results suggested that H2S regulates the inflammatory response induced by burn injury by modulating the levels of TNF-alpha, IL-6, IL-8 and IL-10. Hydrogen Sulfide 29-32 tumor necrosis factor Mus musculus 120-129 23912155-9 2013 These results suggested that H2S regulates the inflammatory response induced by burn injury by modulating the levels of TNF-alpha, IL-6, IL-8 and IL-10. Hydrogen Sulfide 29-32 interleukin 6 Mus musculus 131-135 23912155-9 2013 These results suggested that H2S regulates the inflammatory response induced by burn injury by modulating the levels of TNF-alpha, IL-6, IL-8 and IL-10. Hydrogen Sulfide 29-32 chemokine (C-X-C motif) ligand 15 Mus musculus 137-141 23912155-9 2013 These results suggested that H2S regulates the inflammatory response induced by burn injury by modulating the levels of TNF-alpha, IL-6, IL-8 and IL-10. Hydrogen Sulfide 29-32 interleukin 10 Mus musculus 146-151 24131846-1 2013 OBJECTIVE: To observe the level in plasma hydrogen sulfide (H2S) and the expression of cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) (two key synthetases for endogenous H2S generation in the kidney) in obstructed kidney tissue among rats with tubulointerstitial fibrosis (TIF) induced by unilateral ureteral obstruction (UUO), and to explore the role of H2S in TIF. Hydrogen Sulfide 193-196 cystathionine beta synthase Rattus norvegicus 87-114 24131846-1 2013 OBJECTIVE: To observe the level in plasma hydrogen sulfide (H2S) and the expression of cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) (two key synthetases for endogenous H2S generation in the kidney) in obstructed kidney tissue among rats with tubulointerstitial fibrosis (TIF) induced by unilateral ureteral obstruction (UUO), and to explore the role of H2S in TIF. Hydrogen Sulfide 193-196 cystathionine beta synthase Rattus norvegicus 116-119 24131846-1 2013 OBJECTIVE: To observe the level in plasma hydrogen sulfide (H2S) and the expression of cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) (two key synthetases for endogenous H2S generation in the kidney) in obstructed kidney tissue among rats with tubulointerstitial fibrosis (TIF) induced by unilateral ureteral obstruction (UUO), and to explore the role of H2S in TIF. Hydrogen Sulfide 193-196 cystathionine gamma-lyase Rattus norvegicus 152-155 24131846-1 2013 OBJECTIVE: To observe the level in plasma hydrogen sulfide (H2S) and the expression of cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) (two key synthetases for endogenous H2S generation in the kidney) in obstructed kidney tissue among rats with tubulointerstitial fibrosis (TIF) induced by unilateral ureteral obstruction (UUO), and to explore the role of H2S in TIF. Hydrogen Sulfide 193-196 cystathionine beta synthase Rattus norvegicus 87-114 24131846-1 2013 OBJECTIVE: To observe the level in plasma hydrogen sulfide (H2S) and the expression of cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) (two key synthetases for endogenous H2S generation in the kidney) in obstructed kidney tissue among rats with tubulointerstitial fibrosis (TIF) induced by unilateral ureteral obstruction (UUO), and to explore the role of H2S in TIF. Hydrogen Sulfide 193-196 cystathionine beta synthase Rattus norvegicus 116-119 24131846-1 2013 OBJECTIVE: To observe the level in plasma hydrogen sulfide (H2S) and the expression of cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) (two key synthetases for endogenous H2S generation in the kidney) in obstructed kidney tissue among rats with tubulointerstitial fibrosis (TIF) induced by unilateral ureteral obstruction (UUO), and to explore the role of H2S in TIF. Hydrogen Sulfide 193-196 cystathionine gamma-lyase Rattus norvegicus 152-155 24131846-10 2013 With H2S supplementation, renal tubulointerstitial injury was reduced (P<0.01), the expression of mRNA and protein of CBS and CSE in the kidney tissue and plasma H2S level were upregulated (P<0.01), and the degree of TIF was reduced (P<0.01). Hydrogen Sulfide 5-8 cystathionine beta synthase Rattus norvegicus 121-124 24131846-10 2013 With H2S supplementation, renal tubulointerstitial injury was reduced (P<0.01), the expression of mRNA and protein of CBS and CSE in the kidney tissue and plasma H2S level were upregulated (P<0.01), and the degree of TIF was reduced (P<0.01). Hydrogen Sulfide 5-8 cystathionine gamma-lyase Rattus norvegicus 129-132 24131846-10 2013 With H2S supplementation, renal tubulointerstitial injury was reduced (P<0.01), the expression of mRNA and protein of CBS and CSE in the kidney tissue and plasma H2S level were upregulated (P<0.01), and the degree of TIF was reduced (P<0.01). Hydrogen Sulfide 165-168 cystathionine beta synthase Rattus norvegicus 121-124 24131846-12 2013 CONCLUSIONS: H2S is involved in the development of UUO-induced TIF, and the CBS/H2S and CSE/H2S systems play key roles in this process. Hydrogen Sulfide 80-83 cystathionine beta synthase Rattus norvegicus 76-79 24131846-12 2013 CONCLUSIONS: H2S is involved in the development of UUO-induced TIF, and the CBS/H2S and CSE/H2S systems play key roles in this process. Hydrogen Sulfide 80-83 cystathionine beta synthase Rattus norvegicus 76-79 24043838-1 2013 Cystathionine beta-synthase (CBS) controls the flux of sulfur from methionine to cysteine, a precursor of glutathione, taurine, and H2S. Hydrogen Sulfide 132-135 cystathionine beta-synthase Homo sapiens 29-32 24043838-8 2013 Because of its central role in transsulfuration, redox status, and H2S biogenesis, CBS represents a very attractive therapeutic target. Hydrogen Sulfide 67-70 cystathionine beta-synthase Homo sapiens 83-86 24019484-2 2013 Alternatively, by the transulfuration pathway, homocysteine is transformed to hydrogen sulphide (H2S), through multiple steps involving cystathionine beta-synthase and cystathionine gamma-lyase. Hydrogen Sulfide 78-95 cystathionine beta-synthase Homo sapiens 136-163 24019484-2 2013 Alternatively, by the transulfuration pathway, homocysteine is transformed to hydrogen sulphide (H2S), through multiple steps involving cystathionine beta-synthase and cystathionine gamma-lyase. Hydrogen Sulfide 78-95 cystathionine gamma-lyase Homo sapiens 168-193 24019484-2 2013 Alternatively, by the transulfuration pathway, homocysteine is transformed to hydrogen sulphide (H2S), through multiple steps involving cystathionine beta-synthase and cystathionine gamma-lyase. Hydrogen Sulfide 97-100 cystathionine beta-synthase Homo sapiens 136-163 24019484-2 2013 Alternatively, by the transulfuration pathway, homocysteine is transformed to hydrogen sulphide (H2S), through multiple steps involving cystathionine beta-synthase and cystathionine gamma-lyase. Hydrogen Sulfide 97-100 cystathionine gamma-lyase Homo sapiens 168-193 24019484-7 2013 Similarly, in MTHFR++ carriers, the content of H2S was significantly higher in either platelets or plasma compared with healthy volunteers. Hydrogen Sulfide 47-50 methylenetetrahydrofolate reductase Homo sapiens 14-19 24019484-9 2013 The inhibition of phospholipase A2, cyclooxygenase, or blockade of the thromboxane receptor markedly reduced the effects of H2S. Hydrogen Sulfide 124-127 phospholipase A2 group IB Homo sapiens 18-34 23892315-3 2013 The generated aqueous Co(III) is then applied to simultaneous deodorization of simulated odor gases, namely, ammonia, trimethylamine, hydrogen sulfide, methyl mercaptan, and acetaldehyde, for municipal waste treatment plant emissions. Hydrogen Sulfide 134-150 mitochondrially encoded cytochrome c oxidase III Homo sapiens 22-29 23892315-6 2013 In the case of sulfur compounds, deodorization of methyl mercaptan and hydrogen sulfide are removed by the Co(III)-MEO (Co(III)-mediated electrocatalytic oxidation) process via the formation of acetic acid as intermediate and SO4(2-) as a product. Hydrogen Sulfide 71-87 mitochondrially encoded cytochrome c oxidase III Homo sapiens 110-113 23892315-6 2013 In the case of sulfur compounds, deodorization of methyl mercaptan and hydrogen sulfide are removed by the Co(III)-MEO (Co(III)-mediated electrocatalytic oxidation) process via the formation of acetic acid as intermediate and SO4(2-) as a product. Hydrogen Sulfide 71-87 mitochondrially encoded cytochrome c oxidase III Homo sapiens 123-126 23771150-1 2013 CS2 hydrolase, a zinc-dependent enzyme that converts carbon disulfide to carbon dioxide and hydrogen sulfide, exists as a mixture of octameric ring and hexadecameric catenane forms in solution. Hydrogen Sulfide 92-108 chorionic somatomammotropin hormone 2 Homo sapiens 0-3 24058499-0 2013 Increase or decrease hydrogen sulfide exert opposite lipolysis, but reduce global insulin resistance in high fatty diet induced obese mice. Hydrogen Sulfide 21-37 insulin Homo sapiens 82-89 24058499-3 2013 Thus, we hypothesized that CSE/H2S system regulates lipolysis which contributed to the pathogenesis of insulin resistance. Hydrogen Sulfide 31-34 cystathionase (cystathionine gamma-lyase) Mus musculus 27-30 24058499-3 2013 Thus, we hypothesized that CSE/H2S system regulates lipolysis which contributed to the pathogenesis of insulin resistance. Hydrogen Sulfide 31-34 insulin Homo sapiens 103-110 24058499-11 2013 CONCLUSION: These results implicated that inhibition endogenous CSE/H2S system in adipocytes increased lipolysis by a protein kinase A-perilipin/hormone-sensitive lipase pathway, thus blunted fat mass increase and reduced insulin resistance in obese mice; giving H2S donor decreased lipolysis, also reduced insulin resistance induced by HFD. Hydrogen Sulfide 68-71 cystathionase (cystathionine gamma-lyase) Mus musculus 64-67 24058499-11 2013 CONCLUSION: These results implicated that inhibition endogenous CSE/H2S system in adipocytes increased lipolysis by a protein kinase A-perilipin/hormone-sensitive lipase pathway, thus blunted fat mass increase and reduced insulin resistance in obese mice; giving H2S donor decreased lipolysis, also reduced insulin resistance induced by HFD. Hydrogen Sulfide 68-71 insulin Homo sapiens 222-229 24058499-11 2013 CONCLUSION: These results implicated that inhibition endogenous CSE/H2S system in adipocytes increased lipolysis by a protein kinase A-perilipin/hormone-sensitive lipase pathway, thus blunted fat mass increase and reduced insulin resistance in obese mice; giving H2S donor decreased lipolysis, also reduced insulin resistance induced by HFD. Hydrogen Sulfide 68-71 insulin Homo sapiens 307-314 24058499-11 2013 CONCLUSION: These results implicated that inhibition endogenous CSE/H2S system in adipocytes increased lipolysis by a protein kinase A-perilipin/hormone-sensitive lipase pathway, thus blunted fat mass increase and reduced insulin resistance in obese mice; giving H2S donor decreased lipolysis, also reduced insulin resistance induced by HFD. Hydrogen Sulfide 263-266 cystathionase (cystathionine gamma-lyase) Mus musculus 64-67 24058499-12 2013 Our data showed that increase or decrease H2S induced opposite lipolysis, but had the same effect on insulin resistance. Hydrogen Sulfide 42-45 insulin Homo sapiens 101-108 24058562-0 2013 Hydrogen sulfide preconditioning protects rat liver against ischemia/reperfusion injury by activating Akt-GSK-3beta signaling and inhibiting mitochondrial permeability transition. Hydrogen Sulfide 0-16 AKT serine/threonine kinase 1 Rattus norvegicus 102-105 24058562-0 2013 Hydrogen sulfide preconditioning protects rat liver against ischemia/reperfusion injury by activating Akt-GSK-3beta signaling and inhibiting mitochondrial permeability transition. Hydrogen Sulfide 0-16 glycogen synthase kinase 3 beta Rattus norvegicus 106-115 23838794-0 2013 Inhibition of hydrogen sulfide production by gene silencing attenuates inflammatory activity of LPS-activated RAW264.7 cells. Hydrogen Sulfide 14-30 toll-like receptor 4 Mus musculus 96-99 23838794-1 2013 Hydrogen sulfide is an inflammatory mediator and is produced by the activity of the enzyme cystathionine gamma-lyase (CSE) in macrophages. Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 91-116 23838794-1 2013 Hydrogen sulfide is an inflammatory mediator and is produced by the activity of the enzyme cystathionine gamma-lyase (CSE) in macrophages. Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 118-121 23811964-6 2013 H2S therapy increased the expression of the proangiogenic factor, vascular endothelial cell growth factor, and decreased the angiogenesis inhibitor, angiostatin. Hydrogen Sulfide 0-3 plasminogen Mus musculus 149-160 23811964-7 2013 Further studies revealed that H2S therapy increased the expression of the proliferation marker, Ki67, as well as increased the phosphorylation of endothelial NO synthase and the bioavailability of NO. Hydrogen Sulfide 30-33 antigen identified by monoclonal antibody Ki 67 Mus musculus 96-100 23846260-6 2013 H2S-induced GSNO decomposition was slowed by the presence of other thiols, such as L-cysteine (Cys), N-acetyl-L-cysteine (NAC) and L-glutathione (GSH), but not in the presence of L-methionine (Met) or oxidized glutathione (GSSG). Hydrogen Sulfide 0-3 X-linked Kx blood group Homo sapiens 122-125 23846260-7 2013 In sharp contrast, at pH 6.0, H2S-induced GSNO decomposition was negligible, yet the presence of Cys, NAC and GSH induced the H2S-driven GSNO decomposition (whilst Met and GSSG were inactive). Hydrogen Sulfide 126-129 X-linked Kx blood group Homo sapiens 102-105 23676335-0 2013 Hydrogen sulfide suppresses high glucose-induced expression of intercellular adhesion molecule-1 in endothelial cells. Hydrogen Sulfide 0-16 intercellular adhesion molecule 1 Homo sapiens 63-96 23660955-10 2013 Moreover, H2S reduced the expression of the cleaved caspase-3, NOX4 and the leakage of cyt c from the mitochondria to the cytoplasm. Hydrogen Sulfide 10-13 caspase 3 Homo sapiens 52-61 23660955-10 2013 Moreover, H2S reduced the expression of the cleaved caspase-3, NOX4 and the leakage of cyt c from the mitochondria to the cytoplasm. Hydrogen Sulfide 10-13 NADPH oxidase 4 Homo sapiens 63-67 23660955-10 2013 Moreover, H2S reduced the expression of the cleaved caspase-3, NOX4 and the leakage of cyt c from the mitochondria to the cytoplasm. Hydrogen Sulfide 10-13 cytochrome c, somatic Homo sapiens 87-92 23676335-3 2013 The aims of this study were to determine the effect of H2S on the high glucose (HG)-induced expression of intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells and to explore the possible underlying mechanisms. Hydrogen Sulfide 55-58 intercellular adhesion molecule 1 Homo sapiens 106-139 23676335-3 2013 The aims of this study were to determine the effect of H2S on the high glucose (HG)-induced expression of intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells and to explore the possible underlying mechanisms. Hydrogen Sulfide 55-58 intercellular adhesion molecule 1 Homo sapiens 141-147 23676335-9 2013 These findings indicate that H2S might protect against HG-induced vascular damage by down-regulating ICAM-1 expression in endothelial cells. Hydrogen Sulfide 29-32 intercellular adhesion molecule 1 Homo sapiens 101-107 23515848-0 2013 The effect of certain conditions in the regulation of cystathionine gamma-lyase by exogenous hydrogen sulfide in mammalian cells. Hydrogen Sulfide 93-109 cystathionine gamma-lyase Homo sapiens 54-79 24948218-0 2013 Abstracts of the Second European Conference on the Biology of Hydrogen Sulfide, Sep 8-11, 2013, Exeter, UK. Hydrogen Sulfide 62-78 plexin B1 Homo sapiens 80-83 23771693-6 2013 Late-phase preconditioning with BAY 60-2770 was maintained in HO-1-/- and endothelial nitric oxide synthase knockout mice pretreated with an inhibitor (dl-propargylglycine) of enzymatically produced H2S. Hydrogen Sulfide 199-202 nitric oxide synthase 3, endothelial cell Mus musculus 74-107 23785074-0 2013 Akt/eNOS signaling and PLN S-sulfhydration are involved in H2S-dependent cardiac effects in frog and rat. Hydrogen Sulfide 59-62 AKT serine/threonine kinase 1 Rattus norvegicus 0-3 23785074-0 2013 Akt/eNOS signaling and PLN S-sulfhydration are involved in H2S-dependent cardiac effects in frog and rat. Hydrogen Sulfide 59-62 phospholamban Rattus norvegicus 23-26 23785074-12 2013 H2S effects involve KATP channels, the Akt/NOS-cGMP/PKG pathway, and S-sulfhydration of cardiac proteins. Hydrogen Sulfide 0-3 AKT serine/threonine kinase 1 Rattus norvegicus 39-42 23199280-0 2013 VEGFR2 functions as an H2S-targeting receptor protein kinase with its novel Cys1045-Cys1024 disulfide bond serving as a specific molecular switch for hydrogen sulfide actions in vascular endothelial cells. Hydrogen Sulfide 150-166 kinase insert domain receptor Homo sapiens 0-6 23199280-2 2013 RESULTS: H2S could directly activate vascular endothelial growth factor receptor 2 (VEGFR2) and that a small interfering RNA (siRNA)-mediated knockdown of VEGFR2 inhibited H2S-induced migration of human vascular endothelial cells. Hydrogen Sulfide 9-12 kinase insert domain receptor Homo sapiens 37-82 23199280-2 2013 RESULTS: H2S could directly activate vascular endothelial growth factor receptor 2 (VEGFR2) and that a small interfering RNA (siRNA)-mediated knockdown of VEGFR2 inhibited H2S-induced migration of human vascular endothelial cells. Hydrogen Sulfide 9-12 kinase insert domain receptor Homo sapiens 84-90 23199280-2 2013 RESULTS: H2S could directly activate vascular endothelial growth factor receptor 2 (VEGFR2) and that a small interfering RNA (siRNA)-mediated knockdown of VEGFR2 inhibited H2S-induced migration of human vascular endothelial cells. Hydrogen Sulfide 172-175 kinase insert domain receptor Homo sapiens 37-82 23199280-2 2013 RESULTS: H2S could directly activate vascular endothelial growth factor receptor 2 (VEGFR2) and that a small interfering RNA (siRNA)-mediated knockdown of VEGFR2 inhibited H2S-induced migration of human vascular endothelial cells. Hydrogen Sulfide 172-175 kinase insert domain receptor Homo sapiens 84-90 23199280-2 2013 RESULTS: H2S could directly activate vascular endothelial growth factor receptor 2 (VEGFR2) and that a small interfering RNA (siRNA)-mediated knockdown of VEGFR2 inhibited H2S-induced migration of human vascular endothelial cells. Hydrogen Sulfide 172-175 kinase insert domain receptor Homo sapiens 155-161 23199280-3 2013 H2S promoted angiogenesis in Matrigel plug assay in mice and this effect was attenuated by a VEGF receptor inhibitor. Hydrogen Sulfide 0-3 vascular endothelial growth factor A Homo sapiens 93-97 23199280-4 2013 Using tandem mass spectrometry (MS), we identified a new disulfide complex located between Cys1045 and Cys1024 within VEGFR2 that was labile to H2S-mediated modification. Hydrogen Sulfide 144-147 kinase insert domain receptor Homo sapiens 118-124 23199280-6 2013 Transfection with vectors expressing VEGFR2 (C1045A) caused a significant increase in cell migration, while the migration-promoting effect of H2S disappeared in the cells transfected with VEGFR2 (C1045A). Hydrogen Sulfide 142-145 kinase insert domain receptor Homo sapiens 188-194 23499828-0 2013 Thrombospondin-1 is a CD47-dependent endogenous inhibitor of hydrogen sulfide signaling in T cell activation. Hydrogen Sulfide 61-77 thrombospondin 1 Mus musculus 0-16 23499828-0 2013 Thrombospondin-1 is a CD47-dependent endogenous inhibitor of hydrogen sulfide signaling in T cell activation. Hydrogen Sulfide 61-77 CD47 antigen (Rh-related antigen, integrin-associated signal transducer) Mus musculus 22-26 23713790-0 2013 The hydrogen sulfide donor, GYY4137, exhibits anti-atherosclerotic activity in high fat fed apolipoprotein E(-/-) mice. Hydrogen Sulfide 4-20 apolipoprotein E Homo sapiens 92-108 23515848-5 2013 Exogenous H2S at 120 muM increases the transcription and expression of CSE significantly. Hydrogen Sulfide 10-13 cystathionine gamma-lyase Homo sapiens 71-74 23515848-6 2013 At a concentration of exogenous H2S over 160 muM, the transcription and expression of CSE are inhibited completely. Hydrogen Sulfide 32-35 cystathionine gamma-lyase Homo sapiens 86-89 23515848-7 2013 These findings suggest that CSE expression has not only a feedback to the enzyme itself at lower concentrations of exogenous H2S but also can be up-regulated at higher concentrations, and H2S may become toxic at higher levels. Hydrogen Sulfide 125-128 cystathionine gamma-lyase Homo sapiens 28-31 23515848-7 2013 These findings suggest that CSE expression has not only a feedback to the enzyme itself at lower concentrations of exogenous H2S but also can be up-regulated at higher concentrations, and H2S may become toxic at higher levels. Hydrogen Sulfide 188-191 cystathionine gamma-lyase Homo sapiens 28-31 23080424-4 2013 The aim of the present study is to investigate the role of endogenous H2 S in TNF-alpha-induced insulin resistance by studying 3T3-L1 adipocytes. Hydrogen Sulfide 70-74 tumor necrosis factor Homo sapiens 78-87 23080424-4 2013 The aim of the present study is to investigate the role of endogenous H2 S in TNF-alpha-induced insulin resistance by studying 3T3-L1 adipocytes. Hydrogen Sulfide 70-74 insulin Homo sapiens 96-103 23080424-5 2013 We found that treatment of 3T3-L1 adipocytes with TNF-alpha leads to deficiency in insulin-stimulated glucose consumption and uptake and increase in endogenous H2 S generation. Hydrogen Sulfide 160-164 tumor necrosis factor Homo sapiens 50-59 23080424-6 2013 We show that cystathionine gamma-lyase (CSE) is catalysed in 3T3-L1 adipocytes to generate H2 S and that CSE expression and activity are upregulated by TNF-alpha treatment. Hydrogen Sulfide 91-95 cystathionine gamma-lyase Homo sapiens 13-38 23080424-6 2013 We show that cystathionine gamma-lyase (CSE) is catalysed in 3T3-L1 adipocytes to generate H2 S and that CSE expression and activity are upregulated by TNF-alpha treatment. Hydrogen Sulfide 91-95 cystathionine gamma-lyase Homo sapiens 40-43 23080424-6 2013 We show that cystathionine gamma-lyase (CSE) is catalysed in 3T3-L1 adipocytes to generate H2 S and that CSE expression and activity are upregulated by TNF-alpha treatment. Hydrogen Sulfide 91-95 tumor necrosis factor Homo sapiens 152-161 23515848-1 2013 Cystathionine gamma-lyase (CSE), one of three enzymes in the trans-sulfuration pathway, is responsible for the production of endogenous hydrogen sulfide (H2S) using L-cysteine or L-homocysteine as a substrate. Hydrogen Sulfide 136-152 cystathionine gamma-lyase Homo sapiens 0-25 23515848-1 2013 Cystathionine gamma-lyase (CSE), one of three enzymes in the trans-sulfuration pathway, is responsible for the production of endogenous hydrogen sulfide (H2S) using L-cysteine or L-homocysteine as a substrate. Hydrogen Sulfide 136-152 cystathionine gamma-lyase Homo sapiens 27-30 23515848-1 2013 Cystathionine gamma-lyase (CSE), one of three enzymes in the trans-sulfuration pathway, is responsible for the production of endogenous hydrogen sulfide (H2S) using L-cysteine or L-homocysteine as a substrate. Hydrogen Sulfide 154-157 cystathionine gamma-lyase Homo sapiens 0-25 23515848-1 2013 Cystathionine gamma-lyase (CSE), one of three enzymes in the trans-sulfuration pathway, is responsible for the production of endogenous hydrogen sulfide (H2S) using L-cysteine or L-homocysteine as a substrate. Hydrogen Sulfide 154-157 cystathionine gamma-lyase Homo sapiens 27-30 23515848-2 2013 The regulatory mechanism of CSE by exogenous H2S remains unknown. Hydrogen Sulfide 45-48 cystathionine gamma-lyase Homo sapiens 28-31 23515848-3 2013 The transcription and expression of the CSE gene regulated by exogenous H2S at approximately physiologic concentrations was investigated using luciferase assay, Western blotting, and quantitative RT-PCR. Hydrogen Sulfide 72-75 cystathionine gamma-lyase Homo sapiens 40-43 23515848-4 2013 The results revealed that exogenous H2S down-regulates the transcription and expression of CSE in mammalian cells at 10-80 muM. Hydrogen Sulfide 36-39 cystathionine gamma-lyase Homo sapiens 91-94 23996754-6 2013 Plasma H2S/kidney CSE level was significantly increased following NaHS intervention (P<0.01), which reduce the damage of the kidney tissue and significantly lower plasma and renal KIM-1, NO, BUN, Cr, MPO, and MDA (P<0.01). Hydrogen Sulfide 7-10 hepatitis A virus cellular receptor 1 Rattus norvegicus 183-188 23454157-3 2013 RESULTS: On phenylephrine contracted preparations electrical field stimulation and the H2S donor GYY4137 evoked frequency and concentration dependent relaxation, which was reduced by desensitizing capsaicin sensitive primary afferents with capsaicin, and the blockade of adenosine 5"-triphosphate dependent K(+) channels, cyclooxygenase and cyclooxygenase-1 with glibenclamide, indomethacin and SC560, respectively. Hydrogen Sulfide 87-90 prostaglandin-endoperoxide synthase 1 Homo sapiens 341-357 23454157-9 2013 H2S also promotes the release of sensory neuropeptides and cyclooxygenase-1 pathway derived prostanoids from capsaicin sensitive primary afferents via transient receptor potential A1, transient receptor potential vanilloid 1 and/or related ion channel activation. Hydrogen Sulfide 0-3 prostaglandin-endoperoxide synthase 1 Sus scrofa 59-75 23996754-6 2013 Plasma H2S/kidney CSE level was significantly increased following NaHS intervention (P<0.01), which reduce the damage of the kidney tissue and significantly lower plasma and renal KIM-1, NO, BUN, Cr, MPO, and MDA (P<0.01). Hydrogen Sulfide 7-10 myeloperoxidase Rattus norvegicus 203-206 23702336-0 2013 Hydrogen sulfide restores a normal morphological phenotype in Werner syndrome fibroblasts, attenuates oxidative damage and modulates mTOR pathway. Hydrogen Sulfide 0-16 mechanistic target of rapamycin kinase Homo sapiens 133-137 23702336-4 2013 As we found that the expression levels of the two main H2S producing enzymes, cystathionine beta synthase and cystathionine gamma lyase, were lower in WS cells compared to normal, we investigated the effect of administration of H2S as NaHS (50muM). Hydrogen Sulfide 55-58 cystathionine beta-synthase Homo sapiens 78-105 24187829-9 2013 The results showed that PAG and CSE siRNA could significantly decrease the production of H2S in HepG2 cells and inhibit the proliferation of HepG2 cells at a dose-dependent and time-dependent manner, respectively. Hydrogen Sulfide 89-92 choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity) Homo sapiens 32-35 24187829-13 2013 These results suggested that the CSE/H2S pathway was involved in suppression of HepG2 cell growth and promoted apoptosis of HepG2 cells in an oxidative stress-dependent manner. Hydrogen Sulfide 37-40 choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity) Homo sapiens 33-36 23904600-5 2013 The H2S-producing enzyme cystathionine-gamma-lyase (CSE) was expressed in both neurons and glial cells. Hydrogen Sulfide 4-7 cystathionase (cystathionine gamma-lyase) Mus musculus 25-50 23904600-5 2013 The H2S-producing enzyme cystathionine-gamma-lyase (CSE) was expressed in both neurons and glial cells. Hydrogen Sulfide 4-7 cystathionase (cystathionine gamma-lyase) Mus musculus 52-55 23858469-2 2013 Cystathionine beta-synthase (CBS) contains a prosthetic heme group and catalyzes the production of hydrogen sulfide in mammalian cells. Hydrogen Sulfide 99-115 cystathionine beta-synthase Homo sapiens 0-27 23836652-0 2013 Tumor-derived hydrogen sulfide, produced by cystathionine-beta-synthase, stimulates bioenergetics, cell proliferation, and angiogenesis in colon cancer. Hydrogen Sulfide 14-30 cystathionine beta-synthase Homo sapiens 44-71 23836652-2 2013 Analysis of human colon cancer biopsies and patient-matched normal margin mucosa revealed the selective up-regulation of the H2S-producing enzyme cystathionine-beta-synthase (CBS) in colon cancer, resulting in an increased rate of H2S production. Hydrogen Sulfide 125-128 cystathionine beta-synthase Homo sapiens 146-173 23836652-2 2013 Analysis of human colon cancer biopsies and patient-matched normal margin mucosa revealed the selective up-regulation of the H2S-producing enzyme cystathionine-beta-synthase (CBS) in colon cancer, resulting in an increased rate of H2S production. Hydrogen Sulfide 125-128 cystathionine beta-synthase Homo sapiens 175-178 23836652-2 2013 Analysis of human colon cancer biopsies and patient-matched normal margin mucosa revealed the selective up-regulation of the H2S-producing enzyme cystathionine-beta-synthase (CBS) in colon cancer, resulting in an increased rate of H2S production. Hydrogen Sulfide 231-234 cystathionine beta-synthase Homo sapiens 146-173 23836652-2 2013 Analysis of human colon cancer biopsies and patient-matched normal margin mucosa revealed the selective up-regulation of the H2S-producing enzyme cystathionine-beta-synthase (CBS) in colon cancer, resulting in an increased rate of H2S production. Hydrogen Sulfide 231-234 cystathionine beta-synthase Homo sapiens 175-178 23836652-7 2013 Similarly, CBS silencing of the tumor cells decreased xenograft growth and suppressed neovessel density, suggesting a role for endogenous H2S in tumor angiogenesis. Hydrogen Sulfide 138-141 cystathionine beta-synthase Homo sapiens 11-14 23836652-9 2013 In conclusion, H2S produced from CBS serves to (i) maintain colon cancer cellular bioenergetics, thereby supporting tumor growth and proliferation, and (ii) promote angiogenesis and vasorelaxation, consequently providing the tumor with blood and nutritients. Hydrogen Sulfide 15-18 cystathionine beta-synthase Homo sapiens 33-36 23836652-10 2013 The current findings identify CBS-derived H2S as a tumor growth factor and anticancer drug target. Hydrogen Sulfide 42-45 cystathionine beta-synthase Homo sapiens 30-33 23882260-3 2013 H2S is produced by enzymes from l-cysteine; cystathionine beta-synthase, cystathionine gamma-lyase, and 3-mercaptopyruvate sulfurtransferase (3MST) along with cysteine aminotransferase. Hydrogen Sulfide 0-3 cystathionine beta-synthase Homo sapiens 44-71 23882260-3 2013 H2S is produced by enzymes from l-cysteine; cystathionine beta-synthase, cystathionine gamma-lyase, and 3-mercaptopyruvate sulfurtransferase (3MST) along with cysteine aminotransferase. Hydrogen Sulfide 0-3 cystathionine gamma-lyase Homo sapiens 73-98 23882260-3 2013 H2S is produced by enzymes from l-cysteine; cystathionine beta-synthase, cystathionine gamma-lyase, and 3-mercaptopyruvate sulfurtransferase (3MST) along with cysteine aminotransferase. Hydrogen Sulfide 0-3 mercaptopyruvate sulfurtransferase Homo sapiens 104-140 23858469-2 2013 Cystathionine beta-synthase (CBS) contains a prosthetic heme group and catalyzes the production of hydrogen sulfide in mammalian cells. Hydrogen Sulfide 99-115 cystathionine beta-synthase Homo sapiens 29-32 23858469-7 2013 The accumulation of CBS in mitochondria increased hydrogen sulfide production, which prevented Ca(2+)-mediated cytochrome c release from mitochondria and decreased reactive oxygen species generation. Hydrogen Sulfide 50-66 cystathionine beta-synthase Homo sapiens 20-23 23858469-7 2013 The accumulation of CBS in mitochondria increased hydrogen sulfide production, which prevented Ca(2+)-mediated cytochrome c release from mitochondria and decreased reactive oxygen species generation. Hydrogen Sulfide 50-66 cytochrome c, somatic Homo sapiens 111-123 23698001-0 2013 Structure and kinetic analysis of H2S production by human mercaptopyruvate sulfurtransferase. Hydrogen Sulfide 34-37 mercaptopyruvate sulfurtransferase Homo sapiens 58-92 23698001-4 2013 The kinetics of H2S production by MST from 3-MP was studied at pH 7.4 in the presence of various physiological persulfide acceptors: cysteine, dihydrolipoic acid, glutathione, homocysteine, and thioredoxin, and in the presence of cyanide. Hydrogen Sulfide 16-19 mercaptopyruvate sulfurtransferase Homo sapiens 34-37 23698001-4 2013 The kinetics of H2S production by MST from 3-MP was studied at pH 7.4 in the presence of various physiological persulfide acceptors: cysteine, dihydrolipoic acid, glutathione, homocysteine, and thioredoxin, and in the presence of cyanide. Hydrogen Sulfide 16-19 thioredoxin Homo sapiens 194-205 23293908-0 2013 Hydrogen sulfide treatment promotes glucose uptake by increasing insulin receptor sensitivity and ameliorates kidney lesions in type 2 diabetes. Hydrogen Sulfide 0-16 insulin receptor Rattus norvegicus 65-81 23425024-2 2013 "Hydrogen sulfide treatment promotes glucose uptake by increasing insulin receptor sensitivity and ameliorates kidney lesions in type 2 diabetes." Hydrogen Sulfide 1-17 insulin receptor Homo sapiens 66-82 23885269-6 2013 Moreover, we found that H2S dramatically suppressed the release of TNF-alpha, IL-1beta and IL-6 in the hippocampus. Hydrogen Sulfide 24-27 tumor necrosis factor Rattus norvegicus 67-76 23885269-6 2013 Moreover, we found that H2S dramatically suppressed the release of TNF-alpha, IL-1beta and IL-6 in the hippocampus. Hydrogen Sulfide 24-27 interleukin 1 beta Rattus norvegicus 78-86 23885269-6 2013 Moreover, we found that H2S dramatically suppressed the release of TNF-alpha, IL-1beta and IL-6 in the hippocampus. Hydrogen Sulfide 24-27 interleukin 6 Rattus norvegicus 91-95 23885269-7 2013 Consistently, both immunohistochemistry and Western blotting assays showed that H2S inhibited the upregulation of COX-2 and the activation of NF-kappaB in the hippocampus. Hydrogen Sulfide 80-83 cytochrome c oxidase II, mitochondrial Rattus norvegicus 114-119 23180220-1 2013 L-Cysteine desulfhydrase (DES; EC 4.4.1.1) is the most important enzyme that catalyzes the decomposition of L-cysteine to pyruvate, ammonia, and hydrogen sulfide (H2S), the latter of which has recently been recognized as the third gasotransmitter for multiple signaling events in plants. Hydrogen Sulfide 145-161 L-cysteine desulfhydrase Brassica napus 0-24 23180220-1 2013 L-Cysteine desulfhydrase (DES; EC 4.4.1.1) is the most important enzyme that catalyzes the decomposition of L-cysteine to pyruvate, ammonia, and hydrogen sulfide (H2S), the latter of which has recently been recognized as the third gasotransmitter for multiple signaling events in plants. Hydrogen Sulfide 163-166 L-cysteine desulfhydrase Brassica napus 0-24 23624824-9 2013 Taken together, we demonstrated that p38MAPK-iNOS pathway contributes to chemical hypoxia-induced inflammation and that H2S produces an anti-inflammatory effect in chemical hypoxia-stimulated PC12 cells, which may be partly due to inhibition of ROS-activated p38MAPK-iNOS pathway. Hydrogen Sulfide 120-123 nitric oxide synthase 2 Rattus norvegicus 267-271 23790103-1 2013 Cystathionine beta-synthase (CBS) catalyzes the condensation of homocysteine with serine or cysteine to form cystathionine and water or hydrogen sulfide (H2S), respectively. Hydrogen Sulfide 136-152 cystathionine beta-synthase Homo sapiens 0-27 23790103-1 2013 Cystathionine beta-synthase (CBS) catalyzes the condensation of homocysteine with serine or cysteine to form cystathionine and water or hydrogen sulfide (H2S), respectively. Hydrogen Sulfide 136-152 cystathionine beta-synthase Homo sapiens 29-32 23790103-1 2013 Cystathionine beta-synthase (CBS) catalyzes the condensation of homocysteine with serine or cysteine to form cystathionine and water or hydrogen sulfide (H2S), respectively. Hydrogen Sulfide 154-157 cystathionine beta-synthase Homo sapiens 0-27 23790103-1 2013 Cystathionine beta-synthase (CBS) catalyzes the condensation of homocysteine with serine or cysteine to form cystathionine and water or hydrogen sulfide (H2S), respectively. Hydrogen Sulfide 154-157 cystathionine beta-synthase Homo sapiens 29-32 23297114-0 2013 Hydrogen sulfide reduces cell adhesion and relevant inflammatory triggering by preventing ADAM17-dependent TNF-alpha activation. Hydrogen Sulfide 0-16 ADAM metallopeptidase domain 17 Homo sapiens 90-96 23297114-0 2013 Hydrogen sulfide reduces cell adhesion and relevant inflammatory triggering by preventing ADAM17-dependent TNF-alpha activation. Hydrogen Sulfide 0-16 tumor necrosis factor Homo sapiens 107-116 23297114-3 2013 Results show that H2S prevents the increase in monocyte adhesion induced by tumor necrosis factor-alpha (TNF-alpha). Hydrogen Sulfide 18-21 tumor necrosis factor Homo sapiens 76-103 23297114-3 2013 Results show that H2S prevents the increase in monocyte adhesion induced by tumor necrosis factor-alpha (TNF-alpha). Hydrogen Sulfide 18-21 tumor necrosis factor Homo sapiens 105-114 23297114-7 2013 In addition, H2S significantly reduces activation of ADAM17 by PMA in endothelial cells, with consequent reduction of both ADAM17-dependent TNF-alpha ectodomain shedding and MCP-1 release. Hydrogen Sulfide 13-16 ADAM metallopeptidase domain 17 Homo sapiens 53-59 23297114-7 2013 In addition, H2S significantly reduces activation of ADAM17 by PMA in endothelial cells, with consequent reduction of both ADAM17-dependent TNF-alpha ectodomain shedding and MCP-1 release. Hydrogen Sulfide 13-16 ADAM metallopeptidase domain 17 Homo sapiens 123-129 23297114-7 2013 In addition, H2S significantly reduces activation of ADAM17 by PMA in endothelial cells, with consequent reduction of both ADAM17-dependent TNF-alpha ectodomain shedding and MCP-1 release. Hydrogen Sulfide 13-16 tumor necrosis factor Homo sapiens 140-149 23297114-7 2013 In addition, H2S significantly reduces activation of ADAM17 by PMA in endothelial cells, with consequent reduction of both ADAM17-dependent TNF-alpha ectodomain shedding and MCP-1 release. Hydrogen Sulfide 13-16 C-C motif chemokine ligand 2 Homo sapiens 174-179 23297114-8 2013 In conclusion, H2S is able to prevent endothelial activation by hampering endothelial activation, triggered by TNF-alpha. Hydrogen Sulfide 15-18 tumor necrosis factor Homo sapiens 111-120 23742697-6 2013 L-cysteine, a precursor of H2 S, stimulated NO production whereas blockage of the activity of H2 S-generating enzyme, cystathionine gamma-lyase (CSE), inhibited this action. Hydrogen Sulfide 94-98 cystathionine gamma-lyase Homo sapiens 118-143 23742697-6 2013 L-cysteine, a precursor of H2 S, stimulated NO production whereas blockage of the activity of H2 S-generating enzyme, cystathionine gamma-lyase (CSE), inhibited this action. Hydrogen Sulfide 94-98 cystathionine gamma-lyase Homo sapiens 145-148 23742697-8 2013 LY294002 (Akt/PI3-K inhibitor) or SB203580 (p38 MAPK inhibitor) abolished the effects of H2 S on eNOS phosphorylation, NO production, cell proliferation and tube formation. Hydrogen Sulfide 89-93 AKT serine/threonine kinase 1 Homo sapiens 10-13 23742697-8 2013 LY294002 (Akt/PI3-K inhibitor) or SB203580 (p38 MAPK inhibitor) abolished the effects of H2 S on eNOS phosphorylation, NO production, cell proliferation and tube formation. Hydrogen Sulfide 89-93 nitric oxide synthase 3 Homo sapiens 97-101 23742697-9 2013 Blockade of NO production by eNOS-specific siRNA or nitro-L-arginine methyl ester (L-NAME) reversed, but eNOS overexpression potentiated, the proliferative effect of H2 S on ECs. Hydrogen Sulfide 166-170 nitric oxide synthase 3 Homo sapiens 29-33 23742697-9 2013 Blockade of NO production by eNOS-specific siRNA or nitro-L-arginine methyl ester (L-NAME) reversed, but eNOS overexpression potentiated, the proliferative effect of H2 S on ECs. Hydrogen Sulfide 166-170 nitric oxide synthase 3 Homo sapiens 105-109 23742697-10 2013 Our results suggest that H2 S stimulates the phosphorylation of eNOS through a p38 MAPK and Akt-dependent pathway, thus increasing NO production in ECs and vascular tissues and contributing to H2 S-induced angiogenesis. Hydrogen Sulfide 25-29 nitric oxide synthase 3 Homo sapiens 64-68 23742697-10 2013 Our results suggest that H2 S stimulates the phosphorylation of eNOS through a p38 MAPK and Akt-dependent pathway, thus increasing NO production in ECs and vascular tissues and contributing to H2 S-induced angiogenesis. Hydrogen Sulfide 25-29 AKT serine/threonine kinase 1 Homo sapiens 92-95 23742697-10 2013 Our results suggest that H2 S stimulates the phosphorylation of eNOS through a p38 MAPK and Akt-dependent pathway, thus increasing NO production in ECs and vascular tissues and contributing to H2 S-induced angiogenesis. Hydrogen Sulfide 193-197 nitric oxide synthase 3 Homo sapiens 64-68 23742697-10 2013 Our results suggest that H2 S stimulates the phosphorylation of eNOS through a p38 MAPK and Akt-dependent pathway, thus increasing NO production in ECs and vascular tissues and contributing to H2 S-induced angiogenesis. Hydrogen Sulfide 193-197 AKT serine/threonine kinase 1 Homo sapiens 92-95 23613529-7 2013 It has also been found that nucleotides such as ATP act as mediators of chemically induced nociception and pain and gases, such as hydrogen sulphide and nitric oxide, lead to TRPV1 activation. Hydrogen Sulfide 131-148 transient receptor potential cation channel subfamily V member 1 Homo sapiens 175-180 23698001-1 2013 Mercaptopyruvate sulfurtransferase (MST) is a source of endogenous H2S, a gaseous signaling molecule implicated in a wide range of physiological processes. Hydrogen Sulfide 67-70 mercaptopyruvate sulfurtransferase Homo sapiens 0-34 23698001-1 2013 Mercaptopyruvate sulfurtransferase (MST) is a source of endogenous H2S, a gaseous signaling molecule implicated in a wide range of physiological processes. Hydrogen Sulfide 67-70 mercaptopyruvate sulfurtransferase Homo sapiens 36-39 22657153-5 2013 Concentrations of homocysteine and H(2)S in the plasma of control MsrA(-/-) mice were significantly lower than those in control MsrA(+/+) mice. Hydrogen Sulfide 35-40 methionine sulfoxide reductase A Mus musculus 66-70 23805308-1 2013 3-Mercaptopyruvate sulfurtransferase (3MST) is an important enzyme for the synthesis of hydrogen sulfide (H2S) in the brain. Hydrogen Sulfide 88-104 mercaptopyruvate sulfurtransferase Homo sapiens 0-36 23805308-1 2013 3-Mercaptopyruvate sulfurtransferase (3MST) is an important enzyme for the synthesis of hydrogen sulfide (H2S) in the brain. Hydrogen Sulfide 88-104 mercaptopyruvate sulfurtransferase Homo sapiens 38-42 23805308-1 2013 3-Mercaptopyruvate sulfurtransferase (3MST) is an important enzyme for the synthesis of hydrogen sulfide (H2S) in the brain. Hydrogen Sulfide 106-109 mercaptopyruvate sulfurtransferase Homo sapiens 0-36 23805308-1 2013 3-Mercaptopyruvate sulfurtransferase (3MST) is an important enzyme for the synthesis of hydrogen sulfide (H2S) in the brain. Hydrogen Sulfide 106-109 mercaptopyruvate sulfurtransferase Homo sapiens 38-42 23805308-7 2013 Therefore, cystathionine beta-synthase (CBS), the alternative H2S producing enzyme in the CNS, remains as a more likely potential therapeutic target than 3MST in the treatment of acute stroke through inhibition of H2S production. Hydrogen Sulfide 62-65 cystathionine beta-synthase Homo sapiens 11-38 23805308-7 2013 Therefore, cystathionine beta-synthase (CBS), the alternative H2S producing enzyme in the CNS, remains as a more likely potential therapeutic target than 3MST in the treatment of acute stroke through inhibition of H2S production. Hydrogen Sulfide 62-65 cystathionine beta-synthase Homo sapiens 40-43 23805308-7 2013 Therefore, cystathionine beta-synthase (CBS), the alternative H2S producing enzyme in the CNS, remains as a more likely potential therapeutic target than 3MST in the treatment of acute stroke through inhibition of H2S production. Hydrogen Sulfide 214-217 cystathionine beta-synthase Homo sapiens 11-38 23805308-7 2013 Therefore, cystathionine beta-synthase (CBS), the alternative H2S producing enzyme in the CNS, remains as a more likely potential therapeutic target than 3MST in the treatment of acute stroke through inhibition of H2S production. Hydrogen Sulfide 214-217 cystathionine beta-synthase Homo sapiens 40-43 23774934-5 2013 This simple method was used to access the H2S release in HepG2 (high expression CBS and CSE) and HUVEC (low expression CSE) cell lines. Hydrogen Sulfide 42-45 choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity) Homo sapiens 88-91 23774934-5 2013 This simple method was used to access the H2S release in HepG2 (high expression CBS and CSE) and HUVEC (low expression CSE) cell lines. Hydrogen Sulfide 42-45 choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity) Homo sapiens 119-122 23774934-7 2013 PAG (CSE inhibitor), HA (CBS inhibitor) or the two-inhibitor (PAG+HA) treatment significantly lowered H2S release, respectively: (341.34+-105.90) nmol/(minx10(6) cells), (375.05+-174.50) nmol/(minx10(6) cells), and (204.47+-97.14) nmol/(minx10(6) cells). Hydrogen Sulfide 102-105 choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity) Homo sapiens 5-8 23632630-0 2013 Hydrogen sulfide deficiency and diabetic renal remodeling: role of matrix metalloproteinase-9. Hydrogen Sulfide 0-16 matrix metallopeptidase 9 Mus musculus 67-93 23632630-6 2013 H2S-synthesizing enzymes cystathionine-beta-synthase and cystathionine-gamma-lyase were also diminished. Hydrogen Sulfide 0-3 cystathionine beta-synthase Mus musculus 25-52 23632630-6 2013 H2S-synthesizing enzymes cystathionine-beta-synthase and cystathionine-gamma-lyase were also diminished. Hydrogen Sulfide 0-3 cystathionase (cystathionine gamma-lyase) Mus musculus 57-82 23632630-13 2013 Silencing MMP-9 by siRNA or inhibition of NMDA-R1 by MK801 or H2S treatment preserved connexin-40 and -43. Hydrogen Sulfide 62-65 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 42-49 23632630-13 2013 Silencing MMP-9 by siRNA or inhibition of NMDA-R1 by MK801 or H2S treatment preserved connexin-40 and -43. Hydrogen Sulfide 62-65 gap junction protein, alpha 5 Mus musculus 86-105 22657153-6 2013 I/R reduced the levels of homocysteine and H(2)S in both MsrA(+/+) and MsrA(-/-) mice, and these reductions were significantly more profound in MsrA(-/-) than in MsrA(+/+) mice. Hydrogen Sulfide 43-48 methionine sulfoxide reductase A Mus musculus 57-61 22657153-6 2013 I/R reduced the levels of homocysteine and H(2)S in both MsrA(+/+) and MsrA(-/-) mice, and these reductions were significantly more profound in MsrA(-/-) than in MsrA(+/+) mice. Hydrogen Sulfide 43-48 methionine sulfoxide reductase A Mus musculus 71-75 22657153-6 2013 I/R reduced the levels of homocysteine and H(2)S in both MsrA(+/+) and MsrA(-/-) mice, and these reductions were significantly more profound in MsrA(-/-) than in MsrA(+/+) mice. Hydrogen Sulfide 43-48 methionine sulfoxide reductase A Mus musculus 71-75 22657153-6 2013 I/R reduced the levels of homocysteine and H(2)S in both MsrA(+/+) and MsrA(-/-) mice, and these reductions were significantly more profound in MsrA(-/-) than in MsrA(+/+) mice. Hydrogen Sulfide 43-48 methionine sulfoxide reductase A Mus musculus 71-75 22657153-7 2013 I/R reduced the expression and activities of cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE), both of which are H(2)S-producing enzymes, in the kidneys. Hydrogen Sulfide 134-139 cystathionine beta-synthase Mus musculus 45-72 22657153-7 2013 I/R reduced the expression and activities of cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE), both of which are H(2)S-producing enzymes, in the kidneys. Hydrogen Sulfide 134-139 cystathionase (cystathionine gamma-lyase) Mus musculus 83-108 22657153-7 2013 I/R reduced the expression and activities of cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE), both of which are H(2)S-producing enzymes, in the kidneys. Hydrogen Sulfide 134-139 cystathionase (cystathionine gamma-lyase) Mus musculus 110-113 22657153-11 2013 The data indicate that MsrA regulates H(2)S production during I/R by modulating the expression and activity of the CBS and CSE enzymes. Hydrogen Sulfide 38-43 methionine sulfoxide reductase A Mus musculus 23-27 22657153-11 2013 The data indicate that MsrA regulates H(2)S production during I/R by modulating the expression and activity of the CBS and CSE enzymes. Hydrogen Sulfide 38-43 cystathionase (cystathionine gamma-lyase) Mus musculus 123-126 23525712-2 2013 This effect of H2S to cause vasodilation and vascular smooth muscle cell (VSMC) hyperpolarization was mediated by large-conductance Ca(2+)-activated potassium channels (BKCa). Hydrogen Sulfide 15-18 potassium calcium-activated channel subfamily M alpha 1 Rattus norvegicus 169-173 23525712-7 2013 In PE-constricted arteries, the H2S donor NaHS caused vasodilation that was inhibited by ryanodine (RyR blocker), abluminal or luminal iberiotoxin (IbTx, BKCa blocker), endothelial cell (EC) disruption, and sulfaphenazole [cytochrome P-450 2C (Cyp2C) inhibitor]. Hydrogen Sulfide 32-35 ryanodine receptor 2 Homo sapiens 100-103 23525712-7 2013 In PE-constricted arteries, the H2S donor NaHS caused vasodilation that was inhibited by ryanodine (RyR blocker), abluminal or luminal iberiotoxin (IbTx, BKCa blocker), endothelial cell (EC) disruption, and sulfaphenazole [cytochrome P-450 2C (Cyp2C) inhibitor]. Hydrogen Sulfide 32-35 potassium calcium-activated channel subfamily M alpha 1 Rattus norvegicus 154-158 23525712-7 2013 In PE-constricted arteries, the H2S donor NaHS caused vasodilation that was inhibited by ryanodine (RyR blocker), abluminal or luminal iberiotoxin (IbTx, BKCa blocker), endothelial cell (EC) disruption, and sulfaphenazole [cytochrome P-450 2C (Cyp2C) inhibitor]. Hydrogen Sulfide 32-35 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 223-242 23525712-7 2013 In PE-constricted arteries, the H2S donor NaHS caused vasodilation that was inhibited by ryanodine (RyR blocker), abluminal or luminal iberiotoxin (IbTx, BKCa blocker), endothelial cell (EC) disruption, and sulfaphenazole [cytochrome P-450 2C (Cyp2C) inhibitor]. Hydrogen Sulfide 32-35 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 244-249 23525712-9 2013 Inhibiting cystathionine gamma-lyase (CSE)-derived H2S with beta-cyano-l-alanine (BCA) also reduced VSMC Ca(2+) spark frequency in mesenteric arteries, as did EC disruption. Hydrogen Sulfide 51-54 cystathionine gamma-lyase Rattus norvegicus 11-36 23525712-9 2013 Inhibiting cystathionine gamma-lyase (CSE)-derived H2S with beta-cyano-l-alanine (BCA) also reduced VSMC Ca(2+) spark frequency in mesenteric arteries, as did EC disruption. Hydrogen Sulfide 51-54 cystathionine gamma-lyase Rattus norvegicus 38-41 23525712-14 2013 These results suggest that H2S increases Ca(2+) spark activity in mesenteric artery VSMC through activation of endothelial BKCa channels and Cyp2C, a novel vasodilatory pathway for this emerging signaling molecule. Hydrogen Sulfide 27-30 potassium calcium-activated channel subfamily M alpha 1 Rattus norvegicus 123-127 23525712-14 2013 These results suggest that H2S increases Ca(2+) spark activity in mesenteric artery VSMC through activation of endothelial BKCa channels and Cyp2C, a novel vasodilatory pathway for this emerging signaling molecule. Hydrogen Sulfide 27-30 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 141-146 23499876-0 2013 Brg1-dependent epigenetic control of vascular smooth muscle cell proliferation by hydrogen sulfide. Hydrogen Sulfide 82-98 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 0-4 23499876-3 2013 Microarray analysis indicated that Brahma-related gene 1 (Brg1) and proliferation-related genes including proliferating cell nuclear antigen (Pcna), neurotrophin 3 (Ntf3) and platelet-derived growth factor subunit A (Pdgfalpha) were significantly downregulated by H2S in endothelin-1-stimulated proliferative vascular smooth muscle cells. Hydrogen Sulfide 264-267 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 35-56 23499876-5 2013 Overexpression and knockdown of Brg1 confirmed that Brg1 was crucial for H2S-induced inhibition of vascular smooth muscle cell proliferation. Hydrogen Sulfide 73-76 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 32-36 23499876-5 2013 Overexpression and knockdown of Brg1 confirmed that Brg1 was crucial for H2S-induced inhibition of vascular smooth muscle cell proliferation. Hydrogen Sulfide 73-76 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 52-56 23499876-6 2013 A luciferase reporter assay, real-time PCR and Western blotting demonstrated that H2S inhibited Brg1 transcription and expression. Hydrogen Sulfide 82-85 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 96-100 23499876-7 2013 A DNase I hypersensitivity assay revealed that H2S reversed endothelin-1-stimulated Pcna, Ntf3 and Pdgfalpha chromatin remodeling and vascular smooth muscle cell proliferation. Hydrogen Sulfide 47-50 endothelin 1 Homo sapiens 60-72 23499876-7 2013 A DNase I hypersensitivity assay revealed that H2S reversed endothelin-1-stimulated Pcna, Ntf3 and Pdgfalpha chromatin remodeling and vascular smooth muscle cell proliferation. Hydrogen Sulfide 47-50 proliferating cell nuclear antigen Homo sapiens 84-88 23499876-7 2013 A DNase I hypersensitivity assay revealed that H2S reversed endothelin-1-stimulated Pcna, Ntf3 and Pdgfalpha chromatin remodeling and vascular smooth muscle cell proliferation. Hydrogen Sulfide 47-50 neurotrophin 3 Homo sapiens 90-94 23499876-8 2013 A chromatin immunoprecipitation assay indicated that H2S inhibited the recruitment of Brg1 to the Pcna, Ntf3 and Pdgfalpha promoters. Hydrogen Sulfide 53-56 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 86-90 23499876-8 2013 A chromatin immunoprecipitation assay indicated that H2S inhibited the recruitment of Brg1 to the Pcna, Ntf3 and Pdgfalpha promoters. Hydrogen Sulfide 53-56 proliferating cell nuclear antigen Homo sapiens 98-102 23499876-8 2013 A chromatin immunoprecipitation assay indicated that H2S inhibited the recruitment of Brg1 to the Pcna, Ntf3 and Pdgfalpha promoters. Hydrogen Sulfide 53-56 neurotrophin 3 Homo sapiens 104-108 23499876-9 2013 The results of this study indicate that H2S inhibits vascular smooth muscle cell proliferation via an epigenetic mechanism involving the inhibition of Brg1 transcription and expression, and by reducing the recruitment of Brg1 to the Pcna, Ntf3 and Pdgfalpha promoter regions. Hydrogen Sulfide 40-43 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 151-155 23499876-9 2013 The results of this study indicate that H2S inhibits vascular smooth muscle cell proliferation via an epigenetic mechanism involving the inhibition of Brg1 transcription and expression, and by reducing the recruitment of Brg1 to the Pcna, Ntf3 and Pdgfalpha promoter regions. Hydrogen Sulfide 40-43 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 221-225 23499876-9 2013 The results of this study indicate that H2S inhibits vascular smooth muscle cell proliferation via an epigenetic mechanism involving the inhibition of Brg1 transcription and expression, and by reducing the recruitment of Brg1 to the Pcna, Ntf3 and Pdgfalpha promoter regions. Hydrogen Sulfide 40-43 proliferating cell nuclear antigen Homo sapiens 233-237 23499876-9 2013 The results of this study indicate that H2S inhibits vascular smooth muscle cell proliferation via an epigenetic mechanism involving the inhibition of Brg1 transcription and expression, and by reducing the recruitment of Brg1 to the Pcna, Ntf3 and Pdgfalpha promoter regions. Hydrogen Sulfide 40-43 neurotrophin 3 Homo sapiens 239-243 23488457-2 2013 Two major sources for endogenous enzymatic production of H2S are cystathionine beta synthase (CBS) and cystathionine gamma lyase (CSE). Hydrogen Sulfide 57-60 cystathionine beta-synthase Homo sapiens 65-92 23488457-2 2013 Two major sources for endogenous enzymatic production of H2S are cystathionine beta synthase (CBS) and cystathionine gamma lyase (CSE). Hydrogen Sulfide 57-60 cystathionine beta-synthase Homo sapiens 94-97 23488457-3 2013 In the present study, we examined the selectivity of commonly used pharmacological inhibitors of H2S biosynthesis towards CSE and CBS. Hydrogen Sulfide 97-100 cystathionine beta-synthase Homo sapiens 130-133 23488457-10 2013 Trifluoroalanine and hydroxylamine, two compounds that have also been used to block H2S biosynthesis, blocked the activity of CBS and CSE. Hydrogen Sulfide 84-87 cystathionine beta-synthase Homo sapiens 126-129 23307012-6 2013 Treatment with H2S abated hyperoxia-induced oxidative stress marked by reduced malondialdehyde and peroxynitrite formation, reduced NADPH oxidase activity, enhanced translocation of nuclear factor E2-related factor (Nrf2) into nucleus and increased activity of HO-1. Hydrogen Sulfide 15-18 nuclear factor, erythroid derived 2, like 2 Mus musculus 216-220 23307012-7 2013 Treatment with H2S decreased IL-1beta, MCP-1, and MIP-2, and increased IL-10 expression in lungs of mice exposed to hyperoxia. Hydrogen Sulfide 15-18 interleukin 1 beta Mus musculus 29-37 23307012-7 2013 Treatment with H2S decreased IL-1beta, MCP-1, and MIP-2, and increased IL-10 expression in lungs of mice exposed to hyperoxia. Hydrogen Sulfide 15-18 mast cell protease 1 Mus musculus 39-44 23307012-7 2013 Treatment with H2S decreased IL-1beta, MCP-1, and MIP-2, and increased IL-10 expression in lungs of mice exposed to hyperoxia. Hydrogen Sulfide 15-18 chemokine (C-X-C motif) ligand 2 Mus musculus 50-55 23307012-7 2013 Treatment with H2S decreased IL-1beta, MCP-1, and MIP-2, and increased IL-10 expression in lungs of mice exposed to hyperoxia. Hydrogen Sulfide 15-18 interleukin 10 Mus musculus 71-76 23307012-8 2013 Treatment with H2S decreased NFkappaB activity and iNOS expression in lungs, and reduced NOx content in BAL of mice exposed to hyperoxia. Hydrogen Sulfide 15-18 nitric oxide synthase 2, inducible Mus musculus 51-55 23307012-9 2013 Treatment with H2S reduced lung permeability and suppressed VEGF release and VEGFR2 expression in lungs of mice under oxygen exposure. Hydrogen Sulfide 15-18 kinase insert domain protein receptor Mus musculus 77-83 23131022-6 2013 Moreover, the results of western blotting further proved that H2 S inhibited the expression of UII. Hydrogen Sulfide 62-66 urotensin 2 Homo sapiens 95-98 23131022-0 2013 H2 S inhibits the activation of hepatic stellate cells and downregulates the expression of urotensin II. Hydrogen Sulfide 0-4 urotensin 2 Homo sapiens 91-103 23131022-8 2013 Similarly, the examination of cell apoptosis revealed that H2 S could promote LX-2 cell apoptosis and inhibit the apoptosis-inhibiting effect of UII. Hydrogen Sulfide 59-63 urotensin 2 Homo sapiens 145-148 23131022-9 2013 CONCLUSION: H2 S suppresses fibrosis by inhibiting the activation of hepatic stellate cells and reducing the expression of UII. Hydrogen Sulfide 12-16 urotensin 2 Homo sapiens 123-126 23947022-5 2013 The main gaseous products of CS2 decomposition with the addition of O2 in Ar gas were CO, CO2 COS and SO2, while, with the presence of H2 in Ar gas, the main products of CS2 decomposition were H2S and CH4. Hydrogen Sulfide 193-196 chorionic somatomammotropin hormone 2 Homo sapiens 170-173 23151462-6 2013 In the liver, endotoxemia induced a significant increase in the H2S concentration, and in the expression of the H2S-synthesizing enzymes CSE. Hydrogen Sulfide 112-115 cystathionine gamma-lyase Rattus norvegicus 137-140 23030661-0 2013 p53-Pathway activity and apoptosis in hydrogen sulfide-exposed stem cells separated from human gingival epithelium. Hydrogen Sulfide 38-54 tumor protein p53 Homo sapiens 0-3 23030661-7 2013 The main objective of the present study was to explore the implications of the p53 pathway in OKSCs following exposure to H2S. Hydrogen Sulfide 122-125 tumor protein p53 Homo sapiens 79-82 23588928-0 2013 Hydrogen sulfide prevents H2O2-induced senescence in human umbilical vein endothelial cells through SIRT1 activation. Hydrogen Sulfide 0-16 sirtuin 1 Homo sapiens 100-105 23588928-2 2013 Senescence was induced in human umbilical vein endothelial cells (HUVECs) by incubation in 25 micromol/l H2O2 for 1 h. Senescence-associated beta-galactosidase (SA-beta-gal) activity was examined to determine the effects of H2S on senescent HUVECs. Hydrogen Sulfide 224-227 SH3 domain binding protein 5 Homo sapiens 161-168 23588928-4 2013 Pretreatment with nicotinamide (NAM), a sirtuin 1 (SIRT1) inhibitor, inhibited the reduction in senescence associated with H2S. Hydrogen Sulfide 123-126 sirtuin 1 Homo sapiens 40-49 23588928-4 2013 Pretreatment with nicotinamide (NAM), a sirtuin 1 (SIRT1) inhibitor, inhibited the reduction in senescence associated with H2S. Hydrogen Sulfide 123-126 sirtuin 1 Homo sapiens 51-56 23588928-7 2013 The present study demonstrated that H2S protects against HUVEC senescence, potentially through modulation of SIRT1 activity. Hydrogen Sulfide 36-39 sirtuin 1 Homo sapiens 109-114 23176571-0 2013 Hydrogen sulfide protects against cellular senescence via S-sulfhydration of Keap1 and activation of Nrf2. Hydrogen Sulfide 0-16 kelch-like ECH-associated protein 1 Mus musculus 77-82 23827060-4 2013 CONCLUSION: H2S has protective effects on cerebral ischemia and reperfusion,which may be achieved by improving SOD activity,removing oxygen free radicals,inhibiting lipid peroxidation,and down-regulating the expression of HSP70 in the hippocampus. Hydrogen Sulfide 12-15 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 222-227 23741314-0 2013 Hydrogen sulfide prevents hydrogen peroxide-induced activation of epithelial sodium channel through a PTEN/PI(3,4,5)P3 dependent pathway. Hydrogen Sulfide 0-16 phosphatase and tensin homolog Homo sapiens 102-106 23741314-9 2013 In addition, H2S significantly inhibited H2O2-induced oxidative inactivation of the tumor suppressor phosphatase and tensin homolog (PTEN) which is a negative regulator of PI(3,4,5)P3. Hydrogen Sulfide 13-16 phosphatase and tensin homolog Homo sapiens 133-137 23741314-11 2013 Our data show, for the first time, that H2S prevents H2O2-induced activation of ENaC through a PTEN-PI(3,4,5)P3 dependent pathway. Hydrogen Sulfide 40-43 phosphatase and tensin homolog Homo sapiens 95-99 23176571-0 2013 Hydrogen sulfide protects against cellular senescence via S-sulfhydration of Keap1 and activation of Nrf2. Hydrogen Sulfide 0-16 nuclear factor, erythroid derived 2, like 2 Mus musculus 101-105 23176571-2 2013 Cystathionine gamma-lyase (CSE) is a major H2S-generating enzyme in our body. Hydrogen Sulfide 43-46 cystathionase (cystathionine gamma-lyase) Mus musculus 0-25 23176571-2 2013 Cystathionine gamma-lyase (CSE) is a major H2S-generating enzyme in our body. Hydrogen Sulfide 43-46 cystathionase (cystathionine gamma-lyase) Mus musculus 27-30 23176571-11 2013 CONCLUSION: H2S protects against cellular aging via S-sulfhydration of Keap1 and Nrf2 activation in association with oxidative stress. Hydrogen Sulfide 12-15 kelch-like ECH-associated protein 1 Mus musculus 71-76 23176571-11 2013 CONCLUSION: H2S protects against cellular aging via S-sulfhydration of Keap1 and Nrf2 activation in association with oxidative stress. Hydrogen Sulfide 12-15 nuclear factor, erythroid derived 2, like 2 Mus musculus 81-85 23549590-1 2013 Hydrogen sulfide (H2S) is emerging as an important gasotransmitter but remains difficult to study. Hydrogen Sulfide 0-16 histocompatibility 2, S region (C4, Slp, Bf, C2) Mus musculus 18-21 23691233-1 2013 Hydrogen sulfide (H2S) is a novel neurotransmitter that has been shown to influence cardiovascular functions as well and corticotrophin hormone (CRH) secretion. Hydrogen Sulfide 0-16 corticotropin releasing hormone Homo sapiens 145-148 23691233-1 2013 Hydrogen sulfide (H2S) is a novel neurotransmitter that has been shown to influence cardiovascular functions as well and corticotrophin hormone (CRH) secretion. Hydrogen Sulfide 18-21 corticotropin releasing hormone Homo sapiens 145-148 23675473-12 2013 At 7 days post-reperfusion both 10 and 100 ppm H2S reduced expression of fibronectin by 63% (p<0.05) and 67% (p<0.01) and ANP by 84% and 63% (p<0.05), respectively. Hydrogen Sulfide 47-50 fibronectin 1 Mus musculus 73-84 23449670-3 2013 This study was designed to examine plasticity of voltage-gated Na(+) channel activities and roles for the endogenous hydrogen sulfide-producing enzyme cystathionine beta-synthetase (CBS) in chronic visceral hyperalgesia. Hydrogen Sulfide 117-133 cystathionine beta synthase Rattus norvegicus 151-180 23479260-0 2013 Hydrogen sulfide preconditions the db/db diabetic mouse heart against ischemia-reperfusion injury by activating Nrf2 signaling in an Erk-dependent manner. Hydrogen Sulfide 0-16 nuclear factor, erythroid derived 2, like 2 Mus musculus 112-116 23449670-3 2013 This study was designed to examine plasticity of voltage-gated Na(+) channel activities and roles for the endogenous hydrogen sulfide-producing enzyme cystathionine beta-synthetase (CBS) in chronic visceral hyperalgesia. Hydrogen Sulfide 117-133 cystathionine beta-synthase Homo sapiens 182-185 23479260-0 2013 Hydrogen sulfide preconditions the db/db diabetic mouse heart against ischemia-reperfusion injury by activating Nrf2 signaling in an Erk-dependent manner. Hydrogen Sulfide 0-16 mitogen-activated protein kinase 1 Mus musculus 133-136 24648967-0 2013 Hydrogen sulfide upregulates heme oxygenase-1 expression in rats with volume overload-induced heart failure. Hydrogen Sulfide 0-16 heme oxygenase 1 Rattus norvegicus 29-45 24648967-13 2013 The present study demonstrated that H2S may play a protective role in volume overload-induced CHF by upregulating protein and mRNA expression of HO-1. Hydrogen Sulfide 36-39 heme oxygenase 1 Rattus norvegicus 145-149 23470016-12 2013 CBS activity was detected in Muller cells by fluorescent detection of H2S. Hydrogen Sulfide 70-73 cystathionine beta-synthase Mus musculus 0-3 23667860-2 2013 Sodium hydrosulfide (300 muM), a donor of hydrogen sulfide, reversibly increased the frequency of miniature endplate current without changes in its amplitude-time parameters. Hydrogen Sulfide 42-58 latexin Homo sapiens 25-28 22843253-0 2013 Role of paraoxonase-1 in the protection of hydrogen sulfide-donating sildenafil (ACS6) against homocysteine-induced neurotoxicity. Hydrogen Sulfide 43-59 paraoxonase 1 Rattus norvegicus 8-21 23459758-3 2013 Type I (also called glomus) cells, the site of O2 sensing in the carotid body, express haem oxygenase-2 and cystathionine-gamma-lyase, the enzymes which catalyse the generation of CO and H2S, respectively. Hydrogen Sulfide 187-190 cystathionine gamma-lyase Homo sapiens 92-133 23171981-3 2013 In this study, the effect of H2S on nitric oxide (NO) production, especially through the expression of constitutive nitric oxide synthase (NOS) isoforms-endothelial NOS (eNOS) and neuronal NOS (nNOS) in rat corpus cavernosum (CC) were explored. Hydrogen Sulfide 29-32 nitric oxide synthase 1 Rattus norvegicus 180-192 23171981-3 2013 In this study, the effect of H2S on nitric oxide (NO) production, especially through the expression of constitutive nitric oxide synthase (NOS) isoforms-endothelial NOS (eNOS) and neuronal NOS (nNOS) in rat corpus cavernosum (CC) were explored. Hydrogen Sulfide 29-32 nitric oxide synthase 1 Rattus norvegicus 194-198 23376738-0 2013 L-Cysteine promotes the proliferation and differentiation of neural stem cells via the CBS/H2S pathway. Hydrogen Sulfide 91-94 cystathionine beta-synthase Homo sapiens 87-90 23376738-3 2013 Moreover, pre-treatment with aminooxyacetic acid, the inhibitor of CBS or knockdown of CBS in using siRNA, significantly attenuated the effects of L-cysteine on elevated H2S levels and the cell proliferation; it also effectively suppressed L-cysteine-induced neurogenesis and astrocytogenesis. Hydrogen Sulfide 170-173 cystathionine beta-synthase Homo sapiens 67-70 23376738-3 2013 Moreover, pre-treatment with aminooxyacetic acid, the inhibitor of CBS or knockdown of CBS in using siRNA, significantly attenuated the effects of L-cysteine on elevated H2S levels and the cell proliferation; it also effectively suppressed L-cysteine-induced neurogenesis and astrocytogenesis. Hydrogen Sulfide 170-173 cystathionine beta-synthase Homo sapiens 87-90 23376738-5 2013 Taken together, the present data suggest that L-cysteine can enhance proliferation and differentiation of NSCs via the CBS/H2S pathway, which may serve as a useful inference for elucidating its role in regulating the fate of NSCs in physiological and pathological settings. Hydrogen Sulfide 123-126 cystathionine beta-synthase Homo sapiens 119-122 23589874-6 2013 In particular, Sulfidefluor-7 acetoxymethyl ester allows for direct, real-time visualization of endogenous H2S produced in live human umbilical vein endothelial cells upon stimulation with vascular endothelial growth factor (VEGF). Hydrogen Sulfide 107-110 vascular endothelial growth factor A Homo sapiens 189-223 23589874-6 2013 In particular, Sulfidefluor-7 acetoxymethyl ester allows for direct, real-time visualization of endogenous H2S produced in live human umbilical vein endothelial cells upon stimulation with vascular endothelial growth factor (VEGF). Hydrogen Sulfide 107-110 vascular endothelial growth factor A Homo sapiens 225-229 23589874-7 2013 Moreover, we show that H2S production is dependent on NADPH oxidase-derived hydrogen peroxide (H2O2), which attenuates VEGF receptor 2 phosphorylation and establishes a link for H2S/H2O2 crosstalk. Hydrogen Sulfide 23-26 vascular endothelial growth factor A Homo sapiens 119-123 23537657-0 2013 Oxidative stress suppresses the cellular bioenergetic effect of the 3-mercaptopyruvate sulfurtransferase/hydrogen sulfide pathway. Hydrogen Sulfide 105-121 mercaptopyruvate sulfurtransferase Mus musculus 68-104 23512751-0 2013 Identification of cystathionine beta-synthase inhibitors using a hydrogen sulfide selective probe. Hydrogen Sulfide 65-81 cystathionine beta-synthase Homo sapiens 18-45 23512751-1 2013 Buzzing with activity: A hydrogen sulfide selective fluorogenic probe, 7-azido-4-methylcoumarin (AzMC), serves as a highly sensitive assay for cystathionine beta-synthase activity, and is suitable for the high-throughput discovery of novel enzyme inhibitors. Hydrogen Sulfide 25-41 cystathionine beta-synthase Homo sapiens 143-170 23537657-1 2013 Recent data show that lower concentrations of hydrogen sulfide (H2S), as well as endogenous, intramitochondrial production of H2S by the 3-mercaptopyruvate (3-MP)/3-mercaptopyruvate sulfurtransferase (3-MST) pathway serves as an electron donor and inorganic source of energy to support mitochondrial electron transport and ATP generation in mammalian cells by donating electrons to Complex II. Hydrogen Sulfide 46-62 mercaptopyruvate sulfurtransferase Homo sapiens 163-199 23537657-1 2013 Recent data show that lower concentrations of hydrogen sulfide (H2S), as well as endogenous, intramitochondrial production of H2S by the 3-mercaptopyruvate (3-MP)/3-mercaptopyruvate sulfurtransferase (3-MST) pathway serves as an electron donor and inorganic source of energy to support mitochondrial electron transport and ATP generation in mammalian cells by donating electrons to Complex II. Hydrogen Sulfide 126-129 mercaptopyruvate sulfurtransferase Homo sapiens 163-199 23477661-1 2013 Hydrogen sulfide (H2S) has recently been recognized as an important physiologically relevant gasotransmitter. Hydrogen Sulfide 0-16 histocompatibility 2, S region (C4, Slp, Bf, C2) Mus musculus 18-21 23591335-1 2013 OBJECTIVE: To investigate the role of hydrogen sulfide (H2S) on oxidized-low density lipoprotein (ox-LDL)-stimulated NF-kappaB pathway in human monocytes/macrophages and its mechanisms. Hydrogen Sulfide 38-54 nuclear factor kappa B subunit 1 Homo sapiens 117-126 23591335-1 2013 OBJECTIVE: To investigate the role of hydrogen sulfide (H2S) on oxidized-low density lipoprotein (ox-LDL)-stimulated NF-kappaB pathway in human monocytes/macrophages and its mechanisms. Hydrogen Sulfide 56-59 nuclear factor kappa B subunit 1 Homo sapiens 117-126 23591335-10 2013 The IkappaBalpha expression in the cytoplasma of cells in the ox-LDL+ H2S 100 mumol/L group and ox-LDL + H2S 500 mumol/L group was higher than that in the ox-LDL group, and the nuclear translocation of NF-kappaB p65 in the cells of ox-LDL group was lower than that in the ox-LDL group. Hydrogen Sulfide 70-73 NFKB inhibitor alpha Homo sapiens 4-16 23591335-10 2013 The IkappaBalpha expression in the cytoplasma of cells in the ox-LDL+ H2S 100 mumol/L group and ox-LDL + H2S 500 mumol/L group was higher than that in the ox-LDL group, and the nuclear translocation of NF-kappaB p65 in the cells of ox-LDL group was lower than that in the ox-LDL group. Hydrogen Sulfide 105-108 NFKB inhibitor alpha Homo sapiens 4-16 23591335-12 2013 CONCLUSION: H2S inhibited the activation of NF-kappaB p65 pathway in the ox-LDL-induced human monocytes/macrophages. Hydrogen Sulfide 12-15 RELA proto-oncogene, NF-kB subunit Homo sapiens 44-57 23578012-0 2013 Hydrogen sulphide inhalational toxicity at a petroleum refinery in Sri Lanka: a case series of seven survivors following an industrial accident and a brief review of medical literature. Hydrogen Sulfide 0-17 sorcin Homo sapiens 67-70 23578012-1 2013 UNLABELLED: This case series details clinical observations in 7 survivors of accidental hydrogen sulphide inhalation toxicity at a petroleum refinery in Sri Lanka. Hydrogen Sulfide 88-105 sorcin Homo sapiens 153-156 23376828-10 2013 In addition, H2S, possibly via an overriding CSE source, qualifies as an EDHF. Hydrogen Sulfide 13-16 cystathionase (cystathionine gamma-lyase) Mus musculus 45-48 23395089-1 2013 Cystathionine gamma-lyase (CSE) is one of the major enzymes producing hydrogen sulfide (H2S) in lungs, participating in the regulation of respiratory functions. Hydrogen Sulfide 70-86 cystathionase (cystathionine gamma-lyase) Mus musculus 0-25 23395089-1 2013 Cystathionine gamma-lyase (CSE) is one of the major enzymes producing hydrogen sulfide (H2S) in lungs, participating in the regulation of respiratory functions. Hydrogen Sulfide 70-86 cystathionase (cystathionine gamma-lyase) Mus musculus 27-30 23395089-1 2013 Cystathionine gamma-lyase (CSE) is one of the major enzymes producing hydrogen sulfide (H2S) in lungs, participating in the regulation of respiratory functions. Hydrogen Sulfide 88-91 cystathionase (cystathionine gamma-lyase) Mus musculus 0-25 23395089-1 2013 Cystathionine gamma-lyase (CSE) is one of the major enzymes producing hydrogen sulfide (H2S) in lungs, participating in the regulation of respiratory functions. Hydrogen Sulfide 88-91 cystathionase (cystathionine gamma-lyase) Mus musculus 27-30 23395089-2 2013 The role of CSE-derived H2S in eosinophil-dominant inflammation in allergic diseases has been unclear. Hydrogen Sulfide 24-27 cystathionase (cystathionine gamma-lyase) Mus musculus 12-15 23395089-7 2013 CSE expression was absent and H2S production rate was significantly lower in the lungs of CSE KO mice when compared with WT littermates. Hydrogen Sulfide 30-33 cystathionase (cystathionine gamma-lyase) Mus musculus 90-93 23395089-12 2013 The CSE/H2S system plays a critical protective role in the development of asthma. Hydrogen Sulfide 8-11 cystathionase (cystathionine gamma-lyase) Mus musculus 4-7 23410520-0 2013 Reduced cystathionine gamma-lyase and increased miR-21 expression are associated with increased vascular resistance in growth-restricted pregnancies: hydrogen sulfide as a placental vasodilator. Hydrogen Sulfide 150-166 cystathionine gamma-lyase Homo sapiens 8-33 23410520-0 2013 Reduced cystathionine gamma-lyase and increased miR-21 expression are associated with increased vascular resistance in growth-restricted pregnancies: hydrogen sulfide as a placental vasodilator. Hydrogen Sulfide 150-166 microRNA 21 Homo sapiens 48-54 23410520-3 2013 H2S is produced endogenously by catalytic activity of cystathionine beta-synthase and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-3 cystathionine beta-synthase Homo sapiens 54-81 23410520-3 2013 H2S is produced endogenously by catalytic activity of cystathionine beta-synthase and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-3 cystathionine gamma-lyase Homo sapiens 86-111 23410520-3 2013 H2S is produced endogenously by catalytic activity of cystathionine beta-synthase and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-3 cystathionine gamma-lyase Homo sapiens 113-116 23349187-1 2013 OBJECTIVE: The aim of this study was to determine whether thioredoxin 1 (Trx1) mediates the cardioprotective effects of hydrogen sulfide (H2S) in a model of ischemic-induced heart failure (HF). Hydrogen Sulfide 120-136 thioredoxin 1 Mus musculus 58-71 23349187-1 2013 OBJECTIVE: The aim of this study was to determine whether thioredoxin 1 (Trx1) mediates the cardioprotective effects of hydrogen sulfide (H2S) in a model of ischemic-induced heart failure (HF). Hydrogen Sulfide 120-136 thioredoxin 1 Mus musculus 73-77 23349187-1 2013 OBJECTIVE: The aim of this study was to determine whether thioredoxin 1 (Trx1) mediates the cardioprotective effects of hydrogen sulfide (H2S) in a model of ischemic-induced heart failure (HF). Hydrogen Sulfide 138-141 thioredoxin 1 Mus musculus 58-71 23349187-1 2013 OBJECTIVE: The aim of this study was to determine whether thioredoxin 1 (Trx1) mediates the cardioprotective effects of hydrogen sulfide (H2S) in a model of ischemic-induced heart failure (HF). Hydrogen Sulfide 138-141 thioredoxin 1 Mus musculus 73-77 23349187-3 2013 Treatment with H2S as sodium sulfide (Na2S) not only increased the gene and protein expression of Trx1 in the absence of ischemia but also augmented the HF-induced increase in both. Hydrogen Sulfide 15-18 thioredoxin 1 Mus musculus 98-102 23328265-3 2013 In Arabidopsis, we found that the cytosolic L-cysteine desulfhydrase DES1 is involved in the degradation of cysteine, and therefore responsible for the generation of H2S in this cellular compartment. Hydrogen Sulfide 166-169 L-cysteine desulfhydrase 1 Arabidopsis thaliana 69-73 23215842-6 2013 Expression of the H2S-synthesizing enzymes cystathionine beta-synthase (CBS), cystathionine gamma lyase (CSE) and 3-mercaptopyruvate sulphurtransferase (3-MST) were measured by Western blotting. Hydrogen Sulfide 18-21 cystathionine beta-synthase Homo sapiens 43-70 23760002-7 2013 Moreover, H2S was also found to reduce high-glucose-induced oxidative stress and alter the mRNA and protein expression of Bax and Bcl-2. Hydrogen Sulfide 10-13 BCL2 associated X, apoptosis regulator Rattus norvegicus 122-125 23760002-7 2013 Moreover, H2S was also found to reduce high-glucose-induced oxidative stress and alter the mRNA and protein expression of Bax and Bcl-2. Hydrogen Sulfide 10-13 BCL2, apoptosis regulator Rattus norvegicus 130-135 23449534-2 2013 Exogenous treatment with H2S can induce a reversible hypometabolic state, which can protect organs from ischemia/reperfusion injury, but whether cystathionine gamma-lyase (CSE), which produces endogenous H2S, has similar protective effects is unknown. Hydrogen Sulfide 25-28 cystathionase (cystathionine gamma-lyase) Mus musculus 172-175 23449534-2 2013 Exogenous treatment with H2S can induce a reversible hypometabolic state, which can protect organs from ischemia/reperfusion injury, but whether cystathionine gamma-lyase (CSE), which produces endogenous H2S, has similar protective effects is unknown. Hydrogen Sulfide 204-207 cystathionase (cystathionine gamma-lyase) Mus musculus 145-170 23449534-2 2013 Exogenous treatment with H2S can induce a reversible hypometabolic state, which can protect organs from ischemia/reperfusion injury, but whether cystathionine gamma-lyase (CSE), which produces endogenous H2S, has similar protective effects is unknown. Hydrogen Sulfide 204-207 cystathionase (cystathionine gamma-lyase) Mus musculus 172-175 23449534-4 2013 Compared with wild-type mice, CSE knockout mice had markedly reduced renal production of H2S, and CSE deficiency associated with increased damage and mortality after renal ischemia/reperfusion injury. Hydrogen Sulfide 89-92 cystathionase (cystathionine gamma-lyase) Mus musculus 30-33 23449534-5 2013 Treatment with exogenous H2S rescued CSE knockout mice from the injury and mortality associated with renal ischemia. Hydrogen Sulfide 25-28 cystathionase (cystathionine gamma-lyase) Mus musculus 37-40 23449534-8 2013 In summary, these results suggest that CSE protects against renal ischemia/reperfusion injury, likely by modulating oxidative stress through the production of H2S. Hydrogen Sulfide 159-162 cystathionase (cystathionine gamma-lyase) Mus musculus 39-42 23381473-0 2013 Exogenous application of hydrogen sulfide donor attenuates inflammatory reactions through the L-selectin-involved pathway in the cutaneous reverse passive Arthus reaction. Hydrogen Sulfide 25-41 selectin L Homo sapiens 94-104 23756391-5 2013 MFF increased colonic hydrogen sulfide synthesis in healthy rats, but not in rats with colitis, and had no effect on colonic prostaglandin E2 synthesis. Hydrogen Sulfide 22-38 mitochondrial fission factor Rattus norvegicus 0-3 23063804-2 2013 MATERIALS AND METHODS: We used immunohistochemistry to determine the expression of the H2S synthesis enzymes cystathionine gamma-lyase and cystathionine beta-synthase. Hydrogen Sulfide 87-90 cystathionine gamma-lyase Homo sapiens 109-134 23063804-2 2013 MATERIALS AND METHODS: We used immunohistochemistry to determine the expression of the H2S synthesis enzymes cystathionine gamma-lyase and cystathionine beta-synthase. Hydrogen Sulfide 87-90 cystathionine beta-synthase Homo sapiens 139-166 23063804-8 2013 The H2S donor GYY4137 (0.1 nM to 10 muM) induced potent, concentration dependent relaxation, which was not modified by neuronal voltage gated Na(+) channels, or cystathionine gamma-lyase or cystathionine beta-synthase blockade. Hydrogen Sulfide 4-7 latexin Homo sapiens 36-39 23063804-8 2013 The H2S donor GYY4137 (0.1 nM to 10 muM) induced potent, concentration dependent relaxation, which was not modified by neuronal voltage gated Na(+) channels, or cystathionine gamma-lyase or cystathionine beta-synthase blockade. Hydrogen Sulfide 4-7 cystathionine beta-synthase Homo sapiens 190-217 23063804-9 2013 CONCLUSIONS: Results suggest that endogenous H2S synthesized by cystathionine gamma-lyase and released from intramural nerves acts as a powerful signaling molecule in nitric oxide independent inhibitory transmission to the pig bladder neck. Hydrogen Sulfide 45-48 cystathionine gamma-lyase Homo sapiens 64-89 23325453-4 2013 Expression of Cystathionine-beta-synthase (CBS) mRNA as H2S-producing enzymes in mouse brain was determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Hydrogen Sulfide 56-59 cystathionine beta-synthase Mus musculus 14-41 23325453-4 2013 Expression of Cystathionine-beta-synthase (CBS) mRNA as H2S-producing enzymes in mouse brain was determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Hydrogen Sulfide 56-59 cystathionine beta-synthase Mus musculus 43-46 23325453-8 2013 Hydrogen sulfide in the cortex and hippocampus exhibited dynamic changes after brain injury, in parallel with CBS mRNA and protein expression. Hydrogen Sulfide 0-16 cystathionine beta-synthase Mus musculus 110-113 26105871-2 2013 INTRODUCTION: Cystathionine-b-synthase (CBS) produces the vasodilatory and anti-inflammatory hydrogen sulfide (H2S) by conversion of homocysteine (Hcy). Hydrogen Sulfide 93-109 cystathionine beta-synthase Homo sapiens 14-38 26105871-2 2013 INTRODUCTION: Cystathionine-b-synthase (CBS) produces the vasodilatory and anti-inflammatory hydrogen sulfide (H2S) by conversion of homocysteine (Hcy). Hydrogen Sulfide 93-109 cystathionine beta-synthase Homo sapiens 40-43 26105871-2 2013 INTRODUCTION: Cystathionine-b-synthase (CBS) produces the vasodilatory and anti-inflammatory hydrogen sulfide (H2S) by conversion of homocysteine (Hcy). Hydrogen Sulfide 111-114 cystathionine beta-synthase Homo sapiens 14-38 26105871-2 2013 INTRODUCTION: Cystathionine-b-synthase (CBS) produces the vasodilatory and anti-inflammatory hydrogen sulfide (H2S) by conversion of homocysteine (Hcy). Hydrogen Sulfide 111-114 cystathionine beta-synthase Homo sapiens 40-43 26105871-5 2013 OBJECTIVES: Aberrant CBS gene expression may play a role in hyperhomocysteinemia and decreased H2S and could be involved in pathogenesis of PE. Hydrogen Sulfide 95-98 cystathionine beta-synthase Homo sapiens 21-24 26105871-15 2013 Altered effectiveness of CBS may affect PE through decreased H2S production or Hcy accumulation. Hydrogen Sulfide 61-64 cystathionine beta-synthase Homo sapiens 25-28 23401229-2 2013 Key steps of the syntheses of the sulfanes are the photochemical trifluoromethylation of the thiols with CF3 Hal (Hal=halide) or substitution of alkoxyphosphinediamines with CF3 SSCF3 . Hydrogen Sulfide 34-42 histidine ammonia-lyase Homo sapiens 114-117 23519347-0 2013 Improvement of H2S sensing properties of SnO2-based thick film gas sensors promoted with MoO3 and NiO. Hydrogen Sulfide 15-18 strawberry notch homolog 1 Homo sapiens 41-44 23393010-0 2013 H2S protects against pressure overload-induced heart failure via upregulation of endothelial nitric oxide synthase. Hydrogen Sulfide 0-3 nitric oxide synthase 3, endothelial cell Mus musculus 81-114 23393010-1 2013 BACKGROUND: Cystathionine gamma-lyase (CSE) produces H2S via enzymatic conversion of L-cysteine and plays a critical role in cardiovascular homeostasis. Hydrogen Sulfide 53-56 cystathionase (cystathionine gamma-lyase) Mus musculus 12-37 23393010-1 2013 BACKGROUND: Cystathionine gamma-lyase (CSE) produces H2S via enzymatic conversion of L-cysteine and plays a critical role in cardiovascular homeostasis. Hydrogen Sulfide 53-56 cystathionase (cystathionine gamma-lyase) Mus musculus 39-42 23393010-8 2013 H2S therapy with SG-1002 resulted in cardioprotection during transverse aortic constriction via upregulation of the vascular endothelial growth factor-Akt-endothelial nitric oxide synthase-nitric oxide-cGMP pathway with preserved mitochondrial function, attenuated oxidative stress, and increased myocardial vascular density. Hydrogen Sulfide 0-3 nitric oxide synthase 3, endothelial cell Mus musculus 155-188 23393010-10 2013 Moreover, CSE plays a critical role in the preservation of cardiac function in heart failure, and oral H2S therapy prevents the transition from compensated to decompensated heart failure in part via upregulation of endothelial nitric oxide synthase and increased nitric oxide bioavailability. Hydrogen Sulfide 103-106 nitric oxide synthase 3, endothelial cell Mus musculus 215-248 23489804-6 2013 The expressions of H2S producing enzymes cystathionine beta-synthase, cystathionine gamma-lyase and mercaptopyruvate sulfurtransferase were detected by real-time PCR and western blotting and their tissue distributions were observed by immunohistochemical and immunofluorescent analysis. Hydrogen Sulfide 19-22 cystathionine gamma-lyase Rattus norvegicus 70-95 23275972-2 2013 The gasotransmitter H(2)S is mostly generated from L-cysteine in pancreatic beta cells by cystathionine gamma-lyase (CSE) and has been reported to inhibit insulin release by opening ATP-sensitive K(+) channels. Hydrogen Sulfide 20-25 cystathionase (cystathionine gamma-lyase) Mus musculus 90-115 23275972-2 2013 The gasotransmitter H(2)S is mostly generated from L-cysteine in pancreatic beta cells by cystathionine gamma-lyase (CSE) and has been reported to inhibit insulin release by opening ATP-sensitive K(+) channels. Hydrogen Sulfide 20-25 cystathionase (cystathionine gamma-lyase) Mus musculus 117-120 23275972-14 2013 CONCLUSIONS/INTERPRETATION: Exogenous and endogenous H(2)S inhibit L-type VDCC activity and pancreatic insulin secretion, constituting a novel mechanism for the regulation of insulin secretion by the CSE/H(2)S system. Hydrogen Sulfide 53-58 cystathionase (cystathionine gamma-lyase) Mus musculus 200-203 23543448-0 2013 Decreased expression of p38 MAPK mediates protective effects of hydrogen sulfide on hepatic fibrosis. Hydrogen Sulfide 64-80 mitogen activated protein kinase 14 Rattus norvegicus 24-27 23543448-2 2013 To explore the in vitro and in vivo expression of Phospho-p38, Phospho-Akt and NF-kB in HSCs treated with H2S. Hydrogen Sulfide 106-109 mitogen activated protein kinase 14 Rattus norvegicus 58-61 23543448-2 2013 To explore the in vitro and in vivo expression of Phospho-p38, Phospho-Akt and NF-kB in HSCs treated with H2S. Hydrogen Sulfide 106-109 AKT serine/threonine kinase 1 Rattus norvegicus 71-74 23543448-2 2013 To explore the in vitro and in vivo expression of Phospho-p38, Phospho-Akt and NF-kB in HSCs treated with H2S. Hydrogen Sulfide 106-109 RELA proto-oncogene, NF-kB subunit Rattus norvegicus 79-84 23543448-12 2013 Decreased Phospho-p38 and increased Phospho-Akt expressions may mediate the anti-fibrosis effect by exogenous H2S. Hydrogen Sulfide 110-113 mitogen activated protein kinase 14 Rattus norvegicus 18-21 23543448-12 2013 Decreased Phospho-p38 and increased Phospho-Akt expressions may mediate the anti-fibrosis effect by exogenous H2S. Hydrogen Sulfide 110-113 AKT serine/threonine kinase 1 Rattus norvegicus 44-47 22907821-12 2013 Cysteine and the G1364T and 844ins68 variants of the cystathionine gamma-lyase and cystathionine beta-synthase genes, respectively, are the biological determinants of H(2)S synthesis, and all three are shown here to influence the hypertensive phenotype. Hydrogen Sulfide 167-172 cystathionine gamma-lyase Homo sapiens 53-78 22907821-12 2013 Cysteine and the G1364T and 844ins68 variants of the cystathionine gamma-lyase and cystathionine beta-synthase genes, respectively, are the biological determinants of H(2)S synthesis, and all three are shown here to influence the hypertensive phenotype. Hydrogen Sulfide 167-172 cystathionine beta-synthase Homo sapiens 83-110 23338126-0 2013 Hydrogen sulfide attenuates doxorubicin-induced cardiotoxicity by inhibition of the p38 MAPK pathway in H9c2 cells. Hydrogen Sulfide 0-16 mitogen activated protein kinase 14 Rattus norvegicus 96-99 23338126-4 2013 The DOX-induced increase in expression of p-p38 MAPK was significantly attenuated by pretreatment of H9c2 cells with either 400 microM sodium hydrogen sulfide (NaHS) (a donor of H2S) or 1,000 microM N-acetyl-L-cysteine (NAC, an ROS scavenger) prior to exposure to DOX. Hydrogen Sulfide 202-205 mitogen activated protein kinase 14 Rattus norvegicus 56-59 23338126-7 2013 We also provide novel evidence that exogenous H2S protects H9c2 cells against DOX-induced cardiotoxicity by inhibition of the p38 MAPK pathway. Hydrogen Sulfide 46-49 mitogen activated protein kinase 14 Rattus norvegicus 138-141 23303708-3 2013 The expression and distribution pattern of the H(2) S-synthesizing enzymes cystathione gamma-lyase (CSE) and cystathione beta-synthase (CBS) were investigated in healthy and allergic nasal mucosa. Hydrogen Sulfide 47-53 cystathionine beta-synthase Homo sapiens 109-134 23303708-3 2013 The expression and distribution pattern of the H(2) S-synthesizing enzymes cystathione gamma-lyase (CSE) and cystathione beta-synthase (CBS) were investigated in healthy and allergic nasal mucosa. Hydrogen Sulfide 47-53 cystathionine beta-synthase Homo sapiens 136-139 23303708-10 2013 CONCLUSIONS: The current findings indicate that, in parallel with increased expression levels of CSE and CBS, H(2) S is upregulated in nasal mucosa and plasma of allergic patients. Hydrogen Sulfide 110-116 cystathionine beta-synthase Homo sapiens 105-108 23303708-11 2013 Based on localization of CSE and CBS, H(2) S may play multiple functions in human nasal mucosa, contributing to the development of allergic symptoms such as rhinorrhea, sneezing, and nasal stuffiness. Hydrogen Sulfide 38-44 cystathionine beta-synthase Homo sapiens 33-36 23041593-3 2013 Vascular H(2)S is produced from L-cysteine, catalyzed by cystathionine gamma-lyase (CSE). Hydrogen Sulfide 9-14 cystathionase (cystathionine gamma-lyase) Mus musculus 84-87 23297346-4 2013 Substantial evidence shows that H(2)S is involved in aging by inhibiting free-radical reactions, activating SIRT1, and probably interacting with the age-related gene Klotho. Hydrogen Sulfide 32-37 sirtuin 1 Homo sapiens 108-113 23297346-4 2013 Substantial evidence shows that H(2)S is involved in aging by inhibiting free-radical reactions, activating SIRT1, and probably interacting with the age-related gene Klotho. Hydrogen Sulfide 32-37 klotho Homo sapiens 166-172 23446563-0 2013 Hydrogen sulfide reduces neutrophil recruitment in hind-limb ischemia-reperfusion injury in an L-selectin and ADAM-17-dependent manner. Hydrogen Sulfide 0-16 selectin L Homo sapiens 95-105 23446563-0 2013 Hydrogen sulfide reduces neutrophil recruitment in hind-limb ischemia-reperfusion injury in an L-selectin and ADAM-17-dependent manner. Hydrogen Sulfide 0-16 ADAM metallopeptidase domain 17 Homo sapiens 110-117 23446563-9 2013 RESULTS: Hydrogen sulfide treatment significantly increased L-selectin shedding from human neutrophils following activation by fMLP and interleukin-8 in an ADAM-17-dependent manner. Hydrogen Sulfide 9-25 selectin L Homo sapiens 60-70 23446563-9 2013 RESULTS: Hydrogen sulfide treatment significantly increased L-selectin shedding from human neutrophils following activation by fMLP and interleukin-8 in an ADAM-17-dependent manner. Hydrogen Sulfide 9-25 formyl peptide receptor 1 Homo sapiens 127-131 23446563-9 2013 RESULTS: Hydrogen sulfide treatment significantly increased L-selectin shedding from human neutrophils following activation by fMLP and interleukin-8 in an ADAM-17-dependent manner. Hydrogen Sulfide 9-25 C-X-C motif chemokine ligand 8 Homo sapiens 136-149 23446563-9 2013 RESULTS: Hydrogen sulfide treatment significantly increased L-selectin shedding from human neutrophils following activation by fMLP and interleukin-8 in an ADAM-17-dependent manner. Hydrogen Sulfide 9-25 ADAM metallopeptidase domain 17 Homo sapiens 156-163 23446563-11 2013 CONCLUSIONS: Hydrogen sulfide administration results in the down-regulation of L-selectin expression in activated human neutrophils. Hydrogen Sulfide 13-29 selectin L Homo sapiens 79-89 23413915-3 2013 The aim of this study is to investigate distribution of endogenous H2S synthesizing enzyme cystathionine-beta-synthetase (CBS) expression and role of H2S on excitability and voltage-gated potassium channels of TG neurons. Hydrogen Sulfide 67-70 cystathionine beta synthase Rattus norvegicus 91-120 23413915-3 2013 The aim of this study is to investigate distribution of endogenous H2S synthesizing enzyme cystathionine-beta-synthetase (CBS) expression and role of H2S on excitability and voltage-gated potassium channels of TG neurons. Hydrogen Sulfide 67-70 cystathionine beta synthase Rattus norvegicus 122-125 23413915-14 2013 CONCLUSION: These data suggest that endogenous H2S generating enzyme CBS was co-localized well with Kv1.1 and Kv1.4 in TG neurons and that H2S produces the mechanic pain and increases neuronal excitability, which might be largely mediated by suppressing IK density, thus identifying for the first time a specific molecular mechanism underlying pain and sensitization in TG. Hydrogen Sulfide 47-50 cystathionine beta synthase Rattus norvegicus 69-72 23413915-14 2013 CONCLUSION: These data suggest that endogenous H2S generating enzyme CBS was co-localized well with Kv1.1 and Kv1.4 in TG neurons and that H2S produces the mechanic pain and increases neuronal excitability, which might be largely mediated by suppressing IK density, thus identifying for the first time a specific molecular mechanism underlying pain and sensitization in TG. Hydrogen Sulfide 47-50 potassium voltage-gated channel subfamily A member 1 Rattus norvegicus 100-105 23413915-14 2013 CONCLUSION: These data suggest that endogenous H2S generating enzyme CBS was co-localized well with Kv1.1 and Kv1.4 in TG neurons and that H2S produces the mechanic pain and increases neuronal excitability, which might be largely mediated by suppressing IK density, thus identifying for the first time a specific molecular mechanism underlying pain and sensitization in TG. Hydrogen Sulfide 47-50 potassium voltage-gated channel subfamily A member 4 Rattus norvegicus 110-115 23413915-14 2013 CONCLUSION: These data suggest that endogenous H2S generating enzyme CBS was co-localized well with Kv1.1 and Kv1.4 in TG neurons and that H2S produces the mechanic pain and increases neuronal excitability, which might be largely mediated by suppressing IK density, thus identifying for the first time a specific molecular mechanism underlying pain and sensitization in TG. Hydrogen Sulfide 139-142 cystathionine beta synthase Rattus norvegicus 69-72 23413915-14 2013 CONCLUSION: These data suggest that endogenous H2S generating enzyme CBS was co-localized well with Kv1.1 and Kv1.4 in TG neurons and that H2S produces the mechanic pain and increases neuronal excitability, which might be largely mediated by suppressing IK density, thus identifying for the first time a specific molecular mechanism underlying pain and sensitization in TG. Hydrogen Sulfide 139-142 potassium voltage-gated channel subfamily A member 1 Rattus norvegicus 100-105 23413915-14 2013 CONCLUSION: These data suggest that endogenous H2S generating enzyme CBS was co-localized well with Kv1.1 and Kv1.4 in TG neurons and that H2S produces the mechanic pain and increases neuronal excitability, which might be largely mediated by suppressing IK density, thus identifying for the first time a specific molecular mechanism underlying pain and sensitization in TG. Hydrogen Sulfide 139-142 potassium voltage-gated channel subfamily A member 4 Rattus norvegicus 110-115 23368960-6 2013 (4) Hydrogen sulfide (H(2)S/HS(-)) inhibits CO oxidation but not CO(2) reduction--the complex on/off characteristics are consistent with it binding at the same oxidation level as C(ox) and forming a modified version of this inactive state rather than reacting directly with C(red1). Hydrogen Sulfide 4-20 adenosine deaminase RNA specific B1 Homo sapiens 276-280 23368960-6 2013 (4) Hydrogen sulfide (H(2)S/HS(-)) inhibits CO oxidation but not CO(2) reduction--the complex on/off characteristics are consistent with it binding at the same oxidation level as C(ox) and forming a modified version of this inactive state rather than reacting directly with C(red1). Hydrogen Sulfide 22-27 adenosine deaminase RNA specific B1 Homo sapiens 276-280 23313510-0 2013 Hydrogen sulfide is produced by cystathionine gamma-lyase at the steady-state low intracellular Ca(2+) concentrations. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 32-57 23401229-2 2013 Key steps of the syntheses of the sulfanes are the photochemical trifluoromethylation of the thiols with CF3 Hal (Hal=halide) or substitution of alkoxyphosphinediamines with CF3 SSCF3 . Hydrogen Sulfide 34-42 histidine ammonia-lyase Homo sapiens 109-112 23313510-4 2013 Here we show that H(2)S producing activity of CSE is regulated by intracellular Ca(2+) concentrations. Hydrogen Sulfide 18-23 cystathionine gamma-lyase Homo sapiens 46-49 23313510-5 2013 In the presence of pyridoxal 5"-phosphate (PLP) CSE efficiently produces H(2)S at the steady-state low Ca(2+) concentrations but is suppressed at high Ca(2+) concentrations. Hydrogen Sulfide 73-78 cystathionine gamma-lyase Homo sapiens 48-51 23313510-7 2013 These observations suggest that CSE produces H(2)S at the steady-state in cells and that the production is suppressed when the intracellular Ca(2+) concentrations are increased. Hydrogen Sulfide 45-50 cystathionine gamma-lyase Homo sapiens 32-35 22924591-1 2013 BACKGROUND AND PURPOSE: The Ca(v) 3.2 isoform of T-type Ca(2+) channels (T channels) is sensitized by hydrogen sulfide, a pro-nociceptive gasotransmitter, and also by PKA that mediates PGE(2) -induced hyperalgesia. Hydrogen Sulfide 103-119 calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus 28-37 22872231-2 2013 Cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), the main enzymes in the transsulfuration pathway, catalyze H(2)S production in mammalian tissues. Hydrogen Sulfide 130-135 cystathionine gamma-lyase Homo sapiens 38-63 22928888-13 2013 This release was mediated by a H(2)S-induced activation of TRPA1 channels. Hydrogen Sulfide 31-36 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 59-64 22872231-2 2013 Cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), the main enzymes in the transsulfuration pathway, catalyze H(2)S production in mammalian tissues. Hydrogen Sulfide 130-135 cystathionine beta-synthase Homo sapiens 0-27 22872231-2 2013 Cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), the main enzymes in the transsulfuration pathway, catalyze H(2)S production in mammalian tissues. Hydrogen Sulfide 130-135 cystathionine gamma-lyase Homo sapiens 65-68 22872231-10 2013 CONCLUSION: These findings suggest that CSE expression in the proximal tubules may also regulate tubulointerstitial microcirculation via H(2)S production. Hydrogen Sulfide 137-142 cystathionine gamma-lyase Homo sapiens 40-43 23267760-9 2013 Systemically, infusion of H(2)S increased both the pro-inflammatory response during endotoxemia, as demonstrated by increased TNF-alpha levels, as well as the anti-inflammatory response, as demonstrated by increased IL-10 levels. Hydrogen Sulfide 26-31 tumor necrosis factor Homo sapiens 126-135 23267760-9 2013 Systemically, infusion of H(2)S increased both the pro-inflammatory response during endotoxemia, as demonstrated by increased TNF-alpha levels, as well as the anti-inflammatory response, as demonstrated by increased IL-10 levels. Hydrogen Sulfide 26-31 interleukin 10 Homo sapiens 216-221 23267760-10 2013 In LPS-stimulated whole blood of healthy volunteers, co-incubation with H(2)S had solely anti-inflammatory effects, resulting in decreased TNF-alpha levels and increased IL-10 levels. Hydrogen Sulfide 72-77 tumor necrosis factor Homo sapiens 139-148 23267760-10 2013 In LPS-stimulated whole blood of healthy volunteers, co-incubation with H(2)S had solely anti-inflammatory effects, resulting in decreased TNF-alpha levels and increased IL-10 levels. Hydrogen Sulfide 72-77 interleukin 10 Homo sapiens 170-175 23153577-1 2013 Hydrogen sulfide (H(2)S) is a gaseous neuromodulator endogenously produced in the brain by the enzyme cystathionine beta-synthase (CBS). Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 102-129 23104984-0 2013 Intramitochondrial hydrogen sulfide production by 3-mercaptopyruvate sulfurtransferase maintains mitochondrial electron flow and supports cellular bioenergetics. Hydrogen Sulfide 19-35 mercaptopyruvate sulfurtransferase Homo sapiens 50-86 23104984-4 2013 Low concentrations of H(2)S (0.1-1 muM) elicited a significant increase in mitochondrial function, while higher concentrations of H(2)S (3-30 muM) were inhibitory. Hydrogen Sulfide 22-27 latexin Homo sapiens 35-38 23104984-4 2013 Low concentrations of H(2)S (0.1-1 muM) elicited a significant increase in mitochondrial function, while higher concentrations of H(2)S (3-30 muM) were inhibitory. Hydrogen Sulfide 130-135 latexin Homo sapiens 142-145 23104984-6 2013 3-mercaptopyruvate (3-MP), the substrate of the mitochondrial enzyme 3-mercaptopyruvate sulfurtransferase (3-MST) stimulated mitochondrial H(2)S production and enhanced mitochondrial electron transport and cellular bioenergetics at low concentrations (10-100 nM), while at higher concentrations, it inhibited cellular bioenergetics. Hydrogen Sulfide 139-144 mercaptopyruvate sulfurtransferase Homo sapiens 69-105 23153577-1 2013 Hydrogen sulfide (H(2)S) is a gaseous neuromodulator endogenously produced in the brain by the enzyme cystathionine beta-synthase (CBS). Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 131-134 23153577-1 2013 Hydrogen sulfide (H(2)S) is a gaseous neuromodulator endogenously produced in the brain by the enzyme cystathionine beta-synthase (CBS). Hydrogen Sulfide 18-23 cystathionine beta-synthase Homo sapiens 102-129 23153577-1 2013 Hydrogen sulfide (H(2)S) is a gaseous neuromodulator endogenously produced in the brain by the enzyme cystathionine beta-synthase (CBS). Hydrogen Sulfide 18-23 cystathionine beta-synthase Homo sapiens 131-134 23148920-0 2013 Hydrogen sulfide increases nitric oxide production with calcium-dependent activation of endothelial nitric oxide synthase in endothelial cells. Hydrogen Sulfide 0-16 nitric oxide synthase 3 Homo sapiens 88-121 23216831-6 2013 Use of cyclooxygenase-2 inhibitor, prostaglandin, antibiotic or drugs that are not yet commercially available such as nitric oxide-releasing and hydrogen sulfide (H(2) S)-releasing NSAIDs compounds seem to reduce lower GI injury, but more evidence are needed before any of them are recommended in high-risk patients. Hydrogen Sulfide 163-170 prostaglandin-endoperoxide synthase 2 Homo sapiens 7-23 23148920-4 2013 We investigated whether H(2)S directly regulates endothelial NO synthase (eNOS) activity and NO production in endothelial cells. Hydrogen Sulfide 24-29 nitric oxide synthase 3 Homo sapiens 74-78 23148920-10 2013 The data of this study suggest that H(2)S directly acts on endothelial cells to induce eNOS activation and NO production by releasing calcium from the intracellular store in endoplasmic reticulum, which may explain one of mechanisms of its vasodilator function. Hydrogen Sulfide 36-41 nitric oxide synthase 3 Homo sapiens 87-91 22851450-6 2013 Two metabolic gases, nitric oxide and hydrogen sulfide, which are enzymatically produced, appear to exert their signaling properties through non-enzymatic reaction with GAPDH. Hydrogen Sulfide 38-54 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 169-174 23143058-0 2013 Hydrogen sulfide differentially affects the hepatic vasculature in response to phenylephrine and endothelin 1 during endotoxemia. Hydrogen Sulfide 0-16 endothelin 1 Rattus norvegicus 97-109 23143058-14 2013 In summary, the discrepancies between the hepatic response to PE and ET-1 suggest that H(2)S differentially contributes to microcirculatory dysfunction in the systemic and hepatic microcirculations. Hydrogen Sulfide 87-92 endothelin 1 Rattus norvegicus 69-73 23547844-1 2013 Hydrogen sulfide (H2S), known as an important cellular signaling molecule, plays critical roles in many physiological and/or pathological processes. Hydrogen Sulfide 0-16 histocompatibility 2, S region (C4, Slp, Bf, C2) Mus musculus 18-21 23054084-8 2013 Moreover, the expressions of caspase-3, -8, -9 and the release of cytochrome c were all increased in the apoptotic cells, and the activity of NF-kappaB as well as the phosphorylation of ERK1/2, JNK1/2 and p38 decreased accompanying with the reduction of the serum H(2)S level. Hydrogen Sulfide 264-269 caspase 3 Rattus norvegicus 29-46 23054084-8 2013 Moreover, the expressions of caspase-3, -8, -9 and the release of cytochrome c were all increased in the apoptotic cells, and the activity of NF-kappaB as well as the phosphorylation of ERK1/2, JNK1/2 and p38 decreased accompanying with the reduction of the serum H(2)S level. Hydrogen Sulfide 264-269 mitogen activated protein kinase 3 Rattus norvegicus 186-192 22881598-7 2013 Mice lacking GPBAR1 were more sensitive to gastric and intestinal injury caused by ASA and NSAIDs and exhibited a markedly reduced expression of cystathionine-gamma-liase (CSE), cystathionine-beta-synthase (CBS) and endothelial NOS enzymes required for generation of H(2)S and NO, in the stomach. Hydrogen Sulfide 267-272 G protein-coupled bile acid receptor 1 Mus musculus 13-19 24088256-3 2013 Cocktail method was used to evaluate the influence of chronic hydrogen sulfide poisoning on the activities of cytochrome P450 (CYP450) isoforms CYP1A2, CYP2C9, CYP2B6 and CYP2D6, which were reflected by the changes of pharmacokinetic parameters of 4 specific probe drugs phenacetin, tolbutamide bupropion and metroprolol, respectively. Hydrogen Sulfide 62-78 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 144-150 24088256-3 2013 Cocktail method was used to evaluate the influence of chronic hydrogen sulfide poisoning on the activities of cytochrome P450 (CYP450) isoforms CYP1A2, CYP2C9, CYP2B6 and CYP2D6, which were reflected by the changes of pharmacokinetic parameters of 4 specific probe drugs phenacetin, tolbutamide bupropion and metroprolol, respectively. Hydrogen Sulfide 62-78 cytochrome P450, family 2, subfamily b, polypeptide 3 Rattus norvegicus 160-166 24088256-3 2013 Cocktail method was used to evaluate the influence of chronic hydrogen sulfide poisoning on the activities of cytochrome P450 (CYP450) isoforms CYP1A2, CYP2C9, CYP2B6 and CYP2D6, which were reflected by the changes of pharmacokinetic parameters of 4 specific probe drugs phenacetin, tolbutamide bupropion and metroprolol, respectively. Hydrogen Sulfide 62-78 cytochrome P450, family 2, subfamily d, polypeptide 4 Rattus norvegicus 171-177 24088256-8 2013 Chronic hydrogen sulfide poisoning could induce the activity of CYP1A2 and CYP2B6 of rats. Hydrogen Sulfide 8-24 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 64-70 24088256-8 2013 Chronic hydrogen sulfide poisoning could induce the activity of CYP1A2 and CYP2B6 of rats. Hydrogen Sulfide 8-24 cytochrome P450, family 2, subfamily b, polypeptide 3 Rattus norvegicus 75-81 22881598-10 2013 Inhibition of CSE by DL-propargylglycine completely reversed protection afforded by ciprofloxacin in wild type mice, whereas treating mice with an H(2)S donor restored the protective effects of ciprofloxacin in GPBAR1(-/-) mice. Hydrogen Sulfide 147-152 G protein-coupled bile acid receptor 1 Homo sapiens 211-217 24356372-1 2013 BACKGROUND/AIM: We have demonstrated that exogenous hydrogen sulfide (H2S) protects H9c2 cardiac cells against the doxorubicin (DOX)-induced injuries by inhibiting p38 mitogen-activated protein kinase (MAPK) pathway and that the p38 MAPK/nuclear factor-kappaB (NF-kappaB) pathway is involved in the DOX-induced inflammatory response and cytotoxicity. Hydrogen Sulfide 52-68 mitogen activated protein kinase 14 Rattus norvegicus 164-167 24356372-1 2013 BACKGROUND/AIM: We have demonstrated that exogenous hydrogen sulfide (H2S) protects H9c2 cardiac cells against the doxorubicin (DOX)-induced injuries by inhibiting p38 mitogen-activated protein kinase (MAPK) pathway and that the p38 MAPK/nuclear factor-kappaB (NF-kappaB) pathway is involved in the DOX-induced inflammatory response and cytotoxicity. Hydrogen Sulfide 52-68 mitogen activated protein kinase 14 Rattus norvegicus 229-232 24356372-12 2013 CONCLUSION: The present study has demonstrated the new mechanistic evidence that exogenous H2S attenuates the DOX-induced inflammation and cytotoxicity by inhibiting p38 MAPK/NF-kappaB pathway in H9c2 cardiac cells. Hydrogen Sulfide 91-94 mitogen activated protein kinase 14 Rattus norvegicus 166-169 24356372-1 2013 BACKGROUND/AIM: We have demonstrated that exogenous hydrogen sulfide (H2S) protects H9c2 cardiac cells against the doxorubicin (DOX)-induced injuries by inhibiting p38 mitogen-activated protein kinase (MAPK) pathway and that the p38 MAPK/nuclear factor-kappaB (NF-kappaB) pathway is involved in the DOX-induced inflammatory response and cytotoxicity. Hydrogen Sulfide 70-73 mitogen activated protein kinase 14 Rattus norvegicus 164-167 24356372-1 2013 BACKGROUND/AIM: We have demonstrated that exogenous hydrogen sulfide (H2S) protects H9c2 cardiac cells against the doxorubicin (DOX)-induced injuries by inhibiting p38 mitogen-activated protein kinase (MAPK) pathway and that the p38 MAPK/nuclear factor-kappaB (NF-kappaB) pathway is involved in the DOX-induced inflammatory response and cytotoxicity. Hydrogen Sulfide 70-73 mitogen activated protein kinase 14 Rattus norvegicus 229-232 24356372-2 2013 The present study attempts to test the hypothesis that exogenous H2S might protect cardiomyocytes against the DOX-induced inflammation and cytotoxicity through inhibiting p38 MAPK/NF-kappaB pathway. Hydrogen Sulfide 65-68 mitogen activated protein kinase 14 Rattus norvegicus 171-174 23092319-0 2013 Hydrogen sulfide prevents hyperoxia-induced lung injury by downregulating reactive oxygen species formation and angiopoietin-2 release. Hydrogen Sulfide 0-16 angiopoietin 2 Mus musculus 112-126 23735868-0 2013 Hydrogen sulfide inhibits abnormal proliferation of lymphocytes via AKT/GSK3beta signal pathway in systemic lupus erythematosus patients. Hydrogen Sulfide 0-16 AKT serine/threonine kinase 1 Homo sapiens 68-71 23735868-0 2013 Hydrogen sulfide inhibits abnormal proliferation of lymphocytes via AKT/GSK3beta signal pathway in systemic lupus erythematosus patients. Hydrogen Sulfide 0-16 glycogen synthase kinase 3 beta Homo sapiens 72-80 23735868-15 2013 CONCLUSION: These results demonstrate that H2S inhibits the abnormal activation of lymphocytes from SLE patients throuqh the AKT/GSK3beta signal pathway. Hydrogen Sulfide 43-46 AKT serine/threonine kinase 1 Homo sapiens 125-128 23735868-15 2013 CONCLUSION: These results demonstrate that H2S inhibits the abnormal activation of lymphocytes from SLE patients throuqh the AKT/GSK3beta signal pathway. Hydrogen Sulfide 43-46 glycogen synthase kinase 3 beta Homo sapiens 129-137 23111006-9 2013 DBP [beta (SE)] increased 0.23 (0.08) mmHg per unit of reported hog odor during the 10 min outdoors and 0.12 (0.08) mmHg per 1-ppb increase of H2S concentration in the same hour. Hydrogen Sulfide 143-146 GC vitamin D binding protein Sus scrofa 0-3 23183179-4 2013 Adenovirus-mediated cystathionine gamma-lyase (CSE) overexpression increased endogenous H(2)S production and lowered glycogen content in HepG(2) cells. Hydrogen Sulfide 88-93 cystathionase (cystathionine gamma-lyase) Mus musculus 20-45 23183179-4 2013 Adenovirus-mediated cystathionine gamma-lyase (CSE) overexpression increased endogenous H(2)S production and lowered glycogen content in HepG(2) cells. Hydrogen Sulfide 88-93 cystathionase (cystathionine gamma-lyase) Mus musculus 47-50 23092319-15 2013 In conclusion, H2S protects from HALI by preventing ROS production and angiopoietin-2 release. Hydrogen Sulfide 15-18 angiopoietin 2 Mus musculus 71-85 23864951-7 2013 Interestingly, inhibiting endogenous, CSE-dependent H2S production with PPG did not exacerbate the deleterious vascular changes seen in the untreated fat-fed ApoE(-/-) mice. Hydrogen Sulfide 52-55 cystathionase (cystathionine gamma-lyase) Mus musculus 38-41 23864951-9 2013 Endogenous H2S production via CSE is insufficient to counter the atherogenic effects seen in this model; however exogenous H2S treatment has a significant vasoprotective effect. Hydrogen Sulfide 11-14 cystathionase (cystathionine gamma-lyase) Mus musculus 30-33 23108488-5 2013 We also showed that FA exposure inhibits the expression of cystathionine beta-synthase, the major enzyme responsible for endogenous H(2)S generation in hippocampus and decreases the production of endogenous H(2)S in hippocampus in rats. Hydrogen Sulfide 132-137 cystathionine beta synthase Rattus norvegicus 59-86 23108488-5 2013 We also showed that FA exposure inhibits the expression of cystathionine beta-synthase, the major enzyme responsible for endogenous H(2)S generation in hippocampus and decreases the production of endogenous H(2)S in hippocampus in rats. Hydrogen Sulfide 207-212 cystathionine beta synthase Rattus norvegicus 59-86 23631191-3 2013 In pancreatic beta-cells, H2S can be produced by cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE). Hydrogen Sulfide 26-29 cystathionine beta-synthase Homo sapiens 49-76 23903007-2 2013 Cav3.2 T-channels are functionally modulated by extracellular substances such as hydrogen sulfide and ascorbic acid, by intracellular signaling molecules including protein kinases, and by glycosylation. Hydrogen Sulfide 81-97 calcium voltage-gated channel subunit alpha1 H Homo sapiens 0-6 23340406-2 2013 Hydrogen sulphide is known to be produced from L-cysteine by cystathionine beta-synthase, cystathionine gamma-lyase and 3-mercaptopyruvate sulfurtransferase coupled with cysteine aminotransferase. Hydrogen Sulfide 0-17 cystathionine beta-synthase Homo sapiens 61-88 23340406-2 2013 Hydrogen sulphide is known to be produced from L-cysteine by cystathionine beta-synthase, cystathionine gamma-lyase and 3-mercaptopyruvate sulfurtransferase coupled with cysteine aminotransferase. Hydrogen Sulfide 0-17 mercaptopyruvate sulfurtransferase Homo sapiens 120-156 23340406-3 2013 Here we report an additional biosynthetic pathway for the production of hydrogen sulphide from D-cysteine involving 3-mercaptopyruvate sulfurtransferase and D-amino acid oxidase. Hydrogen Sulfide 72-89 mercaptopyruvate sulfurtransferase Homo sapiens 116-152 23340406-3 2013 Here we report an additional biosynthetic pathway for the production of hydrogen sulphide from D-cysteine involving 3-mercaptopyruvate sulfurtransferase and D-amino acid oxidase. Hydrogen Sulfide 72-89 D-amino acid oxidase Homo sapiens 157-177 23631191-3 2013 In pancreatic beta-cells, H2S can be produced by cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE). Hydrogen Sulfide 26-29 cystathionine gamma-lyase Homo sapiens 86-111 23631191-3 2013 In pancreatic beta-cells, H2S can be produced by cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE). Hydrogen Sulfide 26-29 cystathionine gamma-lyase Homo sapiens 113-116 23273102-1 2013 Hydrogen sulfide (H(2)S), an endogenous gas molecule synthesized by cystathionine-beta-synthetase (CBS), is involved in inflammation and nociceptive signaling. Hydrogen Sulfide 0-16 cystathionine beta synthase Rattus norvegicus 68-97 23273102-1 2013 Hydrogen sulfide (H(2)S), an endogenous gas molecule synthesized by cystathionine-beta-synthetase (CBS), is involved in inflammation and nociceptive signaling. Hydrogen Sulfide 0-16 cystathionine beta synthase Rattus norvegicus 99-102 23273102-1 2013 Hydrogen sulfide (H(2)S), an endogenous gas molecule synthesized by cystathionine-beta-synthetase (CBS), is involved in inflammation and nociceptive signaling. Hydrogen Sulfide 18-23 cystathionine beta synthase Rattus norvegicus 68-97 23273102-1 2013 Hydrogen sulfide (H(2)S), an endogenous gas molecule synthesized by cystathionine-beta-synthetase (CBS), is involved in inflammation and nociceptive signaling. Hydrogen Sulfide 18-23 cystathionine beta synthase Rattus norvegicus 99-102 23273102-5 2013 Intraplantar administration of NaHS (its addition mimics CBS production of H(2)S) or l-cysteine in healthy rats elicited mechanical hyperalgesia. Hydrogen Sulfide 75-81 cystathionine beta synthase Rattus norvegicus 57-60 23393548-5 2013 Analysis of ATP synthesis, mitochondrial membrane potential (DeltaPsim) and cytochrome c release from mitochondria indicated that mitochondrial function was preserved by pretreatment with H2S. Hydrogen Sulfide 188-191 cytochrome c, somatic Homo sapiens 76-88 23178483-1 2013 Hydrogen sulfide (H(2)S) plays a crucial role in the regulation of stomatal closure in plant response to drought stress, and l-cysteine desulfhydrase (LCD) has been identified as being mainly responsible for the degradation of cysteine to generate H(2)S. Hydrogen Sulfide 248-253 Pyridoxal phosphate (PLP)-dependent transferases superfamily protein Arabidopsis thaliana 125-149 23178483-6 2013 The expression of LCD and H(2)S production rate decreased in both the aba3 and abi1 mutants. Hydrogen Sulfide 26-31 Protein phosphatase 2C family protein Arabidopsis thaliana 79-83 23393548-7 2013 In additional experiments, H2S was also found to preserve the activities and protein expressions levels of the antioxidants enzymes, superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase in H2O2 exposed cells. Hydrogen Sulfide 27-30 catalase Homo sapiens 155-163 23393548-9 2013 Interestingly, in the current model, D, L-propargylglycine (PAG), a selective inhibitor of cystathionine gamma-lyase (CSE), abolished the protective effects of H2S donors. Hydrogen Sulfide 160-163 cystathionine gamma-lyase Homo sapiens 91-116 23393548-9 2013 Interestingly, in the current model, D, L-propargylglycine (PAG), a selective inhibitor of cystathionine gamma-lyase (CSE), abolished the protective effects of H2S donors. Hydrogen Sulfide 160-163 cystathionine gamma-lyase Homo sapiens 118-121 23409241-0 2013 Resonant tunneling modulation in quasi-2D Cu(2)O/SnO(2) p-n horizontal-multi-layer heterostructure for room temperature H(2)S sensor application. Hydrogen Sulfide 120-125 strawberry notch homolog 2 Homo sapiens 49-52 23359814-7 2013 CBS silencing deteriorates FA-induced decreases in endogenous H(2)S generation, neurotoxicity, and intracellular ROS accumulation in PC12 cells; while ADMA, a specific inhibitor of NOS significantly attenuates FA-induced decreases in endogenous H(2)S generation, neurotoxicity, and intracellular ROS accumulation in PC12 cells. Hydrogen Sulfide 62-67 cystathionine beta synthase Rattus norvegicus 0-3 23359814-7 2013 CBS silencing deteriorates FA-induced decreases in endogenous H(2)S generation, neurotoxicity, and intracellular ROS accumulation in PC12 cells; while ADMA, a specific inhibitor of NOS significantly attenuates FA-induced decreases in endogenous H(2)S generation, neurotoxicity, and intracellular ROS accumulation in PC12 cells. Hydrogen Sulfide 245-250 cystathionine beta synthase Rattus norvegicus 0-3 23658491-15 2013 There was a decrease in MMP activity with increasing hydrogen sulfide, beginning at 16 muM (P < 0.01) and continuing to 40 muM. Hydrogen Sulfide 53-69 latexin Homo sapiens 87-90 23759691-7 2013 Second, MST can produce H2S (or HS(-)). Hydrogen Sulfide 24-27 mercaptopyruvate sulfurtransferase Mus musculus 8-11 23759691-9 2013 It is concluded that behavioral abnormality in MST-KO mice is caused by MST function defects such as an antioxidant insufficiency or a new transducer, H2S (or HS(-)) and/or SOx deficiency. Hydrogen Sulfide 151-154 mercaptopyruvate sulfurtransferase Mus musculus 47-50 23658491-15 2013 There was a decrease in MMP activity with increasing hydrogen sulfide, beginning at 16 muM (P < 0.01) and continuing to 40 muM. Hydrogen Sulfide 53-69 latexin Homo sapiens 126-129 23658491-16 2013 Moreover, sodium nitroprusside 3 muM was able to overcome the decrease in MMP activity that occurred with hydrogen sulfide 40 muM; this resulted in a more pronounced exponential increase in MMP activity. Hydrogen Sulfide 106-122 latexin Homo sapiens 33-36 23658491-16 2013 Moreover, sodium nitroprusside 3 muM was able to overcome the decrease in MMP activity that occurred with hydrogen sulfide 40 muM; this resulted in a more pronounced exponential increase in MMP activity. Hydrogen Sulfide 106-122 latexin Homo sapiens 126-129 23144459-0 2012 Characterization of patient mutations in human persulfide dioxygenase (ETHE1) involved in H2S catabolism. Hydrogen Sulfide 90-93 ETHE1 persulfide dioxygenase Homo sapiens 71-76 23144459-2 2012 The biogenesis of H(2)S involves the cytoplasmic transsulfuration enzymes, cystathionine beta-synthase and gamma-cystathionase, whereas its catabolism occurs in the mitochondrion and couples to the energy-yielding electron transfer chain. Hydrogen Sulfide 18-23 cystathionine beta-synthase Homo sapiens 75-102 23144459-2 2012 The biogenesis of H(2)S involves the cytoplasmic transsulfuration enzymes, cystathionine beta-synthase and gamma-cystathionase, whereas its catabolism occurs in the mitochondrion and couples to the energy-yielding electron transfer chain. Hydrogen Sulfide 18-23 cystathionine gamma-lyase Homo sapiens 107-126 23124209-1 2012 Human cystathionine beta-synthase (CBS), a novel heme-containing pyridoxal 5"-phosphate enzyme, catalyzes the condensation of homocysteine and serine or cysteine to produce cystathionine and H(2)O or H(2)S, respectively. Hydrogen Sulfide 200-205 cystathionine beta-synthase Homo sapiens 6-33 23258330-0 2012 [Hydrogen sulfide reduces lipopolysaccharide-induced acute lung injury and inhibits expression of phosphorylated p38 MAPK in rats]. Hydrogen Sulfide 1-17 mitogen activated protein kinase 14 Rattus norvegicus 113-116 23258330-7 2012 The results suggest that H2S may reduce LPS-induced ALI through inhibiting the conjugation of p38 MAPK and reducing the expression of ICAM-1. Hydrogen Sulfide 25-28 mitogen activated protein kinase 14 Rattus norvegicus 94-97 23258330-7 2012 The results suggest that H2S may reduce LPS-induced ALI through inhibiting the conjugation of p38 MAPK and reducing the expression of ICAM-1. Hydrogen Sulfide 25-28 intercellular adhesion molecule 1 Rattus norvegicus 134-140 23124209-1 2012 Human cystathionine beta-synthase (CBS), a novel heme-containing pyridoxal 5"-phosphate enzyme, catalyzes the condensation of homocysteine and serine or cysteine to produce cystathionine and H(2)O or H(2)S, respectively. Hydrogen Sulfide 200-205 cystathionine beta-synthase Homo sapiens 35-38 23124209-4 2012 The reactions of L-serine and L-cysteine with CBS resulted in the formation of a common aminoacrylate intermediate (k(obs) = 0.96 +- 0.02 and 0.38 +- 0.01 mM(-1) s(-1), respectively, at 24 C) with concomitant loss of H(2)O and H(2)S and without detectable accumulation of the external aldimine or other intermediates. Hydrogen Sulfide 228-233 cystathionine beta-synthase Homo sapiens 46-49 23249427-3 2012 The aim of this study was to investigate roles of endogenous hydrogen sulfide (H2S) producing enzyme cystathionine beta-synthetase (CBS) and p65 nuclear factor-kappa B subunits in CVH. Hydrogen Sulfide 61-77 cystathionine beta synthase Rattus norvegicus 101-130 22841986-2 2012 H(2)S can be synthesized from l-cysteine by cystathionine beta-synthetase (CBS) or cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-5 cystathionine gamma-lyase Homo sapiens 83-108 22841986-2 2012 H(2)S can be synthesized from l-cysteine by cystathionine beta-synthetase (CBS) or cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-5 cystathionine gamma-lyase Homo sapiens 110-113 23074218-0 2012 Vitamin D up-regulates glucose transporter 4 (GLUT4) translocation and glucose utilization mediated by cystathionine-gamma-lyase (CSE) activation and H2S formation in 3T3L1 adipocytes. Hydrogen Sulfide 150-153 solute carrier family 2 member 4 Homo sapiens 46-51 23074218-5 2012 The effect of 1,25(OH)(2)D(3) on GLUT4 translocation, glucose utilization, and H(2)S formation was prevented by propargylglycine, an inhibitor of CSE that catalyzes H(2)S formation. Hydrogen Sulfide 79-84 cystathionine gamma-lyase Homo sapiens 146-149 23074218-5 2012 The effect of 1,25(OH)(2)D(3) on GLUT4 translocation, glucose utilization, and H(2)S formation was prevented by propargylglycine, an inhibitor of CSE that catalyzes H(2)S formation. Hydrogen Sulfide 165-170 solute carrier family 2 member 4 Homo sapiens 33-38 23074218-5 2012 The effect of 1,25(OH)(2)D(3) on GLUT4 translocation, glucose utilization, and H(2)S formation was prevented by propargylglycine, an inhibitor of CSE that catalyzes H(2)S formation. Hydrogen Sulfide 165-170 cystathionine gamma-lyase Homo sapiens 146-149 23043860-1 2012 Endogenous hydrogen sulfide is produced by cystathionine-gamma-lyase and cystathionine-beta-synthase in a variety of tissues and has recently been implicated in the regulation of cardiac functions. Hydrogen Sulfide 11-27 cystathionine gamma-lyase Rattus norvegicus 43-68 23043860-1 2012 Endogenous hydrogen sulfide is produced by cystathionine-gamma-lyase and cystathionine-beta-synthase in a variety of tissues and has recently been implicated in the regulation of cardiac functions. Hydrogen Sulfide 11-27 cystathionine beta synthase Rattus norvegicus 73-100 23249427-3 2012 The aim of this study was to investigate roles of endogenous hydrogen sulfide (H2S) producing enzyme cystathionine beta-synthetase (CBS) and p65 nuclear factor-kappa B subunits in CVH. Hydrogen Sulfide 61-77 cystathionine beta synthase Rattus norvegicus 132-135 23249427-3 2012 The aim of this study was to investigate roles of endogenous hydrogen sulfide (H2S) producing enzyme cystathionine beta-synthetase (CBS) and p65 nuclear factor-kappa B subunits in CVH. Hydrogen Sulfide 79-82 cystathionine beta synthase Rattus norvegicus 101-130 23249427-3 2012 The aim of this study was to investigate roles of endogenous hydrogen sulfide (H2S) producing enzyme cystathionine beta-synthetase (CBS) and p65 nuclear factor-kappa B subunits in CVH. Hydrogen Sulfide 79-82 cystathionine beta synthase Rattus norvegicus 132-135 23046222-19 2012 Supplemental H(2) S decreased expression of the pro-inflammatory markers toll-like receptor 4, tumour necrosis factor alpha, interleukin 8, C-C chemokine receptor type 5, interferon gamma and interleukin 2 (P < 0.05). Hydrogen Sulfide 13-19 C-C motif chemokine receptor 5 Rattus norvegicus 140-205 22981831-9 2012 Hydrogen sulfide reduced also the thrombin- or TRAP-induced platelet adhesion to fibrinogen (for 0.00001 and 0.0001 mM NaHS, p<0.05; 0.001-1 mM NaHS, p<0.01; 5 and 10 mM NaHS, p<0.001). Hydrogen Sulfide 0-16 coagulation factor II, thrombin Homo sapiens 34-42 22981831-9 2012 Hydrogen sulfide reduced also the thrombin- or TRAP-induced platelet adhesion to fibrinogen (for 0.00001 and 0.0001 mM NaHS, p<0.05; 0.001-1 mM NaHS, p<0.01; 5 and 10 mM NaHS, p<0.001). Hydrogen Sulfide 0-16 TRAP Homo sapiens 47-51 22841676-8 2012 H(2)S production was measured by a colorimetric assay in basal and stimulated conditions with L-cysteine and in response to sildenafil (1, 3, 10, and 30 muM), 8-bromo-cyclic guanosine monophosphate (8-bromo-cGMP; 100 muM) or dibutyryl-cyclic adenosine monophosphate (dibutyryl-cAMP; 100 muM). Hydrogen Sulfide 0-5 latexin Homo sapiens 153-156 22841676-8 2012 H(2)S production was measured by a colorimetric assay in basal and stimulated conditions with L-cysteine and in response to sildenafil (1, 3, 10, and 30 muM), 8-bromo-cyclic guanosine monophosphate (8-bromo-cGMP; 100 muM) or dibutyryl-cyclic adenosine monophosphate (dibutyryl-cAMP; 100 muM). Hydrogen Sulfide 0-5 latexin Homo sapiens 217-220 22841676-8 2012 H(2)S production was measured by a colorimetric assay in basal and stimulated conditions with L-cysteine and in response to sildenafil (1, 3, 10, and 30 muM), 8-bromo-cyclic guanosine monophosphate (8-bromo-cGMP; 100 muM) or dibutyryl-cyclic adenosine monophosphate (dibutyryl-cAMP; 100 muM). Hydrogen Sulfide 0-5 latexin Homo sapiens 217-220 22841676-12 2012 RESULTS AND LIMITATIONS: CBS and CSE are present in the human bladder dome and efficiently convert L-cysteine into H(2)S. Hydrogen Sulfide 115-120 cystathionine gamma-lyase Homo sapiens 33-36 23226785-7 2012 The concentration of H(2)S at the first minute of reperfusion in the IPO 2" group was higher compared to that of the IR group, which correlated with cardioprotection including improved heart contractile function and reduced infarct size and LDH levels. Hydrogen Sulfide 21-26 transportin 1 Homo sapiens 69-74 23242725-3 2012 OBJECTIVE: Aim of this study was to identify whether hydrogen sulfide (H2S) protects heroin withdrawal rat is related with adenylate cyclase (AC)-cAMP-protein kinase A (PKA)-cAMP response element-binding protein (CREB) signaling pathway in heroin-dependent rat"s nucleus accumbens or not. Hydrogen Sulfide 53-69 cAMP responsive element binding protein 1 Rattus norvegicus 213-217 23242725-3 2012 OBJECTIVE: Aim of this study was to identify whether hydrogen sulfide (H2S) protects heroin withdrawal rat is related with adenylate cyclase (AC)-cAMP-protein kinase A (PKA)-cAMP response element-binding protein (CREB) signaling pathway in heroin-dependent rat"s nucleus accumbens or not. Hydrogen Sulfide 71-74 cAMP responsive element binding protein 1 Rattus norvegicus 213-217 23242725-7 2012 Exogenous H2S can decrease the high activities of AC, PKA and the high levels of cAMP, p-CREB caused by heroin. Hydrogen Sulfide 10-13 cAMP responsive element binding protein 1 Rattus norvegicus 89-93 23242725-8 2012 Furthermore, exogenous H2S can decrease the high level of p-NR1 and can increase the low levels of p-NR2A and p-NR2B caused by heroin. Hydrogen Sulfide 23-26 glutamate ionotropic receptor NMDA type subunit 2A Rattus norvegicus 101-105 23242725-8 2012 Furthermore, exogenous H2S can decrease the high level of p-NR1 and can increase the low levels of p-NR2A and p-NR2B caused by heroin. Hydrogen Sulfide 23-26 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 112-116 23242725-9 2012 It is surprising that exogenous H2S treatment alone was able to raise the activities of AC and PKA as well as the levels of cAMP, p-CREB, p-NR1, p-NR2A and p-NR2B. Hydrogen Sulfide 32-35 cAMP responsive element binding protein 1 Rattus norvegicus 132-136 23242725-9 2012 It is surprising that exogenous H2S treatment alone was able to raise the activities of AC and PKA as well as the levels of cAMP, p-CREB, p-NR1, p-NR2A and p-NR2B. Hydrogen Sulfide 32-35 glutamate ionotropic receptor NMDA type subunit 2A Rattus norvegicus 147-151 23242725-9 2012 It is surprising that exogenous H2S treatment alone was able to raise the activities of AC and PKA as well as the levels of cAMP, p-CREB, p-NR1, p-NR2A and p-NR2B. Hydrogen Sulfide 32-35 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 158-162 23242725-10 2012 CONCLUSIONS: Exogenous H2S decreases naloxone-precipitated withdrawal signs, maybe through decreasing AC/cAMP/PKA/CREB/NMDR signaling pathway in heroin-dependent rats" nucleus accumbens. Hydrogen Sulfide 23-26 cAMP responsive element binding protein 1 Rattus norvegicus 114-118 22434643-2 2012 The colonic mucosal thiosulfate sulfurtransferase (TST) enzyme removes H(2) S by conversion to the less toxic thiocyanate. Hydrogen Sulfide 71-77 thiosulfate sulfurtransferase Homo sapiens 20-49 22434643-2 2012 The colonic mucosal thiosulfate sulfurtransferase (TST) enzyme removes H(2) S by conversion to the less toxic thiocyanate. Hydrogen Sulfide 71-77 thiosulfate sulfurtransferase Homo sapiens 51-54 23132229-4 2012 Serum H(2)S levels in psoriasis patients were significantly lower than those of healthy controls (16.69 +- 5.47 muM vs. 34.5 +- 6.39 muM). Hydrogen Sulfide 6-11 latexin Homo sapiens 112-115 22831549-0 2012 Hydrogen sulfide inhibits the translational expression of hypoxia-inducible factor-1alpha. Hydrogen Sulfide 0-16 hypoxia inducible factor 1 subunit alpha Homo sapiens 58-89 22831549-1 2012 BACKGROUND AND PURPOSE: The accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha) is under the influence of hydrogen sulfide (H(2) S), which regulates hypoxia responses. Hydrogen Sulfide 115-131 hypoxia inducible factor 1 subunit alpha Homo sapiens 44-75 22831549-1 2012 BACKGROUND AND PURPOSE: The accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha) is under the influence of hydrogen sulfide (H(2) S), which regulates hypoxia responses. Hydrogen Sulfide 115-131 hypoxia inducible factor 1 subunit alpha Homo sapiens 77-87 22831549-2 2012 The regulation of HIF-1alpha accumulation by H(2) S has been shown, but the mechanisms for this effect are largely elusive and controversial. Hydrogen Sulfide 45-51 hypoxia inducible factor 1 subunit alpha Homo sapiens 18-28 22831549-12 2012 CONCLUSIONS AND IMPLICATIONS: H(2) S suppresses HIF-1alpha translation by enhancing eIF2alpha phosphorylation under hypoxia. Hydrogen Sulfide 30-36 hypoxia inducible factor 1 subunit alpha Homo sapiens 48-58 22831549-12 2012 CONCLUSIONS AND IMPLICATIONS: H(2) S suppresses HIF-1alpha translation by enhancing eIF2alpha phosphorylation under hypoxia. Hydrogen Sulfide 30-36 eukaryotic translation initiation factor 2A Homo sapiens 84-93 23132229-4 2012 Serum H(2)S levels in psoriasis patients were significantly lower than those of healthy controls (16.69 +- 5.47 muM vs. 34.5 +- 6.39 muM). Hydrogen Sulfide 6-11 latexin Homo sapiens 133-136 23132229-8 2012 Exogenous H(2)S inhibited the TNF-alpha-mediated upregulation of NO, IL-6 and IL-8 in a dose-dependent manner. Hydrogen Sulfide 10-15 tumor necrosis factor Homo sapiens 30-39 23132229-8 2012 Exogenous H(2)S inhibited the TNF-alpha-mediated upregulation of NO, IL-6 and IL-8 in a dose-dependent manner. Hydrogen Sulfide 10-15 interleukin 6 Homo sapiens 69-73 23132229-8 2012 Exogenous H(2)S inhibited the TNF-alpha-mediated upregulation of NO, IL-6 and IL-8 in a dose-dependent manner. Hydrogen Sulfide 10-15 C-X-C motif chemokine ligand 8 Homo sapiens 78-82 23132229-9 2012 In addition, H(2)S inhibited TNF-alpha-mediated activation of p38, extracellular-signal-regulated kinase and nuclear factor kappa B. Hydrogen Sulfide 13-18 tumor necrosis factor Homo sapiens 29-38 23132229-9 2012 In addition, H(2)S inhibited TNF-alpha-mediated activation of p38, extracellular-signal-regulated kinase and nuclear factor kappa B. Hydrogen Sulfide 13-18 mitogen-activated protein kinase 14 Homo sapiens 62-65 23122812-2 2012 Cystathionine gamma-lyase (CSE) is believed to be the major H(2)S-generating enzyme in the heart. Hydrogen Sulfide 60-65 cystathionase (cystathionine gamma-lyase) Mus musculus 0-25 23122812-2 2012 Cystathionine gamma-lyase (CSE) is believed to be the major H(2)S-generating enzyme in the heart. Hydrogen Sulfide 60-65 cystathionase (cystathionine gamma-lyase) Mus musculus 27-30 23122812-11 2012 In the presence of an CSE inhibitor, D,L-propargylglycine, H(2)S production rate of heart tissues from WT mice was inhibited by approximately 80%. Hydrogen Sulfide 59-64 cystathionase (cystathionine gamma-lyase) Mus musculus 22-25 22476058-2 2012 The enzymes that produce H(2)S - mainly cystathionine-beta-synthase and cystathionine-gamma-lyase - are expressed in pulmonary and airway tissues. Hydrogen Sulfide 25-30 cystathionine beta-synthase Homo sapiens 40-67 23122812-12 2012 It appears that CSE mediates mostly endogenous H(2)S production in heart tissues. Hydrogen Sulfide 47-52 cystathionase (cystathionine gamma-lyase) Mus musculus 16-19 22977242-0 2012 Allosteric communication between the pyridoxal 5"-phosphate (PLP) and heme sites in the H2S generator human cystathionine beta-synthase. Hydrogen Sulfide 88-91 pyridoxal phosphatase Homo sapiens 61-64 22977242-0 2012 Allosteric communication between the pyridoxal 5"-phosphate (PLP) and heme sites in the H2S generator human cystathionine beta-synthase. Hydrogen Sulfide 88-91 cystathionine beta-synthase Homo sapiens 108-135 22744006-1 2012 H(2)S generated by the enzyme cystathionine-gamma-lyase (CSE) has been implicated in O(2) sensing by the carotid body. Hydrogen Sulfide 0-5 cystathionase (cystathionine gamma-lyase) Mus musculus 30-55 22744006-1 2012 H(2)S generated by the enzyme cystathionine-gamma-lyase (CSE) has been implicated in O(2) sensing by the carotid body. Hydrogen Sulfide 0-5 cystathionase (cystathionine gamma-lyase) Mus musculus 57-60 22744006-10 2012 These results demonstrate that H(2)S generated by CSE is a physiologic mediator of the glomus cell"s response to hypoxia. Hydrogen Sulfide 31-36 cystathionase (cystathionine gamma-lyase) Mus musculus 50-53 22989474-0 2012 Relationship between hydrogen sulfide levels and HDL-cholesterol, adiponectin, and potassium levels in the blood of healthy subjects. Hydrogen Sulfide 21-37 adiponectin, C1Q and collagen domain containing Homo sapiens 66-77 22989474-5 2012 This is the first demonstration of an association of circulating levels of H(2)S with the HDL, LDL, and adiponectin homeostasis in the blood of healthy humans. Hydrogen Sulfide 75-80 adiponectin, C1Q and collagen domain containing Homo sapiens 104-115 23226735-0 2012 Cystathionine beta-synthase-derived hydrogen sulfide regulates lipopolysaccharide-induced apoptosis of the BRL rat hepatic cell line in vitro. Hydrogen Sulfide 36-52 cystathionine beta synthase Rattus norvegicus 0-27 23226735-1 2012 Hydrogen sulfide (H(2)S), is a member of the novel family of endogenous gaseous transmitters, termed "gasotransmitters exhibiting diverse physiological activities, and is generated in mammalian tissues mainly by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST) in conjunction with cysteine (aspartate) aminotranferase (CAT). Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 212-239 23226735-1 2012 Hydrogen sulfide (H(2)S), is a member of the novel family of endogenous gaseous transmitters, termed "gasotransmitters exhibiting diverse physiological activities, and is generated in mammalian tissues mainly by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST) in conjunction with cysteine (aspartate) aminotranferase (CAT). Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 241-244 23226735-1 2012 Hydrogen sulfide (H(2)S), is a member of the novel family of endogenous gaseous transmitters, termed "gasotransmitters exhibiting diverse physiological activities, and is generated in mammalian tissues mainly by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST) in conjunction with cysteine (aspartate) aminotranferase (CAT). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 247-272 23226735-1 2012 Hydrogen sulfide (H(2)S), is a member of the novel family of endogenous gaseous transmitters, termed "gasotransmitters exhibiting diverse physiological activities, and is generated in mammalian tissues mainly by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST) in conjunction with cysteine (aspartate) aminotranferase (CAT). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 274-277 23226735-1 2012 Hydrogen sulfide (H(2)S), is a member of the novel family of endogenous gaseous transmitters, termed "gasotransmitters exhibiting diverse physiological activities, and is generated in mammalian tissues mainly by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST) in conjunction with cysteine (aspartate) aminotranferase (CAT). Hydrogen Sulfide 18-23 cystathionine beta-synthase Homo sapiens 212-239 23226735-1 2012 Hydrogen sulfide (H(2)S), is a member of the novel family of endogenous gaseous transmitters, termed "gasotransmitters exhibiting diverse physiological activities, and is generated in mammalian tissues mainly by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST) in conjunction with cysteine (aspartate) aminotranferase (CAT). Hydrogen Sulfide 18-23 cystathionine beta-synthase Homo sapiens 241-244 23226735-1 2012 Hydrogen sulfide (H(2)S), is a member of the novel family of endogenous gaseous transmitters, termed "gasotransmitters exhibiting diverse physiological activities, and is generated in mammalian tissues mainly by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST) in conjunction with cysteine (aspartate) aminotranferase (CAT). Hydrogen Sulfide 18-23 cystathionine gamma-lyase Homo sapiens 247-272 23226735-1 2012 Hydrogen sulfide (H(2)S), is a member of the novel family of endogenous gaseous transmitters, termed "gasotransmitters exhibiting diverse physiological activities, and is generated in mammalian tissues mainly by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST) in conjunction with cysteine (aspartate) aminotranferase (CAT). Hydrogen Sulfide 18-23 cystathionine gamma-lyase Homo sapiens 274-277 23226735-9 2012 Pretreatment with the CBS inhibitor aminooxyacetic acid (AOAA) or CBS small interfering RNA (siRNA) decreased LPS-enhanced H(2)S production. Hydrogen Sulfide 123-128 cystathionine beta-synthase Homo sapiens 22-25 23226735-9 2012 Pretreatment with the CBS inhibitor aminooxyacetic acid (AOAA) or CBS small interfering RNA (siRNA) decreased LPS-enhanced H(2)S production. Hydrogen Sulfide 123-128 cystathionine beta-synthase Homo sapiens 66-69 22476058-2 2012 The enzymes that produce H(2)S - mainly cystathionine-beta-synthase and cystathionine-gamma-lyase - are expressed in pulmonary and airway tissues. Hydrogen Sulfide 25-30 cystathionine gamma-lyase Homo sapiens 72-97 22664830-8 2012 Exogenous application of H(2)S donors, like hypoxia, stimulate the carotid body activity and CSE knockout mice exhibit severely impaired sensory excitation by hypoxia, suggesting that CSE catalyzed H(2)S is an excitatory gas messenger. Hydrogen Sulfide 25-30 cystathionase (cystathionine gamma-lyase) Mus musculus 93-96 22664830-8 2012 Exogenous application of H(2)S donors, like hypoxia, stimulate the carotid body activity and CSE knockout mice exhibit severely impaired sensory excitation by hypoxia, suggesting that CSE catalyzed H(2)S is an excitatory gas messenger. Hydrogen Sulfide 25-30 cystathionase (cystathionine gamma-lyase) Mus musculus 184-187 22664830-8 2012 Exogenous application of H(2)S donors, like hypoxia, stimulate the carotid body activity and CSE knockout mice exhibit severely impaired sensory excitation by hypoxia, suggesting that CSE catalyzed H(2)S is an excitatory gas messenger. Hydrogen Sulfide 198-203 cystathionase (cystathionine gamma-lyase) Mus musculus 93-96 22664830-8 2012 Exogenous application of H(2)S donors, like hypoxia, stimulate the carotid body activity and CSE knockout mice exhibit severely impaired sensory excitation by hypoxia, suggesting that CSE catalyzed H(2)S is an excitatory gas messenger. Hydrogen Sulfide 198-203 cystathionase (cystathionine gamma-lyase) Mus musculus 184-187 22816429-2 2012 This study determined the effects of H(2) S derived from AtLCD and AtDCD on cadmium (Cd) toxicity in Escherichia coli. Hydrogen Sulfide 37-43 Pyridoxal phosphate (PLP)-dependent transferases superfamily protein Arabidopsis thaliana 57-62 23144183-1 2012 In Arabidopsis thaliana, DES1 is the only identified L-Cysteine desulfhydrase located in the cytosol, and it is involved in the degradation of cysteine and the concomitant production of H(2)S in this cell compartment. Hydrogen Sulfide 186-191 L-cysteine desulfhydrase 1 Arabidopsis thaliana 25-29 22895544-0 2012 Hydrogen sulfide protects PC12 cells against reactive oxygen species and extracellular signal-regulated kinase 1/2-mediated downregulation of glutamate transporter-1 expression induced by chemical hypoxia. Hydrogen Sulfide 0-16 mitogen activated protein kinase 3 Rattus norvegicus 85-126 22895544-0 2012 Hydrogen sulfide protects PC12 cells against reactive oxygen species and extracellular signal-regulated kinase 1/2-mediated downregulation of glutamate transporter-1 expression induced by chemical hypoxia. Hydrogen Sulfide 0-16 solute carrier family 1 member 2 Rattus norvegicus 154-189 22895544-4 2012 In the present study, we investigated the role of glutamate transporter-1 (GLT-1) in the protection of H2S against chemical hypoxia-induced injury in PC12 cells. Hydrogen Sulfide 103-106 solute carrier family 1 member 2 Rattus norvegicus 50-73 22895544-4 2012 In the present study, we investigated the role of glutamate transporter-1 (GLT-1) in the protection of H2S against chemical hypoxia-induced injury in PC12 cells. Hydrogen Sulfide 103-106 solute carrier family 1 member 2 Rattus norvegicus 75-80 22895544-6 2012 Pretreatment with NaHS (a donor of H2S) reversed the CoCl2-induced downregulation of GLT-1 expression. Hydrogen Sulfide 35-38 solute carrier family 1 member 2 Homo sapiens 85-90 22895544-7 2012 Pretreatment with DHK (a selective inhibitor of GLT-1) for 30 min prior to NaHS preconditioning significantly inhibited the cytoprotection of H2S against CoCl2-induced injuries, leading to an increase in cytotoxicity and apoptosis as well as to a loss of mitochondrial membrane potential (MMP). Hydrogen Sulfide 142-145 solute carrier family 1 member 2 Rattus norvegicus 48-53 22895544-9 2012 Collectively, we demonstrated for the first time that ROS and extracellular signal-regulated kinase 1/2 (ERK1/2)-mediated reduction of GLT-1 expression may be involved in chemical hypoxia-induced neural injury and that H2S attenuates this injury partly by upregulating GLT-1 expression in PC12 cells. Hydrogen Sulfide 219-222 mitogen activated protein kinase 3 Rattus norvegicus 62-103 22895544-9 2012 Collectively, we demonstrated for the first time that ROS and extracellular signal-regulated kinase 1/2 (ERK1/2)-mediated reduction of GLT-1 expression may be involved in chemical hypoxia-induced neural injury and that H2S attenuates this injury partly by upregulating GLT-1 expression in PC12 cells. Hydrogen Sulfide 219-222 mitogen activated protein kinase 3 Rattus norvegicus 105-111 22895544-9 2012 Collectively, we demonstrated for the first time that ROS and extracellular signal-regulated kinase 1/2 (ERK1/2)-mediated reduction of GLT-1 expression may be involved in chemical hypoxia-induced neural injury and that H2S attenuates this injury partly by upregulating GLT-1 expression in PC12 cells. Hydrogen Sulfide 219-222 solute carrier family 1 member 2 Rattus norvegicus 135-140 22895544-9 2012 Collectively, we demonstrated for the first time that ROS and extracellular signal-regulated kinase 1/2 (ERK1/2)-mediated reduction of GLT-1 expression may be involved in chemical hypoxia-induced neural injury and that H2S attenuates this injury partly by upregulating GLT-1 expression in PC12 cells. Hydrogen Sulfide 219-222 solute carrier family 1 member 2 Rattus norvegicus 269-274 22906137-0 2012 H2S relaxes vas deferens smooth muscle by modulating the large conductance Ca2+ -activated K+ (BKCa) channels via a redox mechanism. Hydrogen Sulfide 0-3 potassium calcium-activated channel subfamily M alpha 1 Rattus norvegicus 95-99 23059761-2 2012 H(2)S is biosynthesized in mammalian tissues by cystathionine-beta-synthase and cystathionine-gamma-lyase. Hydrogen Sulfide 0-5 cystathionine beta-synthase Homo sapiens 48-75 23059761-2 2012 H(2)S is biosynthesized in mammalian tissues by cystathionine-beta-synthase and cystathionine-gamma-lyase. Hydrogen Sulfide 0-5 cystathionine gamma-lyase Homo sapiens 80-105 23124382-3 2012 In this study, we found that the vascular H(2)S-producing enzyme, cystathionine-gamma-lyase (CSE), was down-regulated by oscillatory shear stress (OSS) among various vaso-regulators. Hydrogen Sulfide 42-47 cystathionine gamma-lyase Homo sapiens 66-91 23124382-3 2012 In this study, we found that the vascular H(2)S-producing enzyme, cystathionine-gamma-lyase (CSE), was down-regulated by oscillatory shear stress (OSS) among various vaso-regulators. Hydrogen Sulfide 42-47 cystathionine gamma-lyase Homo sapiens 93-96 23124382-8 2012 These data suggest that down-regulation of CSE resulting in decreased levels of H(2)S is a key factor for OSS-associated atherogenesis and further suggest that regulation of H(2)S production can be a potential target for preventing cardiovascular diseases. Hydrogen Sulfide 80-85 cystathionine gamma-lyase Homo sapiens 43-46 23124382-8 2012 These data suggest that down-regulation of CSE resulting in decreased levels of H(2)S is a key factor for OSS-associated atherogenesis and further suggest that regulation of H(2)S production can be a potential target for preventing cardiovascular diseases. Hydrogen Sulfide 174-179 cystathionine gamma-lyase Homo sapiens 43-46 22511607-2 2012 In mitochondria, cyanide is a potent inhibitor of the cytochrome c oxidase and is metabolized by the beta-cyanoalanine synthase CYS-C1, catalyzing the conversion of cysteine and cyanide to hydrogen sulfide and beta-cyanoalanine. Hydrogen Sulfide 189-205 cysteine synthase C1 Arabidopsis thaliana 128-134 22511607-3 2012 The hydrogen sulfide released also inhibits the cytochrome c oxidase and needs to be detoxified by the O-acetylserine(thiol)lyase mitochondrial isoform, OAS-C, which catalyzes the incorporation of sulfide to O-acetylserine to produce cysteine, thus generating a cyclic pathway in the mitochondria. Hydrogen Sulfide 4-20 O-acetylserine (thiol) lyase Arabidopsis thaliana 153-158 23144183-3 2012 Mutations of L-CYS DESULFHYDRASE 1 (DES1) impede H(2)S generation in the Arabidopsis cytosol and strongly affect plant metabolism. Hydrogen Sulfide 49-54 L-cysteine desulfhydrase 1 Arabidopsis thaliana 36-40 23020085-4 2012 However, the bystander effects were increased when the irradiated cells were pretreated with an inhibitor of cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), the synthases of endogenous hydrogen sulfide (H(2)S). Hydrogen Sulfide 208-224 cystathionine beta-synthase Homo sapiens 109-136 23020085-4 2012 However, the bystander effects were increased when the irradiated cells were pretreated with an inhibitor of cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), the synthases of endogenous hydrogen sulfide (H(2)S). Hydrogen Sulfide 208-224 cystathionine gamma-lyase Homo sapiens 147-172 23020085-4 2012 However, the bystander effects were increased when the irradiated cells were pretreated with an inhibitor of cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), the synthases of endogenous hydrogen sulfide (H(2)S). Hydrogen Sulfide 208-224 cystathionine gamma-lyase Homo sapiens 174-177 23020085-7 2012 However, the activity of caspase-3 increased in the hypoxic bystander cells, and this could be regulated by both NaHS and the inhibitor of endogenous H(2)S. Hydrogen Sulfide 150-155 caspase 3 Homo sapiens 25-34 22884438-0 2012 Role of KATP channels and TRPV1 receptors in hydrogen sulfide-enhanced gastric emptying of liquid in awake mice. Hydrogen Sulfide 45-61 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 26-31 22884438-10 2012 These data suggest that H(2)S donors-induced acceleration of gastric emptying and relaxation of pyloric sphincter muscle by K(ATP) channel and TRPV1 receptor activations. Hydrogen Sulfide 24-29 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 143-148 23290060-0 2012 [Alternation of thioredoxin system in postconditioning with hydrogen sulfide against hepatic ischemia-reperfusion injury in rats]. Hydrogen Sulfide 60-76 thioredoxin 1 Rattus norvegicus 16-27 23290060-1 2012 OBJECTIVE: To explore the relationship between the protection of hydrogen sulfide (H(2)S) against hepatic ischemia-reperfusion injury and thioredoxin system in rats. Hydrogen Sulfide 65-81 thioredoxin 1 Rattus norvegicus 138-149 23290060-1 2012 OBJECTIVE: To explore the relationship between the protection of hydrogen sulfide (H(2)S) against hepatic ischemia-reperfusion injury and thioredoxin system in rats. Hydrogen Sulfide 83-88 thioredoxin 1 Rattus norvegicus 138-149 23290060-11 2012 It indicated that the postconditioning with H(2)S could reduce the inhibition of Trx system and boost tissue antioxidant capacity. Hydrogen Sulfide 44-49 thioredoxin 1 Rattus norvegicus 81-84 23290060-12 2012 CONCLUSION: Hydrogen sulfide postconditioning can enhance the cellular Trx system and play a protective role in hepatic ischemia-reperfusion injury. Hydrogen Sulfide 12-28 thioredoxin 1 Rattus norvegicus 71-74 22948409-10 2012 However, H2S-mediated protection was abolished by AG-490, the JAK2 inhibitor. Hydrogen Sulfide 9-12 Janus kinase 2 Rattus norvegicus 62-66 22842066-0 2012 Hydrogen sulfide modulates the release of nitric oxide and VEGF in human keratinocytes. Hydrogen Sulfide 0-16 vascular endothelial growth factor A Homo sapiens 59-63 22842066-2 2012 The present study aimed to: (i) characterize the in vitro effects of H(2)S on human keratinocyte"s proliferation and death; (ii) investigate the ability of H(2)S to modulate VEGF and NO production; (iii) examine the intracellular signaling pathways involved in VEGF and NO modulatory effect. Hydrogen Sulfide 156-161 vascular endothelial growth factor A Homo sapiens 174-178 22842066-2 2012 The present study aimed to: (i) characterize the in vitro effects of H(2)S on human keratinocyte"s proliferation and death; (ii) investigate the ability of H(2)S to modulate VEGF and NO production; (iii) examine the intracellular signaling pathways involved in VEGF and NO modulatory effect. Hydrogen Sulfide 156-161 vascular endothelial growth factor A Homo sapiens 261-265 22842066-3 2012 We found that exogenous application of H(2)S (NaHS and GYY4137 as H(2)S donors) significantly enhances NO through increase of iNOS, in a manner Akt-dependent. Hydrogen Sulfide 39-44 inositol-3-phosphate synthase 1 Homo sapiens 126-130 22842066-3 2012 We found that exogenous application of H(2)S (NaHS and GYY4137 as H(2)S donors) significantly enhances NO through increase of iNOS, in a manner Akt-dependent. Hydrogen Sulfide 39-44 AKT serine/threonine kinase 1 Homo sapiens 144-147 22842066-3 2012 We found that exogenous application of H(2)S (NaHS and GYY4137 as H(2)S donors) significantly enhances NO through increase of iNOS, in a manner Akt-dependent. Hydrogen Sulfide 66-71 inositol-3-phosphate synthase 1 Homo sapiens 126-130 22842066-3 2012 We found that exogenous application of H(2)S (NaHS and GYY4137 as H(2)S donors) significantly enhances NO through increase of iNOS, in a manner Akt-dependent. Hydrogen Sulfide 66-71 AKT serine/threonine kinase 1 Homo sapiens 144-147 22592920-0 2012 Hydrogen sulfide attenuates particulate matter-induced human lung endothelial barrier disruption via combined reactive oxygen species scavenging and Akt activation. Hydrogen Sulfide 0-16 AKT serine/threonine kinase 1 Homo sapiens 149-152 22646666-1 2012 BACKGROUND AND PURPOSE: Hydrogen sulfide (H(2) S), generated by enzymes such as cystathionine-gamma-lyase (CSE) from L-cysteine, facilitates pain signals by activating the Ca(v) 3.2 T-type Ca(2+) channels. Hydrogen Sulfide 24-40 cystathionase (cystathionine gamma-lyase) Mus musculus 80-105 22646666-1 2012 BACKGROUND AND PURPOSE: Hydrogen sulfide (H(2) S), generated by enzymes such as cystathionine-gamma-lyase (CSE) from L-cysteine, facilitates pain signals by activating the Ca(v) 3.2 T-type Ca(2+) channels. Hydrogen Sulfide 24-40 cystathionase (cystathionine gamma-lyase) Mus musculus 107-110 22646666-1 2012 BACKGROUND AND PURPOSE: Hydrogen sulfide (H(2) S), generated by enzymes such as cystathionine-gamma-lyase (CSE) from L-cysteine, facilitates pain signals by activating the Ca(v) 3.2 T-type Ca(2+) channels. Hydrogen Sulfide 24-40 caveolin 3 Mus musculus 172-179 22646666-1 2012 BACKGROUND AND PURPOSE: Hydrogen sulfide (H(2) S), generated by enzymes such as cystathionine-gamma-lyase (CSE) from L-cysteine, facilitates pain signals by activating the Ca(v) 3.2 T-type Ca(2+) channels. Hydrogen Sulfide 42-48 cystathionase (cystathionine gamma-lyase) Mus musculus 80-105 22646666-1 2012 BACKGROUND AND PURPOSE: Hydrogen sulfide (H(2) S), generated by enzymes such as cystathionine-gamma-lyase (CSE) from L-cysteine, facilitates pain signals by activating the Ca(v) 3.2 T-type Ca(2+) channels. Hydrogen Sulfide 42-48 cystathionase (cystathionine gamma-lyase) Mus musculus 107-110 22646666-1 2012 BACKGROUND AND PURPOSE: Hydrogen sulfide (H(2) S), generated by enzymes such as cystathionine-gamma-lyase (CSE) from L-cysteine, facilitates pain signals by activating the Ca(v) 3.2 T-type Ca(2+) channels. Hydrogen Sulfide 42-48 caveolin 3 Mus musculus 172-179 22646666-6 2012 Phosphorylation of ERK in the spinal dorsal horn was determined immunohistochemically following intravesical administration of NaHS, an H(2) S donor. Hydrogen Sulfide 136-142 mitogen-activated protein kinase 1 Homo sapiens 19-22 22646666-13 2012 CONCLUSION AND IMPLICATIONS: Endogenous H(2) S, generated by up-regulated CSE, caused bladder pain and referred hyperalgesia through the activation of Ca(v) 3.2 channels, one of the T-type Ca(2+) channels, in mice with cyclophosphamide-induced cystitis. Hydrogen Sulfide 40-46 cystathionase (cystathionine gamma-lyase) Mus musculus 74-77 22646666-13 2012 CONCLUSION AND IMPLICATIONS: Endogenous H(2) S, generated by up-regulated CSE, caused bladder pain and referred hyperalgesia through the activation of Ca(v) 3.2 channels, one of the T-type Ca(2+) channels, in mice with cyclophosphamide-induced cystitis. Hydrogen Sulfide 40-46 calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus 151-160 22982226-2 2012 Here, we investigated whether hydrogen sulfide (H(2)S)/cystathionine gamma-lyase (CSE) pathway could serve the protective role toward radiation in normal human liver cells. Hydrogen Sulfide 30-46 cystathionine gamma-lyase Homo sapiens 55-80 23316304-0 2012 Hydrogen sulfide stimulates ischemic vascular remodeling through nitric oxide synthase and nitrite reduction activity regulating hypoxia-inducible factor-1alpha and vascular endothelial growth factor-dependent angiogenesis. Hydrogen Sulfide 0-16 hypoxia inducible factor 1, alpha subunit Mus musculus 129-160 23025523-14 2012 In addition, myeloperoxidase levels were increased in serum after LPS challenge and this was prevented by H2S inhalation. Hydrogen Sulfide 106-109 myeloperoxidase Mus musculus 13-28 22982226-9 2012 In conclusion, our finding demonstrates that H(2)S/CSE pathway plays a radioprotection role by inhibiting radiation-induced ROS production, P53 phosphorylation, NF-kappaB activation and decrease of Bcl-2/Bax, indicating that modulation of H(2)S may be a novel protection strategy for liver radiation injury in radiotherapy. Hydrogen Sulfide 45-50 tumor protein p53 Homo sapiens 140-143 22982226-9 2012 In conclusion, our finding demonstrates that H(2)S/CSE pathway plays a radioprotection role by inhibiting radiation-induced ROS production, P53 phosphorylation, NF-kappaB activation and decrease of Bcl-2/Bax, indicating that modulation of H(2)S may be a novel protection strategy for liver radiation injury in radiotherapy. Hydrogen Sulfide 45-50 BCL2 apoptosis regulator Homo sapiens 198-203 22982226-9 2012 In conclusion, our finding demonstrates that H(2)S/CSE pathway plays a radioprotection role by inhibiting radiation-induced ROS production, P53 phosphorylation, NF-kappaB activation and decrease of Bcl-2/Bax, indicating that modulation of H(2)S may be a novel protection strategy for liver radiation injury in radiotherapy. Hydrogen Sulfide 45-50 BCL2 associated X, apoptosis regulator Homo sapiens 204-207 22360462-5 2012 We further found that deficiency of mitochondrial uncoupling protein 2 (UCP2), which reduces reactive oxygen species (ROS) production and functions as upstream to the K-ATP channel in determining vulnerability of DA neurons, abolished the protective effects of H(2)S against either DA neuron degeneration in the PD mouse model or MPP(+)-induced injury in primary mesencephalic neurons. Hydrogen Sulfide 261-266 uncoupling protein 2 (mitochondrial, proton carrier) Mus musculus 36-70 22884808-0 2012 Hydrogen sulfide regulates cardiac sarcoplasmic reticulum Ca(2+) uptake via K(ATP) channel and PI3K/Akt pathway. Hydrogen Sulfide 0-16 AKT serine/threonine kinase 1 Rattus norvegicus 100-103 22884808-7 2012 Glibenclamide (a K(ATP) channel blocker) blocked the inhibitory effects of H(2)S on PLB and Akt phosphorylation. Hydrogen Sulfide 75-80 AKT serine/threonine kinase 1 Rattus norvegicus 92-95 22884808-10 2012 SIGNIFICANCE: Endogenous H(2)S transiently and reversibly inhibits SR Ca(2+) uptake in rat heart SR because of downregulated SERCA activity associated with PLB phosphorylation by the PI3K/Akt or K(ATP) channel. Hydrogen Sulfide 25-30 AKT serine/threonine kinase 1 Rattus norvegicus 188-191 22360462-5 2012 We further found that deficiency of mitochondrial uncoupling protein 2 (UCP2), which reduces reactive oxygen species (ROS) production and functions as upstream to the K-ATP channel in determining vulnerability of DA neurons, abolished the protective effects of H(2)S against either DA neuron degeneration in the PD mouse model or MPP(+)-induced injury in primary mesencephalic neurons. Hydrogen Sulfide 261-266 uncoupling protein 2 (mitochondrial, proton carrier) Mus musculus 72-76 22360462-7 2012 Furthermore, H(2)S exerted neuroprotective effect via enhancing UCP2-mediated antioxidation and subsequently suppressing ROS-triggered endoplasmic reticulum stress as well as ultimately inhibiting caspase 12-induced neuronal apoptosis. Hydrogen Sulfide 13-18 uncoupling protein 2 (mitochondrial, proton carrier) Mus musculus 64-68 22360462-7 2012 Furthermore, H(2)S exerted neuroprotective effect via enhancing UCP2-mediated antioxidation and subsequently suppressing ROS-triggered endoplasmic reticulum stress as well as ultimately inhibiting caspase 12-induced neuronal apoptosis. Hydrogen Sulfide 13-18 caspase 12 Mus musculus 197-207 22360462-8 2012 INNOVATION AND CONCLUSION: H(2)S protects DA neurons against degeneration in a UCP2 rather than Kir6.2/K-ATP channel-dependent mechanism, which will give us an insight into the potential of H(2)S in terms of opening up new therapeutic avenues for PD. Hydrogen Sulfide 27-32 uncoupling protein 2 (mitochondrial, proton carrier) Mus musculus 79-83 22903887-4 2012 Here, we show that AAV2/8-mediated, ETHE1-gene transfer to the liver of a genetically, metabolically and clinically faithful EE mouse model resulted in full restoration of SDO activity, correction of plasma thiosulfate, a biomarker reflecting the accumulation of H(2)S, and spectacular clinical improvement. Hydrogen Sulfide 263-268 ethylmalonic encephalopathy 1 Mus musculus 36-41 22900817-5 2012 In one wine MOX increased the concentration of H(2)S and methyl mercaptan during maturation. Hydrogen Sulfide 47-52 monooxygenase DBH like 1 Homo sapiens 12-15 22392688-1 2012 INTRODUCTION: On August 2006, a cargo ship illegally dumped 500 t of toxic waste containing high concentrations of hydrogen sulphide in numerous sites across Abidjan. Hydrogen Sulfide 115-132 inositol polyphosphate-5-phosphatase D Homo sapiens 38-42 22034194-1 2012 Cystathionine gamma-lyase (CSE) is the major H(2)S-generating enzyme in vascular smooth muscle cells (SMCs). Hydrogen Sulfide 45-50 cystathionine gamma-lyase Homo sapiens 0-25 22034194-1 2012 Cystathionine gamma-lyase (CSE) is the major H(2)S-generating enzyme in vascular smooth muscle cells (SMCs). Hydrogen Sulfide 45-50 cystathionine gamma-lyase Homo sapiens 27-30 22034194-6 2012 Interestingly, miR-21 overexpression significantly repressed the protein expressions of both CSE and SP1, inhibited H(2)S production, stimulated SMC proliferation, and reduced SMC differentiation marker gene expression, respectively. Hydrogen Sulfide 116-121 microRNA 21 Homo sapiens 15-21 22034194-10 2012 Take together, these results suggest that miR-21 participates in CSE/H(2)S-mediated-SMC differentiation by targeting SP1. Hydrogen Sulfide 69-74 microRNA 21 Homo sapiens 42-48 22034194-10 2012 Take together, these results suggest that miR-21 participates in CSE/H(2)S-mediated-SMC differentiation by targeting SP1. Hydrogen Sulfide 69-74 cystathionine gamma-lyase Homo sapiens 65-68 23000765-9 2012 CONCLUSION: Exogenous hydrogen sulfide can effectively inhibit the development of hepatic fibrosis, reduce the expression of TGF-beta1, and decrease the the sediment of extracellular matrix in the liver tissues. Hydrogen Sulfide 22-38 transforming growth factor, beta 1 Rattus norvegicus 125-134 23193672-2 2012 In mammalians, H2S is mainly synthesized by two proteases, cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE). Hydrogen Sulfide 15-18 cystathionine beta-synthase Homo sapiens 59-86 23193672-2 2012 In mammalians, H2S is mainly synthesized by two proteases, cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE). Hydrogen Sulfide 15-18 cystathionine gamma-lyase Homo sapiens 97-122 23193672-2 2012 In mammalians, H2S is mainly synthesized by two proteases, cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE). Hydrogen Sulfide 15-18 cystathionine gamma-lyase Homo sapiens 124-127 22641084-3 2012 Here we show that H(2)S activates mouse transient receptor potential ankyrin 1 (TRPA1) channels and elicits acute pain, using TRPA1-gene deficient mice (TRPA1(-/-)) and heterologous expression system. Hydrogen Sulfide 18-23 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 40-78 22641084-3 2012 Here we show that H(2)S activates mouse transient receptor potential ankyrin 1 (TRPA1) channels and elicits acute pain, using TRPA1-gene deficient mice (TRPA1(-/-)) and heterologous expression system. Hydrogen Sulfide 18-23 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 80-85 22641084-3 2012 Here we show that H(2)S activates mouse transient receptor potential ankyrin 1 (TRPA1) channels and elicits acute pain, using TRPA1-gene deficient mice (TRPA1(-/-)) and heterologous expression system. Hydrogen Sulfide 18-23 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 126-131 22641084-3 2012 Here we show that H(2)S activates mouse transient receptor potential ankyrin 1 (TRPA1) channels and elicits acute pain, using TRPA1-gene deficient mice (TRPA1(-/-)) and heterologous expression system. Hydrogen Sulfide 18-23 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 126-131 22641084-4 2012 In wild-type mouse sensory neurons, H(2)S increased the intracellular Ca(2+) concentration ([Ca(2+)](i)), which was inhibited by ruthenium red (a nonselective TRP channel blocker) and HC-030031 (a TRPA1 blocker). Hydrogen Sulfide 36-41 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 197-202 22641084-5 2012 H(2)S-responsive neurons highly corresponded to TRPA1 agonist-sensitive ones. Hydrogen Sulfide 0-5 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 48-53 22641084-6 2012 [Ca(2+)](i) responses to H(2)S were observed in neurons from transient receptor potential vanilloid 1 (TRPV1(-/-)) mice but not from TRPA1(-/-) mice. Hydrogen Sulfide 25-30 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 103-108 22641084-7 2012 Heterologously expressed mouse TRPA1, but not mouse TRPV1, was activated by H(2)S. Hydrogen Sulfide 76-81 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 31-36 22641084-9 2012 Analyses of the TRPA1 mutant channel revealed that two cysteine residues located in the N-terminal internal domain were responsible for the activation by H(2)S. Hydrogen Sulfide 154-159 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 16-21 22641084-10 2012 Intraplantar injection of H(2)S into the mouse hind paw caused acute pain which was significantly less in TRPA1(-/-) mice. Hydrogen Sulfide 26-31 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 106-111 22641084-12 2012 These results suggest that H(2)S functions as a nociceptive messenger through the activation of TRPA1 channels. Hydrogen Sulfide 27-32 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 96-101 22641084-13 2012 TRPA1 may be a therapeutic target for H(2)S-related algesic action, especially under inflammatory conditions. Hydrogen Sulfide 38-43 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 0-5 22852582-0 2012 Human sulfide:quinone oxidoreductase catalyzes the first step in hydrogen sulfide metabolism and produces a sulfane sulfur metabolite. Hydrogen Sulfide 65-81 crystallin zeta Homo sapiens 14-36 22852582-1 2012 Sulfide:quinone oxidoreductase (SQOR) is a membrane-bound enzyme that catalyzes the first step in the mitochondrial metabolism of H(2)S. Hydrogen Sulfide 130-135 crystallin zeta Homo sapiens 8-30 22852582-1 2012 Sulfide:quinone oxidoreductase (SQOR) is a membrane-bound enzyme that catalyzes the first step in the mitochondrial metabolism of H(2)S. Hydrogen Sulfide 130-135 sulfide quinone oxidoreductase Homo sapiens 32-36 22852582-3 2012 Recombinant SQOR contains noncovalently bound FAD and catalyzes the two-electron oxidation of H(2)S to S(0) (sulfane sulfur) using CoQ(1) as an electron acceptor. Hydrogen Sulfide 94-99 sulfide quinone oxidoreductase Homo sapiens 12-16 22852582-7 2012 Oxidation of H(2)S by SQOR with sulfite as the sulfane sulfur acceptor is rapid and highly efficient at physiological pH (k(cat)/K(m,H(2)S) = 2.9 x 10(7) M(-1) s(-1)). Hydrogen Sulfide 13-18 sulfide quinone oxidoreductase Homo sapiens 22-26 22852582-7 2012 Oxidation of H(2)S by SQOR with sulfite as the sulfane sulfur acceptor is rapid and highly efficient at physiological pH (k(cat)/K(m,H(2)S) = 2.9 x 10(7) M(-1) s(-1)). Hydrogen Sulfide 47-54 sulfide quinone oxidoreductase Homo sapiens 22-26 22721614-0 2012 The role of transient receptor potential ankyrin 1 (TRPA1) receptor activation in hydrogen-sulphide-induced CGRP-release and vasodilation. Hydrogen Sulfide 82-99 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 12-50 22721614-9 2012 We conclude that H(2)S activates TRPA1 receptors causing CGRP release from sensory nerves of rat tracheae, as well as inducing cutaneous vasodilatation in the mouse ear. Hydrogen Sulfide 17-22 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 33-38 22721614-9 2012 We conclude that H(2)S activates TRPA1 receptors causing CGRP release from sensory nerves of rat tracheae, as well as inducing cutaneous vasodilatation in the mouse ear. Hydrogen Sulfide 17-22 calcitonin-related polypeptide alpha Rattus norvegicus 57-61 22721614-11 2012 Our results highlight that TRPA1 receptor activation should be considered as a potential mechanism of vasoactive effects of H(2)S. Hydrogen Sulfide 124-129 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 27-32 22837466-3 2012 We also found that cooling of hamster cells increased endogenous production of H(2)S through the enzyme cystathionine-beta-synthase (CBS). Hydrogen Sulfide 79-84 cystathionine beta-synthase-like protein Mesocricetus auratus 133-136 22837466-15 2012 Our data indicate that increased production of H(2)S through CBS in hamster lungs during torpor contributes to remodeling by inhibition of gelatinase activity and possibly by suppression of the inflammatory response. Hydrogen Sulfide 47-52 cystathionine beta-synthase-like protein Mesocricetus auratus 61-64 22721614-0 2012 The role of transient receptor potential ankyrin 1 (TRPA1) receptor activation in hydrogen-sulphide-induced CGRP-release and vasodilation. Hydrogen Sulfide 82-99 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 52-57 22721614-0 2012 The role of transient receptor potential ankyrin 1 (TRPA1) receptor activation in hydrogen-sulphide-induced CGRP-release and vasodilation. Hydrogen Sulfide 82-99 calcitonin/calcitonin-related polypeptide, alpha Mus musculus 108-112 22721614-2 2012 We investigated whether the hydrogen sulphide (H(2)S)-evoked CGRP release from sensory neurons of isolated rat tracheae and H(2)S-induced increases in the microcirculation of the mouse ear were mediated by TRPA1 receptor activation. Hydrogen Sulfide 28-45 calcitonin-related polypeptide alpha Rattus norvegicus 61-65 22721614-2 2012 We investigated whether the hydrogen sulphide (H(2)S)-evoked CGRP release from sensory neurons of isolated rat tracheae and H(2)S-induced increases in the microcirculation of the mouse ear were mediated by TRPA1 receptor activation. Hydrogen Sulfide 28-45 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 206-211 22721614-2 2012 We investigated whether the hydrogen sulphide (H(2)S)-evoked CGRP release from sensory neurons of isolated rat tracheae and H(2)S-induced increases in the microcirculation of the mouse ear were mediated by TRPA1 receptor activation. Hydrogen Sulfide 47-52 calcitonin-related polypeptide alpha Rattus norvegicus 61-65 22721614-2 2012 We investigated whether the hydrogen sulphide (H(2)S)-evoked CGRP release from sensory neurons of isolated rat tracheae and H(2)S-induced increases in the microcirculation of the mouse ear were mediated by TRPA1 receptor activation. Hydrogen Sulfide 47-52 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 206-211 22721614-2 2012 We investigated whether the hydrogen sulphide (H(2)S)-evoked CGRP release from sensory neurons of isolated rat tracheae and H(2)S-induced increases in the microcirculation of the mouse ear were mediated by TRPA1 receptor activation. Hydrogen Sulfide 124-129 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 206-211 22934072-8 2012 TRPA1 also detects other gaseous molecules such as hydrogen sulfide (H(2)S) and carbon dioxide (CO(2)). Hydrogen Sulfide 51-67 transient receptor potential cation channel subfamily A member 1 Homo sapiens 0-5 22934072-8 2012 TRPA1 also detects other gaseous molecules such as hydrogen sulfide (H(2)S) and carbon dioxide (CO(2)). Hydrogen Sulfide 69-74 transient receptor potential cation channel subfamily A member 1 Homo sapiens 0-5 22428706-2 2012 This study was done to evaluate the redox-dependent signalling events that regulate the expression of the H(2) S synthesising enzyme cystathionine-gamma-lyase (CSE) in rat mesangial cells. Hydrogen Sulfide 106-112 cystathionine gamma-lyase Rattus norvegicus 133-158 22428706-2 2012 This study was done to evaluate the redox-dependent signalling events that regulate the expression of the H(2) S synthesising enzyme cystathionine-gamma-lyase (CSE) in rat mesangial cells. Hydrogen Sulfide 106-112 cystathionine gamma-lyase Rattus norvegicus 160-163 22519544-1 2012 UNLABELLED: Recently, cystathionine-gamma-lyase (CSE) was found to provide the major physiological pathway for H(2) S, the third member of the gasotransmitter family. Hydrogen Sulfide 111-117 cystathionine gamma-lyase Homo sapiens 22-47 22519544-1 2012 UNLABELLED: Recently, cystathionine-gamma-lyase (CSE) was found to provide the major physiological pathway for H(2) S, the third member of the gasotransmitter family. Hydrogen Sulfide 111-117 cystathionine gamma-lyase Homo sapiens 49-52 21541705-0 2012 Hydrogen sulfide down-regulates the expression and release of osteoprotegerin (OPG) by vascular endothelial cells. Hydrogen Sulfide 0-16 TNF receptor superfamily member 11b Homo sapiens 62-77 21541705-0 2012 Hydrogen sulfide down-regulates the expression and release of osteoprotegerin (OPG) by vascular endothelial cells. Hydrogen Sulfide 0-16 TNF receptor superfamily member 11b Homo sapiens 79-82 22716165-6 2012 Animals treated with H2 S showed attenuated serum ALT and AST levels and reduced necrotic lesions after 24 h. IRI animals had increased Bcl-2 mRNA expression and increased active Caspase 3 protein, which were both significantly lower in H2 S treated animals. Hydrogen Sulfide 21-25 glutamic pyruvic transaminase, soluble Mus musculus 50-53 22934046-8 2012 This objective is achieved by discussing the involvement of H(2)S in the regulation of (1) ion channels such as calcium (L-type, T-type, and intracellular stores), potassium (K(ATP) and small conductance channels) and chloride channels, (2) glutamate transporters such as EAAT1/GLAST and the L-cystine/glutamate antiporter. Hydrogen Sulfide 60-65 solute carrier family 1 member 3 Homo sapiens 272-277 22934046-8 2012 This objective is achieved by discussing the involvement of H(2)S in the regulation of (1) ion channels such as calcium (L-type, T-type, and intracellular stores), potassium (K(ATP) and small conductance channels) and chloride channels, (2) glutamate transporters such as EAAT1/GLAST and the L-cystine/glutamate antiporter. Hydrogen Sulfide 60-65 solute carrier family 1 member 3 Homo sapiens 278-283 22716165-6 2012 Animals treated with H2 S showed attenuated serum ALT and AST levels and reduced necrotic lesions after 24 h. IRI animals had increased Bcl-2 mRNA expression and increased active Caspase 3 protein, which were both significantly lower in H2 S treated animals. Hydrogen Sulfide 21-25 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 58-61 22716165-6 2012 Animals treated with H2 S showed attenuated serum ALT and AST levels and reduced necrotic lesions after 24 h. IRI animals had increased Bcl-2 mRNA expression and increased active Caspase 3 protein, which were both significantly lower in H2 S treated animals. Hydrogen Sulfide 21-25 B cell leukemia/lymphoma 2 Mus musculus 136-141 22221071-7 2012 Inhaled H(2)S suppressed LPS-induced upregulation of inflammatory cytokines, while it markedly induced anti-inflammatory interleukin (IL)-10 in the liver. Hydrogen Sulfide 8-13 interleukin 10 Mus musculus 121-140 22781905-2 2012 H(2)S is predominantly formed from Cys or its derivatives by the enzymes cystathionine beta-synthase and cystathionine gamma-lyase. Hydrogen Sulfide 0-5 cystathionine beta-synthase Homo sapiens 73-100 22781905-2 2012 H(2)S is predominantly formed from Cys or its derivatives by the enzymes cystathionine beta-synthase and cystathionine gamma-lyase. Hydrogen Sulfide 0-5 cystathionine gamma-lyase Homo sapiens 105-130 22517358-0 2012 Increased endogenous H2S generation by CBS, CSE, and 3MST gene therapy improves ex vivo renovascular relaxation in hyperhomocysteinemia. Hydrogen Sulfide 21-24 cystathionine gamma-lyase Homo sapiens 44-47 22517358-0 2012 Increased endogenous H2S generation by CBS, CSE, and 3MST gene therapy improves ex vivo renovascular relaxation in hyperhomocysteinemia. Hydrogen Sulfide 21-24 mercaptopyruvate sulfurtransferase Homo sapiens 53-57 22517358-2 2012 Endogenously, H(2)S is produced as a metabolite of homocysteine (Hcy) by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST). Hydrogen Sulfide 14-19 cystathionine beta-synthase Homo sapiens 73-100 22517358-2 2012 Endogenously, H(2)S is produced as a metabolite of homocysteine (Hcy) by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST). Hydrogen Sulfide 14-19 cystathionine gamma-lyase Homo sapiens 108-133 22517358-2 2012 Endogenously, H(2)S is produced as a metabolite of homocysteine (Hcy) by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST). Hydrogen Sulfide 14-19 cystathionine gamma-lyase Homo sapiens 135-138 22517358-2 2012 Endogenously, H(2)S is produced as a metabolite of homocysteine (Hcy) by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST). Hydrogen Sulfide 14-19 mercaptopyruvate sulfurtransferase Homo sapiens 145-181 22517358-2 2012 Endogenously, H(2)S is produced as a metabolite of homocysteine (Hcy) by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST). Hydrogen Sulfide 14-19 mercaptopyruvate sulfurtransferase Homo sapiens 183-187 22517358-5 2012 Ex vivo renal artery culture with CBS, CSE, and 3MST triple gene therapy generated more H(2)S in the presence of Hcy, and these arteries were more responsive to endothelial-dependent vasodilation compared with nontransfected arteries treated with high Hcy. Hydrogen Sulfide 88-93 mercaptopyruvate sulfurtransferase Homo sapiens 48-52 22517358-10 2012 Together, these results suggest that H(2)S plays a key role in renovasculopathy during HHcy and is mediated through Akt/FoxO3 pathways. Hydrogen Sulfide 37-42 AKT serine/threonine kinase 1 Homo sapiens 116-119 22517358-10 2012 Together, these results suggest that H(2)S plays a key role in renovasculopathy during HHcy and is mediated through Akt/FoxO3 pathways. Hydrogen Sulfide 37-42 forkhead box O3 Homo sapiens 120-125 22517358-11 2012 We conclude that conversion of Hcy to H(2)S by CBS, CSE, or 3MST triple gene therapy improves renovascular function in HHcy. Hydrogen Sulfide 38-43 mercaptopyruvate sulfurtransferase Homo sapiens 60-64 22555844-3 2012 We found in the present study that exogenous application of sodium hydrosulfide (NaHS; an H(2)S donor, 100 muM) significantly attenuated 6-OHDA (50 muM)-induced cell death. Hydrogen Sulfide 90-95 latexin Homo sapiens 148-151 22555844-6 2012 The protective effect of H(2)S on ER stress was attenuated by blockade of Akt activity with an Akt inhibitor or inhibition of heat shock protein (Hsp)90 with geldanamycin but not by suppression of ERK1/2 with PD-98059. Hydrogen Sulfide 25-30 AKT serine/threonine kinase 1 Homo sapiens 74-77 22555844-6 2012 The protective effect of H(2)S on ER stress was attenuated by blockade of Akt activity with an Akt inhibitor or inhibition of heat shock protein (Hsp)90 with geldanamycin but not by suppression of ERK1/2 with PD-98059. Hydrogen Sulfide 25-30 AKT serine/threonine kinase 1 Homo sapiens 95-98 22555844-6 2012 The protective effect of H(2)S on ER stress was attenuated by blockade of Akt activity with an Akt inhibitor or inhibition of heat shock protein (Hsp)90 with geldanamycin but not by suppression of ERK1/2 with PD-98059. Hydrogen Sulfide 25-30 heat shock protein 90 alpha family class A member 1 Homo sapiens 146-152 22555844-9 2012 In conclusion, the protective effect of H(2)S against 6-OHDA-induced ER stress injury in SH-SY5Y cells involves the Akt-Hsp90 pathway. Hydrogen Sulfide 40-45 AKT serine/threonine kinase 1 Homo sapiens 116-119 22555844-9 2012 In conclusion, the protective effect of H(2)S against 6-OHDA-induced ER stress injury in SH-SY5Y cells involves the Akt-Hsp90 pathway. Hydrogen Sulfide 40-45 heat shock protein 90 alpha family class A member 1 Homo sapiens 120-125 22229673-5 2012 The production of H(2)S by the pathway, which is regulated by Ca(2+) and facilitated by thioredoxin and dihydrolipoic acid, is also involved in H(2)S signaling as well as cytoprotection. Hydrogen Sulfide 18-23 thioredoxin Homo sapiens 88-99 22229673-5 2012 The production of H(2)S by the pathway, which is regulated by Ca(2+) and facilitated by thioredoxin and dihydrolipoic acid, is also involved in H(2)S signaling as well as cytoprotection. Hydrogen Sulfide 144-149 thioredoxin Homo sapiens 88-99 22570497-4 2012 Exposure of endothelial cells to H(2)S increases intracellular cyclic guanosine 5"-monophosphate (cGMP) in a NO-dependent manner, and activated protein kinase G (PKG) and its downstream effector, the vasodilator-stimulated phosphoprotein (VASP). Hydrogen Sulfide 33-38 protein kinase cGMP-dependent 1 Homo sapiens 144-160 22017202-3 2012 RECENT ADVANCES: The production of endogenous H(2)S has been attributed to three key enzymes, cystathionine gamma-lyase (CSE), cystathionine beta-synthase, and 3-mercaptopyruvate sulfurtransferase. Hydrogen Sulfide 46-51 cystathionine gamma-lyase Homo sapiens 94-119 22017202-3 2012 RECENT ADVANCES: The production of endogenous H(2)S has been attributed to three key enzymes, cystathionine gamma-lyase (CSE), cystathionine beta-synthase, and 3-mercaptopyruvate sulfurtransferase. Hydrogen Sulfide 46-51 cystathionine gamma-lyase Homo sapiens 121-124 22017202-5 2012 In particular, important roles in cardiovascular disorder processes are ascribed to the CSE/H(2)S pathway, such as atherosclerosis, myocardial infarction, hypertension, and shock. Hydrogen Sulfide 92-97 cystathionine gamma-lyase Homo sapiens 88-91 22017202-6 2012 CRITICAL ISSUES: Many biological activities and molecular mechanisms of H(2)S in the cardiovascular system have been demonstrated in studies using different tools, such as the genetic overexpression of CSE, the direct administration of H(2)S donors, or the use of H(2)S-releasing pro-drugs. Hydrogen Sulfide 72-77 cystathionine gamma-lyase Homo sapiens 202-205 22034938-7 2012 Inhibition of H(2)S metabolism results from atorvastatin-induced decrease in coenzyme Q, which is a cofactor of H(2)S oxidation by sulfide:quinone oxidoreductase. Hydrogen Sulfide 14-19 crystallin zeta Homo sapiens 139-161 22300342-0 2012 Hydrogen sulfide-induced mechanical hyperalgesia and allodynia require activation of both Cav3.2 and TRPA1 channels in mice. Hydrogen Sulfide 0-16 calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus 90-96 22300342-0 2012 Hydrogen sulfide-induced mechanical hyperalgesia and allodynia require activation of both Cav3.2 and TRPA1 channels in mice. Hydrogen Sulfide 0-16 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 101-106 22300342-1 2012 BACKGROUND AND PURPOSE: Hydrogen sulfide, a gasotransmitter, facilitates somatic pain signals via activation of Ca(v)3.2 T-type calcium channels in rats. Hydrogen Sulfide 24-40 caveolin 3 Rattus norvegicus 112-118 22300342-2 2012 Given evidence for the activation of transient receptor potential ankyrin-1 (TRPA1) channels by H(2)S, we asked whether TRPA1 channels, in addition to Ca(v)3.2 channels, contribute to the H(2)S-induced mechanical hyperalgesia and allodynia in mice. Hydrogen Sulfide 96-101 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 37-75 22300342-2 2012 Given evidence for the activation of transient receptor potential ankyrin-1 (TRPA1) channels by H(2)S, we asked whether TRPA1 channels, in addition to Ca(v)3.2 channels, contribute to the H(2)S-induced mechanical hyperalgesia and allodynia in mice. Hydrogen Sulfide 96-101 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 77-82 22300342-8 2012 CONCLUSIONS AND IMPLICATIONS: Mechanical hyperalgesia and allodynia induced by NaHS/H(2)S required activation of both Ca(v)3.2 and TRPA1 channels in mice. Hydrogen Sulfide 84-89 calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus 118-126 22300342-8 2012 CONCLUSIONS AND IMPLICATIONS: Mechanical hyperalgesia and allodynia induced by NaHS/H(2)S required activation of both Ca(v)3.2 and TRPA1 channels in mice. Hydrogen Sulfide 84-89 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 131-136 22016355-3 2012 It is mainly synthesized by 2 enzymes, including cystathionine beta-synthase and cystathionine gamma-lysase, which utilize L-cysteine as substrate to produce H(2)S. Hydrogen Sulfide 158-163 cystathionine beta-synthase Homo sapiens 49-76 26105277-18 2012 CBS and CSE, the enzymes involved in the production of H2S, were down-regulated in SHR rats and, as a consequence the H2S production was significantly reduced. Hydrogen Sulfide 55-58 cystathionine beta-synthase Homo sapiens 0-3 26105277-18 2012 CBS and CSE, the enzymes involved in the production of H2S, were down-regulated in SHR rats and, as a consequence the H2S production was significantly reduced. Hydrogen Sulfide 55-58 cystathionine gamma-lyase Homo sapiens 8-11 26105277-18 2012 CBS and CSE, the enzymes involved in the production of H2S, were down-regulated in SHR rats and, as a consequence the H2S production was significantly reduced. Hydrogen Sulfide 118-121 cystathionine beta-synthase Homo sapiens 0-3 26105277-18 2012 CBS and CSE, the enzymes involved in the production of H2S, were down-regulated in SHR rats and, as a consequence the H2S production was significantly reduced. Hydrogen Sulfide 118-121 cystathionine gamma-lyase Homo sapiens 8-11 22680986-7 2012 In addition, the assay was used to determine K(M) and V(max) for natural substrates of cystathionine gamma-lyase (CSE), the main enzyme responsible for H(2)S production in peripheral tissues. Hydrogen Sulfide 152-157 cystathionine gamma-lyase Homo sapiens 87-112 22680986-7 2012 In addition, the assay was used to determine K(M) and V(max) for natural substrates of cystathionine gamma-lyase (CSE), the main enzyme responsible for H(2)S production in peripheral tissues. Hydrogen Sulfide 152-157 cystathionine gamma-lyase Homo sapiens 114-117 22570497-4 2012 Exposure of endothelial cells to H(2)S increases intracellular cyclic guanosine 5"-monophosphate (cGMP) in a NO-dependent manner, and activated protein kinase G (PKG) and its downstream effector, the vasodilator-stimulated phosphoprotein (VASP). Hydrogen Sulfide 33-38 protein kinase cGMP-dependent 1 Homo sapiens 162-165 22570497-4 2012 Exposure of endothelial cells to H(2)S increases intracellular cyclic guanosine 5"-monophosphate (cGMP) in a NO-dependent manner, and activated protein kinase G (PKG) and its downstream effector, the vasodilator-stimulated phosphoprotein (VASP). Hydrogen Sulfide 33-38 vasodilator stimulated phosphoprotein Homo sapiens 200-237 22570497-4 2012 Exposure of endothelial cells to H(2)S increases intracellular cyclic guanosine 5"-monophosphate (cGMP) in a NO-dependent manner, and activated protein kinase G (PKG) and its downstream effector, the vasodilator-stimulated phosphoprotein (VASP). Hydrogen Sulfide 33-38 vasodilator stimulated phosphoprotein Homo sapiens 239-243 22570497-5 2012 Inhibition of endothelial isoform of NO synthase (eNOS) or PKG-I abolishes the H(2)S-stimulated angiogenic response, and attenuated H(2)S-stimulated vasorelaxation, demonstrating the requirement of NO in vascular H(2)S signaling. Hydrogen Sulfide 79-84 protein kinase cGMP-dependent 1 Homo sapiens 59-62 22570497-6 2012 Conversely, silencing of the H(2)S-producing enzyme cystathionine-gamma-lyase abolishes NO-stimulated cGMP accumulation and angiogenesis and attenuates the acetylcholine-induced vasorelaxation, indicating a partial requirement of H(2)S in the vascular activity of NO. Hydrogen Sulfide 29-34 cystathionine gamma-lyase Homo sapiens 52-77 22570497-6 2012 Conversely, silencing of the H(2)S-producing enzyme cystathionine-gamma-lyase abolishes NO-stimulated cGMP accumulation and angiogenesis and attenuates the acetylcholine-induced vasorelaxation, indicating a partial requirement of H(2)S in the vascular activity of NO. Hydrogen Sulfide 230-235 cystathionine gamma-lyase Homo sapiens 52-77 22570497-7 2012 The actions of H(2)S and NO converge at cGMP; though H(2)S does not directly activate soluble guanylyl cyclase, it maintains a tonic inhibitory effect on PDE5, thereby delaying the degradation of cGMP. Hydrogen Sulfide 15-20 phosphodiesterase 5A Homo sapiens 154-158 22570497-7 2012 The actions of H(2)S and NO converge at cGMP; though H(2)S does not directly activate soluble guanylyl cyclase, it maintains a tonic inhibitory effect on PDE5, thereby delaying the degradation of cGMP. Hydrogen Sulfide 53-58 phosphodiesterase 5A Homo sapiens 154-158 22570497-8 2012 H(2)S also activates PI3K/Akt, and increases eNOS phosphorylation at its activating site S1177. Hydrogen Sulfide 0-5 AKT serine/threonine kinase 1 Homo sapiens 26-29 22694815-0 2012 The role of AKT1 and autophagy in the protective effect of hydrogen sulphide against hepatic ischemia/reperfusion injury in mice. Hydrogen Sulfide 59-76 thymoma viral proto-oncogene 1 Mus musculus 12-16 22694815-3 2012 This study was designed to investigate the role of the PtdIns3K-AKT1 pathways and autophagy in the protective effect of H 2S against hepatic I/R injury. Hydrogen Sulfide 120-124 thymoma viral proto-oncogene 1 Mus musculus 64-68 22694815-9 2012 H 2S preconditioning activated PtdIns3K-AKT1 signaling in hepatocytes. Hydrogen Sulfide 0-4 thymoma viral proto-oncogene 1 Mus musculus 40-44 22694815-13 2012 Taken together, H 2S protects against hepatocytic A/R and hepatic I/R injuries, at least in part, through AKT1 activation but not autophagy. Hydrogen Sulfide 16-20 thymoma viral proto-oncogene 1 Mus musculus 106-110 22360859-3 2012 According to the data that cystathionine gamma-lyase (CSE) gene, catalyzed H(2)S production in trans-sulfuration pathway, was upregulated in Akt stably transformed mouse embryonic fibroblast cells, the mechanisms that elevated CSE expression by PI3K/Akt signaling pathway and its biological functions in cell survival were studied. Hydrogen Sulfide 75-80 cystathionase (cystathionine gamma-lyase) Mus musculus 27-52 22546230-5 2012 The aim of this study was to determine effects of inhibiting hydrogen sulphide biosynthesis by DL-propargyl glycine (an irreversible inhibitor of cystathionine gamma-lyase) on inflammation, necrosis and renal function, following treatment with gentamicin in rats. Hydrogen Sulfide 61-78 cystathionine gamma-lyase Rattus norvegicus 146-171 22360859-3 2012 According to the data that cystathionine gamma-lyase (CSE) gene, catalyzed H(2)S production in trans-sulfuration pathway, was upregulated in Akt stably transformed mouse embryonic fibroblast cells, the mechanisms that elevated CSE expression by PI3K/Akt signaling pathway and its biological functions in cell survival were studied. Hydrogen Sulfide 75-80 cystathionase (cystathionine gamma-lyase) Mus musculus 54-57 22360859-3 2012 According to the data that cystathionine gamma-lyase (CSE) gene, catalyzed H(2)S production in trans-sulfuration pathway, was upregulated in Akt stably transformed mouse embryonic fibroblast cells, the mechanisms that elevated CSE expression by PI3K/Akt signaling pathway and its biological functions in cell survival were studied. Hydrogen Sulfide 75-80 thymoma viral proto-oncogene 1 Mus musculus 141-144 22360859-9 2012 In addition, we explored that the endogenous H(2)S production was connected with the regulated CSE expression, and CSE/H(2)S promoted human hepatocellular carcinoma cell proliferation via cell cycle progression regulation. Hydrogen Sulfide 45-50 cystathionine gamma-lyase Homo sapiens 95-98 22360859-9 2012 In addition, we explored that the endogenous H(2)S production was connected with the regulated CSE expression, and CSE/H(2)S promoted human hepatocellular carcinoma cell proliferation via cell cycle progression regulation. Hydrogen Sulfide 119-124 cystathionine gamma-lyase Homo sapiens 115-118 22669619-0 2012 Hydrogen sulfide: in the aftermath of argininosuccinate lyase and nitric oxide deficiency. Hydrogen Sulfide 0-16 argininosuccinate lyase Homo sapiens 38-61 22391326-5 2012 Thus, down regulation of CBS during early-onset preeclampsia may result in less H(2)S-production and may aid in the anti-angiogenic state. Hydrogen Sulfide 80-85 cystathionine beta-synthase Homo sapiens 25-28 23675260-4 2012 It seems that a potent interaction of hydrogen sulfide with vascular endothelial growth factor (VEGF) becomes important in angiogenesis, in the process of wound healing, but also in tumor angiogenesis. Hydrogen Sulfide 38-54 vascular endothelial growth factor A Homo sapiens 60-94 23675260-4 2012 It seems that a potent interaction of hydrogen sulfide with vascular endothelial growth factor (VEGF) becomes important in angiogenesis, in the process of wound healing, but also in tumor angiogenesis. Hydrogen Sulfide 38-54 vascular endothelial growth factor A Homo sapiens 96-100 23675260-8 2012 We attempt to provide recent insights into mechanisms by which CSE-dependent hydrogen sulfide plays a role in the regulation of vascular tone by perivascular adipose tissue. Hydrogen Sulfide 77-93 choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity) Homo sapiens 63-66 22508960-6 2012 In voltage-clamped (-40 mV) cells, H2S increased the frequency of iberiotoxin-sensitive, Ca2+ spark-induced transient Ca2+-activated K+ (KCa) currents ~1.83-fold, but did not alter the amplitude of these events. Hydrogen Sulfide 35-38 casein kappa Homo sapiens 137-140 22508960-10 2012 Iberiotoxin, a KCa channel blocker, reduced H2S-induced hyperpolarization by ~51%. Hydrogen Sulfide 44-47 casein kappa Homo sapiens 15-18 22503984-0 2012 Hydrogen sulfide decreases the levels of ROS by inhibiting mitochondrial complex IV and increasing SOD activities in cardiomyocytes under ischemia/reperfusion. Hydrogen Sulfide 0-16 superoxide dismutase 2 Homo sapiens 99-102 22503984-5 2012 We found that H(2)S inhibited mitochondrial complex IV activity and increased the activities of superoxide dismutases (SODs), including Mn-SOD and CuZn-SOD. Hydrogen Sulfide 14-19 superoxide dismutase 2 Homo sapiens 136-142 22306852-5 2012 Homogenates from rat corpus cavernosum convert l-cysteine to H(2)S and this was partially inhibited by a CSE inhibitor, propargylglycine. Hydrogen Sulfide 61-66 cystathionine gamma-lyase Rattus norvegicus 105-108 22306852-7 2012 This neurogenic relaxation was significantly enhanced by inhibition of CSE by propargylglycine indicating that endogenously produced H(2)S may have a negative regulatory role in neurogenic relaxation of rat corpus cavernosum. Hydrogen Sulfide 133-138 cystathionine gamma-lyase Rattus norvegicus 71-74 22403348-9 2012 H(2)S in 21% O(2) increased Akt-P(Ser473) and GSK-3beta-P(Ser9) in the heart whereas phosphorylation was decreased by H(2)S in 10.5% O(2), indicating O(2) dependence in regulating cardiac signaling pathways. Hydrogen Sulfide 0-5 AKT serine/threonine kinase 1 Rattus norvegicus 28-31 22020834-7 2012 Our findings of diffuse vascular damage of target critical organs are in keeping with the hypothesis that the pathologic effects of ETHE1 deficiency may stem from high levels of circulating hydrogen sulphide rather than the inability of specific organs to detoxify its endogenous production. Hydrogen Sulfide 190-207 ETHE1 persulfide dioxygenase Homo sapiens 132-137 22513461-10 2012 ROS, as an upstream regulator of HIF-1alpha, may be involved in the migration-promoting effect of H2S. Hydrogen Sulfide 98-101 hypoxia inducible factor 1 subunit alpha Macaca mulatta 33-43 22370476-2 2012 Sea bass slices wrapped with LEO film had the retarded growth of lactic acid bacteria (LAB), psychrophilic bacteria and spoilage microorganisms including H2S-producing bacteria and Enterobacteriaceae throughout storage of 12 days in comparison with the control and those wrapped with gelatin film without LEO (G film) (P<0.05). Hydrogen Sulfide 154-157 S13 erythroblastosis (avian) oncogene homolog Homo sapiens 0-3 22244329-0 2012 Hydrogen sulfide-linked sulfhydration of NF-kappaB mediates its antiapoptotic actions. Hydrogen Sulfide 0-16 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 41-50 22274539-6 2012 We were able to detect H(2)S produced from sodium hydrogen sulfide (NaHS) added at concentrations as low as 10 muM. Hydrogen Sulfide 23-28 latexin Homo sapiens 111-114 22274539-7 2012 Following a 24-h incubation of endothelial-like or vascular smooth muscle cells with 50 muM NaHS, we were able to recover twice more H(2)S than conventional methods. Hydrogen Sulfide 133-138 latexin Homo sapiens 88-91 22323590-3 2012 Cystathionine gamma-lyase (CSE) is a major H(2)S-producing enzyme in the cardiovascular system that uses cysteine as the main substrate. Hydrogen Sulfide 43-48 cystathionine gamma-lyase Homo sapiens 0-25 22323590-3 2012 Cystathionine gamma-lyase (CSE) is a major H(2)S-producing enzyme in the cardiovascular system that uses cysteine as the main substrate. Hydrogen Sulfide 43-48 cystathionine gamma-lyase Homo sapiens 27-30 22323590-7 2012 Tom20 siRNA significantly inhibited mitochondrial translocation of CSE and mitochondrial H(2)S production. Hydrogen Sulfide 89-94 translocase of outer mitochondrial membrane 20 Homo sapiens 0-5 22323590-9 2012 Translocation of CSE to mitochondria metabolized cysteine, produced H(2)S inside mitochondria, and increased ATP production. Hydrogen Sulfide 68-73 cystathionine gamma-lyase Homo sapiens 17-20 22323590-12 2012 These results suggest that translocation of CSE to mitochondria on specific stress stimulations is a unique mechanism to promote H(2)S production inside mitochondria, which subsequently sustains mitochondrial ATP production under hypoxic conditions. Hydrogen Sulfide 129-134 cystathionine gamma-lyase Homo sapiens 44-47 22158625-0 2012 Hydrogen sulfide inhibits high glucose-induced matrix protein synthesis by activating AMP-activated protein kinase in renal epithelial cells. Hydrogen Sulfide 0-16 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 86-114 22158625-10 2012 Renal cortical content of cystathionine beta-synthase and cystathionine gamma-lyase, hydrogen sulfide-generating enzymes, was significantly reduced in mice with type 1 diabetes or type 2 diabetes, coinciding with renal hypertrophy and matrix accumulation. Hydrogen Sulfide 85-101 cystathionine beta-synthase Mus musculus 26-53 22158625-10 2012 Renal cortical content of cystathionine beta-synthase and cystathionine gamma-lyase, hydrogen sulfide-generating enzymes, was significantly reduced in mice with type 1 diabetes or type 2 diabetes, coinciding with renal hypertrophy and matrix accumulation. Hydrogen Sulfide 85-101 cystathionase (cystathionine gamma-lyase) Mus musculus 58-83 22316301-4 2012 Therefore, we hypothesized that exogenous H2S can affect the expression of circadian clock genes mediated by sirt1 thereby affecting body"s lipid metabolism. Hydrogen Sulfide 42-45 sirtuin 1 Mus musculus 109-114 22316301-6 2012 Thus the effect of H2S were observed on 24-hour dynamic expression of 4 central circadian clock genes and sirt1gene in primary cultured hepatocytes. Hydrogen Sulfide 19-22 sirtuin 1 Mus musculus 106-111 22316301-8 2012 And detected that the expression level and the peak of circadian clock genes decreased gradually and H2S could maintain the expression and amplitude of circadian clock genes such as Clock, Per2, Bmal1 and Rev-erbalphawithin a certain period time. Hydrogen Sulfide 101-104 period circadian clock 2 Mus musculus 189-193 22316301-8 2012 And detected that the expression level and the peak of circadian clock genes decreased gradually and H2S could maintain the expression and amplitude of circadian clock genes such as Clock, Per2, Bmal1 and Rev-erbalphawithin a certain period time. Hydrogen Sulfide 101-104 aryl hydrocarbon receptor nuclear translocator-like Mus musculus 195-200 22316301-8 2012 And detected that the expression level and the peak of circadian clock genes decreased gradually and H2S could maintain the expression and amplitude of circadian clock genes such as Clock, Per2, Bmal1 and Rev-erbalphawithin a certain period time. Hydrogen Sulfide 101-104 REV3 like, DNA directed polymerase zeta catalytic subunit Mus musculus 205-208 22316301-9 2012 Accordingly the expression level of sirt1 in H2S group was significantly higher than that in the control group. Hydrogen Sulfide 45-48 sirtuin 1 Mus musculus 36-41 22316301-11 2012 We speculated that H2S has changed NAD+/NADH content ratio in hepatocytes and enhanced the activity of SIRT1 protein directly or indirectly, so as to maintain the rhythm of expression of circadian clock genes, they play a role in the prevention and treatment of lipid metabolism-related disease caused by the biological clock disorders. Hydrogen Sulfide 19-22 sirtuin 1 Mus musculus 103-108 22167178-7 2012 Nanomolar levels of H(2)S (50-500 nM) enhance T cell activation assessed by CD69 expression, interleukin-2 expression, and CD25 levels. Hydrogen Sulfide 20-25 CD69 molecule Homo sapiens 76-80 22167178-7 2012 Nanomolar levels of H(2)S (50-500 nM) enhance T cell activation assessed by CD69 expression, interleukin-2 expression, and CD25 levels. Hydrogen Sulfide 20-25 interleukin 2 Homo sapiens 93-106 22167178-7 2012 Nanomolar levels of H(2)S (50-500 nM) enhance T cell activation assessed by CD69 expression, interleukin-2 expression, and CD25 levels. Hydrogen Sulfide 20-25 interleukin 2 receptor subunit alpha Homo sapiens 123-127 22167178-9 2012 Furthermore, activation increases the capacity of T cells to make H(2)S via increased expression of cystathionine gamma-lyase and cystathionine beta-synthase. Hydrogen Sulfide 66-71 cystathionine gamma-lyase Homo sapiens 100-125 22167178-9 2012 Furthermore, activation increases the capacity of T cells to make H(2)S via increased expression of cystathionine gamma-lyase and cystathionine beta-synthase. Hydrogen Sulfide 66-71 cystathionine beta-synthase Homo sapiens 130-157 22004513-0 2012 Hydrogen sulfide inhibits hypoxia- but not anoxia-induced hypoxia-inducible factor 1 activation in a von hippel-lindau- and mitochondria-dependent manner. Hydrogen Sulfide 0-16 von Hippel-Lindau tumor suppressor Mus musculus 101-118 22004513-3 2012 However, the effect of H(2)S on HIF-1 activity under hypoxic conditions is largely unknown in mammalian cells. Hydrogen Sulfide 23-28 hypoxia inducible factor 1 subunit alpha Homo sapiens 32-37 22004513-4 2012 In this study, we tried to elucidate the effect of H(2)S on hypoxia-induced HIF-1 activation adopting cultured cells and mice. Hydrogen Sulfide 51-56 hypoxia inducible factor 1 subunit alpha Homo sapiens 76-81 22004513-7 2012 Experimental evidence adopting von Hippel-Lindau (VHL)- or mitochondria-deficient cells indicated that H(2)S did not affect neosynthesis of HIF-1alpha protein but destabilized HIF-1alpha in a VHL- and mitochondria-dependent manner. Hydrogen Sulfide 103-108 von Hippel-Lindau tumor suppressor Mus musculus 31-48 22004513-7 2012 Experimental evidence adopting von Hippel-Lindau (VHL)- or mitochondria-deficient cells indicated that H(2)S did not affect neosynthesis of HIF-1alpha protein but destabilized HIF-1alpha in a VHL- and mitochondria-dependent manner. Hydrogen Sulfide 103-108 von Hippel-Lindau tumor suppressor Mus musculus 50-53 22004513-7 2012 Experimental evidence adopting von Hippel-Lindau (VHL)- or mitochondria-deficient cells indicated that H(2)S did not affect neosynthesis of HIF-1alpha protein but destabilized HIF-1alpha in a VHL- and mitochondria-dependent manner. Hydrogen Sulfide 103-108 hypoxia inducible factor 1, alpha subunit Mus musculus 176-186 22004513-7 2012 Experimental evidence adopting von Hippel-Lindau (VHL)- or mitochondria-deficient cells indicated that H(2)S did not affect neosynthesis of HIF-1alpha protein but destabilized HIF-1alpha in a VHL- and mitochondria-dependent manner. Hydrogen Sulfide 103-108 von Hippel-Lindau tumor suppressor Mus musculus 192-195 22004513-8 2012 We also demonstrate that exogenously administered H(2)S inhibited HIF-1-dependent gene expression in mice. Hydrogen Sulfide 50-55 hypoxia inducible factor 1 subunit alpha Homo sapiens 66-71 22004513-9 2012 INNOVATION: For the first time, we show that H(2)S modulates intracellular O(2) homeostasis and regulates activation of HIF-1 and the subsequent gene expression induced by hypoxia by using an in vitro system with established cell lines and an in vivo system in mice. Hydrogen Sulfide 45-50 hypoxia inducible factor 1 subunit alpha Homo sapiens 120-125 22004513-10 2012 CONCLUSIONS: We demonstrate that H(2)S inhibits hypoxia-induced HIF-1 activation in a VHL- and mitochondria-dependent manner. Hydrogen Sulfide 33-38 hypoxia inducible factor 1 subunit alpha Homo sapiens 64-69 22004513-10 2012 CONCLUSIONS: We demonstrate that H(2)S inhibits hypoxia-induced HIF-1 activation in a VHL- and mitochondria-dependent manner. Hydrogen Sulfide 33-38 von Hippel-Lindau tumor suppressor Mus musculus 86-89 23704250-0 2013 Sulfane sustains vascular health: insights into cystathionine gamma-lyase function. Hydrogen Sulfide 0-7 cystathionine gamma-lyase Homo sapiens 48-73 23704251-0 2013 Dysregulation of hydrogen sulfide producing enzyme cystathionine gamma-lyase contributes to maternal hypertension and placental abnormalities in preeclampsia. Hydrogen Sulfide 17-33 cystathionine gamma-lyase Homo sapiens 51-76 23704251-2 2013 Hydrogen sulfide (H2S), a gaseous messenger produced mainly by cystathionine gamma-lyase (CSE), is a proangiogenic vasodilator. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 63-88 23704251-2 2013 Hydrogen sulfide (H2S), a gaseous messenger produced mainly by cystathionine gamma-lyase (CSE), is a proangiogenic vasodilator. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 90-93 23704251-2 2013 Hydrogen sulfide (H2S), a gaseous messenger produced mainly by cystathionine gamma-lyase (CSE), is a proangiogenic vasodilator. Hydrogen Sulfide 18-21 cystathionine gamma-lyase Homo sapiens 63-88 23704251-2 2013 Hydrogen sulfide (H2S), a gaseous messenger produced mainly by cystathionine gamma-lyase (CSE), is a proangiogenic vasodilator. Hydrogen Sulfide 18-21 cystathionine gamma-lyase Homo sapiens 90-93 23704251-4 2013 METHODS AND RESULTS: Plasma levels of H2S were significantly decreased in women with preeclampsia (P<0.01), which was associated with reduced placental CSE expression as determined by real-time polymerase chain reaction and immunohistochemistry. Hydrogen Sulfide 38-41 cystathionine gamma-lyase Homo sapiens 155-158 23704251-8 2013 Finally, a slow-releasing H2S-generating compound, GYY4137, inhibited circulating soluble fms-like tyrosine kinase-1 and soluble endoglin levels and restored fetal growth in mice that was compromised by DL-propargylglycine treatment, demonstrating that the effect of CSE inhibitor was attributable to inhibition of H2S production. Hydrogen Sulfide 26-29 endoglin Mus musculus 129-137 23704251-8 2013 Finally, a slow-releasing H2S-generating compound, GYY4137, inhibited circulating soluble fms-like tyrosine kinase-1 and soluble endoglin levels and restored fetal growth in mice that was compromised by DL-propargylglycine treatment, demonstrating that the effect of CSE inhibitor was attributable to inhibition of H2S production. Hydrogen Sulfide 26-29 cystathionase (cystathionine gamma-lyase) Mus musculus 267-270 23704251-9 2013 CONCLUSIONS: These results imply that endogenous H2S is required for healthy placental vasculature and that a decrease in CSE/H2S activity may contribute to the pathogenesis of preeclampsia. Hydrogen Sulfide 126-129 cystathionine gamma-lyase Homo sapiens 122-125 23704252-1 2013 BACKGROUND: Cystathionine gamma-lyase (CSE) produces hydrogen sulfide (H2S) in the cardiovascular system. Hydrogen Sulfide 53-69 cystathionase (cystathionine gamma-lyase) Mus musculus 12-37 23704252-1 2013 BACKGROUND: Cystathionine gamma-lyase (CSE) produces hydrogen sulfide (H2S) in the cardiovascular system. Hydrogen Sulfide 53-69 cystathionase (cystathionine gamma-lyase) Mus musculus 39-42 23704252-1 2013 BACKGROUND: Cystathionine gamma-lyase (CSE) produces hydrogen sulfide (H2S) in the cardiovascular system. Hydrogen Sulfide 71-74 cystathionase (cystathionine gamma-lyase) Mus musculus 12-37 23704252-1 2013 BACKGROUND: Cystathionine gamma-lyase (CSE) produces hydrogen sulfide (H2S) in the cardiovascular system. Hydrogen Sulfide 71-74 cystathionase (cystathionine gamma-lyase) Mus musculus 39-42 23704252-11 2013 The CSE/H2S pathway is an important therapeutic target for protection against atherosclerosis. Hydrogen Sulfide 8-11 cystathionase (cystathionine gamma-lyase) Mus musculus 4-7 21950400-0 2012 Sulphide quinone reductase contributes to hydrogen sulphide metabolism in murine peripheral tissues but not in the CNS. Hydrogen Sulfide 42-59 crystallin, zeta Mus musculus 9-26 21679296-4 2012 The expression and enzymatic activity of the H(2)S synthesizing enzymes cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) were determined by Western blot and zinc-trap spectrophotometry, respectively. Hydrogen Sulfide 45-50 cystathionine beta-synthase Homo sapiens 72-99 21679296-4 2012 The expression and enzymatic activity of the H(2)S synthesizing enzymes cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) were determined by Western blot and zinc-trap spectrophotometry, respectively. Hydrogen Sulfide 45-50 cystathionine gamma-lyase Homo sapiens 110-135 21679296-4 2012 The expression and enzymatic activity of the H(2)S synthesizing enzymes cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) were determined by Western blot and zinc-trap spectrophotometry, respectively. Hydrogen Sulfide 45-50 cystathionine gamma-lyase Homo sapiens 137-140 21679296-8 2012 Endogenous H(2) S synthesis was inhibited by siRNA-mediated knockdown of CSE and CBS and pharmacological inhibitors D,L-propargylglycine and aminoxyacetate, respectively. Hydrogen Sulfide 11-17 cystathionine gamma-lyase Homo sapiens 73-76 21679296-12 2012 These data suggest CSE is an inducible source of H(2)S in cultured HACs and MPCs. Hydrogen Sulfide 49-54 cystathionine gamma-lyase Homo sapiens 19-22 22203419-7 2012 Pretreatment with sodium hydrosulfide (NaHS, a H(2)S donor) before DOX exposure markedly suppressed DOX-induced overexpressions of GRP78 and CHOP, cytotoxicity and oxidative stress. Hydrogen Sulfide 47-52 heat shock protein family A (Hsp70) member 5 Homo sapiens 131-136 22203419-7 2012 Pretreatment with sodium hydrosulfide (NaHS, a H(2)S donor) before DOX exposure markedly suppressed DOX-induced overexpressions of GRP78 and CHOP, cytotoxicity and oxidative stress. Hydrogen Sulfide 47-52 DNA damage inducible transcript 3 Homo sapiens 141-145 22245911-9 2012 H2S decreased the levels of Ang-II in the heart, but not in plasma. Hydrogen Sulfide 0-3 angiotensinogen Rattus norvegicus 40-46 22245911-10 2012 In addition, H2S also improved the expression of connexin 43 (Cx43). Hydrogen Sulfide 13-16 gap junction protein, alpha 1 Rattus norvegicus 61-72 22245911-10 2012 In addition, H2S also improved the expression of connexin 43 (Cx43). Hydrogen Sulfide 13-16 gap junction protein, alpha 1 Rattus norvegicus 74-78 22245911-11 2012 Our results suggest that H2S can significantly suppress cardiac hypertrophy and fibrosis induced by overloaded pressure, possibly by inhibiting the activity of intracardiac Ang-II and by modifying expression of Cx43. Hydrogen Sulfide 25-28 angiotensinogen Rattus norvegicus 197-203 22245911-11 2012 Our results suggest that H2S can significantly suppress cardiac hypertrophy and fibrosis induced by overloaded pressure, possibly by inhibiting the activity of intracardiac Ang-II and by modifying expression of Cx43. Hydrogen Sulfide 25-28 gap junction protein, alpha 1 Rattus norvegicus 247-251 22535897-8 2012 Many new technologies have been developed to detect endogenous H(2)S production, and novel H(2)S-delivery compounds have been invented to aid therapeutic intervention of diseases related to abnormal H(2)S metabolism. Hydrogen Sulfide 91-96 activation induced cytidine deaminase Homo sapiens 138-141 22499119-9 2012 In contrast, DL-propargylglycine, an inhibitor of cystathionine gamma-lyase, the main enzyme for H(2)S production in hearts, showed opposite effects to NaHS. Hydrogen Sulfide 97-102 cystathionine gamma-lyase Rattus norvegicus 50-75 22281027-2 2012 Seedlings pretreated with 200 muM NaHS as a donor of H(2)S for 24h and subsequently exposed to 100 muM AlCl(3) for 24h had significantly longer roots than those without NaHS. Hydrogen Sulfide 53-58 latexin Homo sapiens 30-33 22209867-0 2012 Hydrogen sulfide-releasing aspirin suppresses NF-kappaB signaling in estrogen receptor negative breast cancer cells in vitro and in vivo. Hydrogen Sulfide 0-16 nuclear factor kappa B subunit 1 Homo sapiens 46-55 22262763-5 2012 IL-12 repression could also be induced by propargylglycine in vitro in monocytes and dendritic cells (DCs), a phenomenon not mediated by changes to nuclear factor-kappa B or hydrogen sulfide but that occurred together with a modulation of intracellular cysteine content. Hydrogen Sulfide 174-190 interleukin 12B Rattus norvegicus 0-5 22268103-5 2012 The PKG inhibitor KT5283 (KT; 1 mg/kg ip) or dl-propargylglycine (PAG; 50 mg/kg ip) the inhibitor of the H(2)S-producing enzyme cystathionine-gamma-lyase (CSE) were given 10 and 30 min before cinaciguat. Hydrogen Sulfide 105-110 cystathionase (cystathionine gamma-lyase) Mus musculus 128-153 22240755-0 2012 S-propargyl-cysteine, a novel hydrogen sulfide-modulated agent, attenuated tumor necrosis factor-alpha-induced inflammatory signaling and dysfunction in endothelial cells. Hydrogen Sulfide 30-46 tumor necrosis factor Homo sapiens 75-102 22405203-0 2012 CYSL-1 interacts with the O2-sensing hydroxylase EGL-9 to promote H2S-modulated hypoxia-induced behavioral plasticity in C. elegans. Hydrogen Sulfide 66-69 Cysteine synthase 1 Caenorhabditis elegans 0-6 22405203-0 2012 CYSL-1 interacts with the O2-sensing hydroxylase EGL-9 to promote H2S-modulated hypoxia-induced behavioral plasticity in C. elegans. Hydrogen Sulfide 66-69 Hypoxia-inducible factor prolyl hydroxylase Caenorhabditis elegans 49-54 22405203-7 2012 These findings demonstrate that CYSL-1 acts to transduce signals from H(2)S to EGL-9 to regulate O(2)-dependent behavioral plasticity in C. elegans. Hydrogen Sulfide 70-75 Cysteine synthase 1 Caenorhabditis elegans 32-38 22133746-0 2012 Protein phosphorylation involved in the gene expression of the hydrogen sulphide producing enzyme cystathionine gamma-lyase in the pancreatic beta-cell. Hydrogen Sulfide 63-80 cystathionase (cystathionine gamma-lyase) Mus musculus 98-123 22133746-1 2012 Cystathionine gamma-lyase (CSE) is one of the major enzymes for the production of hydrogen sulphide (H(2)S), a multifunctional gasotransmitter in the pancreatic beta-cell. Hydrogen Sulfide 82-99 cystathionase (cystathionine gamma-lyase) Mus musculus 0-25 22133746-1 2012 Cystathionine gamma-lyase (CSE) is one of the major enzymes for the production of hydrogen sulphide (H(2)S), a multifunctional gasotransmitter in the pancreatic beta-cell. Hydrogen Sulfide 82-99 cystathionase (cystathionine gamma-lyase) Mus musculus 27-30 22133746-1 2012 Cystathionine gamma-lyase (CSE) is one of the major enzymes for the production of hydrogen sulphide (H(2)S), a multifunctional gasotransmitter in the pancreatic beta-cell. Hydrogen Sulfide 101-106 cystathionase (cystathionine gamma-lyase) Mus musculus 0-25 22133746-1 2012 Cystathionine gamma-lyase (CSE) is one of the major enzymes for the production of hydrogen sulphide (H(2)S), a multifunctional gasotransmitter in the pancreatic beta-cell. Hydrogen Sulfide 101-106 cystathionase (cystathionine gamma-lyase) Mus musculus 27-30 22403551-1 2012 The aim of this study was to identify the actions of stimulation of endogenous production of H(2)S by cysteine, the substrate for the two H(2)S-producing enzymes, cystathionine-beta-synthase and cystathionine-gamma-lyase, on ion transport across rat distal colon. Hydrogen Sulfide 93-98 cystathionine beta synthase Rattus norvegicus 163-190 22403551-1 2012 The aim of this study was to identify the actions of stimulation of endogenous production of H(2)S by cysteine, the substrate for the two H(2)S-producing enzymes, cystathionine-beta-synthase and cystathionine-gamma-lyase, on ion transport across rat distal colon. Hydrogen Sulfide 93-98 cystathionine gamma-lyase Rattus norvegicus 195-220 22403551-1 2012 The aim of this study was to identify the actions of stimulation of endogenous production of H(2)S by cysteine, the substrate for the two H(2)S-producing enzymes, cystathionine-beta-synthase and cystathionine-gamma-lyase, on ion transport across rat distal colon. Hydrogen Sulfide 138-143 cystathionine beta synthase Rattus norvegicus 163-190 22403551-1 2012 The aim of this study was to identify the actions of stimulation of endogenous production of H(2)S by cysteine, the substrate for the two H(2)S-producing enzymes, cystathionine-beta-synthase and cystathionine-gamma-lyase, on ion transport across rat distal colon. Hydrogen Sulfide 138-143 cystathionine gamma-lyase Rattus norvegicus 195-220 22808324-7 2012 Cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) are well known as H(2)S-producing enzymes. Hydrogen Sulfide 88-93 cystathionine beta-synthase Homo sapiens 0-27 22808324-7 2012 Cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) are well known as H(2)S-producing enzymes. Hydrogen Sulfide 88-93 cystathionine gamma-lyase Homo sapiens 38-63 22808324-7 2012 Cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) are well known as H(2)S-producing enzymes. Hydrogen Sulfide 88-93 cystathionine gamma-lyase Homo sapiens 65-68 22368256-6 2012 In human gingival fibroblasts, H(2)S inhibits not only cytochrome c oxidase activity but also superoxide dismutase activity. Hydrogen Sulfide 31-36 cytochrome c, somatic Homo sapiens 55-67 22368256-11 2012 It is concluded that the Bax apoptotic pathway and the mitochondrial pathway are activated by H(2)S. Hydrogen Sulfide 94-99 BCL2 associated X, apoptosis regulator Homo sapiens 25-28 22314625-2 2012 The enzymes cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS) had long been speculated to generate H2S, and inhibitors of these enzymes had been employed to characterize influences of H2S in various organs. Hydrogen Sulfide 119-122 cystathionase (cystathionine gamma-lyase) Mus musculus 12-37 22314625-2 2012 The enzymes cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS) had long been speculated to generate H2S, and inhibitors of these enzymes had been employed to characterize influences of H2S in various organs. Hydrogen Sulfide 119-122 cystathionase (cystathionine gamma-lyase) Mus musculus 39-42 22314625-2 2012 The enzymes cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS) had long been speculated to generate H2S, and inhibitors of these enzymes had been employed to characterize influences of H2S in various organs. Hydrogen Sulfide 119-122 cystathionine beta-synthase Mus musculus 48-75 22314625-2 2012 The enzymes cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS) had long been speculated to generate H2S, and inhibitors of these enzymes had been employed to characterize influences of H2S in various organs. Hydrogen Sulfide 204-207 cystathionase (cystathionine gamma-lyase) Mus musculus 12-37 22314625-2 2012 The enzymes cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS) had long been speculated to generate H2S, and inhibitors of these enzymes had been employed to characterize influences of H2S in various organs. Hydrogen Sulfide 204-207 cystathionase (cystathionine gamma-lyase) Mus musculus 39-42 22314625-2 2012 The enzymes cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS) had long been speculated to generate H2S, and inhibitors of these enzymes had been employed to characterize influences of H2S in various organs. Hydrogen Sulfide 204-207 cystathionine beta-synthase Mus musculus 48-75 22314625-3 2012 Definitive evidence that H2S is a physiologic regulator came with the development of mice with targeted deletion of CSE and CBS. Hydrogen Sulfide 25-28 cystathionase (cystathionine gamma-lyase) Mus musculus 116-119 22314625-4 2012 Best characterized is the role of H2S, formed by CSE, as an endothelial derived relaxing factor that normally regulates blood pressure by acting through ATP-sensitive potassium channels. Hydrogen Sulfide 34-37 cystathionase (cystathionine gamma-lyase) Mus musculus 49-52 22331189-5 2012 Recent studies using metabolomics revealed that CO inhibits cystathionine beta-synthase (CBS), which generates H(2)S, another gaseous mediator. Hydrogen Sulfide 111-116 cystathionine beta-synthase Homo sapiens 60-87 22331189-5 2012 Recent studies using metabolomics revealed that CO inhibits cystathionine beta-synthase (CBS), which generates H(2)S, another gaseous mediator. Hydrogen Sulfide 111-116 cystathionine beta-synthase Homo sapiens 89-92 22349394-8 2012 Hypoxia-evoked H(2)S generation in the carotid body requires the interaction of CSE with HO-2, which generates CO. Hydrogen Sulfide 15-20 cystathionase (cystathionine gamma-lyase) Mus musculus 80-83 22349394-8 2012 Hypoxia-evoked H(2)S generation in the carotid body requires the interaction of CSE with HO-2, which generates CO. Hydrogen Sulfide 15-20 heme oxygenase 2 Mus musculus 89-93 22134701-0 2012 Inhibition of ROS-activated ERK1/2 pathway contributes to the protection of H2S against chemical hypoxia-induced injury in H9c2 cells. Hydrogen Sulfide 76-79 mitogen activated protein kinase 3 Rattus norvegicus 28-34 22134701-2 2012 However, the roles of extracellular signal-regulated protein kinases 1/2 (ERK1/2) in H(2)S-induced cardioprotection have not been completely elucidated. Hydrogen Sulfide 85-90 mitogen activated protein kinase 3 Rattus norvegicus 74-80 22134701-6 2012 More importantly, U0126, a selective inhibitor of ERK1/2, mimicked the above cytoprotection of H(2)S against CoCl(2)-induced injury in H9c2 cells. Hydrogen Sulfide 95-100 mitogen activated protein kinase 3 Rattus norvegicus 50-56 22134701-7 2012 In conclusion, these results indicate that H(2)S protects H9c2 cells against chemical hypoxia-induced injury partially by inhibiting ROS-mediated activation of ERK1/2. Hydrogen Sulfide 43-48 mitogen activated protein kinase 3 Rattus norvegicus 160-166 21161531-0 2012 Inhibitors of p38 and ERK1/2 MAPkinase and hydrogen sulphide block constitutive and IL-1beta-induced IL-6 and IL-8 expression in the human chondrocyte cell line C-28/I2. Hydrogen Sulfide 43-60 mitogen-activated protein kinase 3 Homo sapiens 22-28 21161531-0 2012 Inhibitors of p38 and ERK1/2 MAPkinase and hydrogen sulphide block constitutive and IL-1beta-induced IL-6 and IL-8 expression in the human chondrocyte cell line C-28/I2. Hydrogen Sulfide 43-60 interleukin 1 beta Homo sapiens 84-92 21161531-0 2012 Inhibitors of p38 and ERK1/2 MAPkinase and hydrogen sulphide block constitutive and IL-1beta-induced IL-6 and IL-8 expression in the human chondrocyte cell line C-28/I2. Hydrogen Sulfide 43-60 interleukin 6 Homo sapiens 101-105 21161531-0 2012 Inhibitors of p38 and ERK1/2 MAPkinase and hydrogen sulphide block constitutive and IL-1beta-induced IL-6 and IL-8 expression in the human chondrocyte cell line C-28/I2. Hydrogen Sulfide 43-60 C-X-C motif chemokine ligand 8 Homo sapiens 110-114 21800153-0 2012 Involvement of K(ATP)/PI (3)K/AKT/Bcl-2 pathway in hydrogen sulfide-induced neuroprotection against the toxicity of 1-methy-4-phenylpyridinium ion. Hydrogen Sulfide 51-67 AKT serine/threonine kinase 1 Rattus norvegicus 30-33 21800153-0 2012 Involvement of K(ATP)/PI (3)K/AKT/Bcl-2 pathway in hydrogen sulfide-induced neuroprotection against the toxicity of 1-methy-4-phenylpyridinium ion. Hydrogen Sulfide 51-67 BCL2, apoptosis regulator Rattus norvegicus 34-39 21800153-4 2012 These data provided the evidence that the neuroprotective action of H(2)S against MPP(+) toxicity to PC12 cells is via the K(ATP)/PI(3)K/AKT/Bcl-2 pathway. Hydrogen Sulfide 68-73 AKT serine/threonine kinase 1 Rattus norvegicus 137-140 21800153-4 2012 These data provided the evidence that the neuroprotective action of H(2)S against MPP(+) toxicity to PC12 cells is via the K(ATP)/PI(3)K/AKT/Bcl-2 pathway. Hydrogen Sulfide 68-73 BCL2, apoptosis regulator Rattus norvegicus 141-146 21920536-1 2012 OBJECTIVE: To explore the predictive value of plasma hydrogen sulfide (H(2)S) in differentiating between vasovagal syncope (VVS) and postural orthostatic tachycardia syndrome (POTS) in children. Hydrogen Sulfide 53-69 VVS Homo sapiens 124-127 21920536-5 2012 RESULTS: Plasma levels of H(2)S were significantly higher in children with VVS (95.3+-3.8 mumol/L) and POTS (100.9+-2.1 mumol/L) than in children in the control group (82.6+-6.5 mumol/L). Hydrogen Sulfide 26-31 VVS Homo sapiens 75-78 21920536-6 2012 Compared with the VVS group, the POTS group had plasma levels of H(2)S that were significantly increased. Hydrogen Sulfide 65-70 VVS Homo sapiens 18-21 22460462-1 2012 Hydrogen sulfide (H(2)S) is generated from L-cysteine by certain enzymes including cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (CBS), and causes excitation of nociceptors mainly via activation of Ca(v)3.2 T-type Ca(2+) channels in the peripheral tissue, facilitating somatic and colonic pain. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Rattus norvegicus 83-108 22460462-1 2012 Hydrogen sulfide (H(2)S) is generated from L-cysteine by certain enzymes including cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (CBS), and causes excitation of nociceptors mainly via activation of Ca(v)3.2 T-type Ca(2+) channels in the peripheral tissue, facilitating somatic and colonic pain. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Rattus norvegicus 110-113 22460462-1 2012 Hydrogen sulfide (H(2)S) is generated from L-cysteine by certain enzymes including cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (CBS), and causes excitation of nociceptors mainly via activation of Ca(v)3.2 T-type Ca(2+) channels in the peripheral tissue, facilitating somatic and colonic pain. Hydrogen Sulfide 0-16 cystathionine beta synthase Rattus norvegicus 119-146 22460462-1 2012 Hydrogen sulfide (H(2)S) is generated from L-cysteine by certain enzymes including cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (CBS), and causes excitation of nociceptors mainly via activation of Ca(v)3.2 T-type Ca(2+) channels in the peripheral tissue, facilitating somatic and colonic pain. Hydrogen Sulfide 0-16 caveolin 3 Rattus norvegicus 216-222 22460462-1 2012 Hydrogen sulfide (H(2)S) is generated from L-cysteine by certain enzymes including cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (CBS), and causes excitation of nociceptors mainly via activation of Ca(v)3.2 T-type Ca(2+) channels in the peripheral tissue, facilitating somatic and colonic pain. Hydrogen Sulfide 18-23 cystathionine gamma-lyase Rattus norvegicus 83-108 22460462-1 2012 Hydrogen sulfide (H(2)S) is generated from L-cysteine by certain enzymes including cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (CBS), and causes excitation of nociceptors mainly via activation of Ca(v)3.2 T-type Ca(2+) channels in the peripheral tissue, facilitating somatic and colonic pain. Hydrogen Sulfide 18-23 cystathionine gamma-lyase Rattus norvegicus 110-113 22460462-1 2012 Hydrogen sulfide (H(2)S) is generated from L-cysteine by certain enzymes including cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (CBS), and causes excitation of nociceptors mainly via activation of Ca(v)3.2 T-type Ca(2+) channels in the peripheral tissue, facilitating somatic and colonic pain. Hydrogen Sulfide 18-23 cystathionine beta synthase Rattus norvegicus 119-146 22460462-1 2012 Hydrogen sulfide (H(2)S) is generated from L-cysteine by certain enzymes including cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (CBS), and causes excitation of nociceptors mainly via activation of Ca(v)3.2 T-type Ca(2+) channels in the peripheral tissue, facilitating somatic and colonic pain. Hydrogen Sulfide 18-23 caveolin 3 Rattus norvegicus 216-222 22460462-2 2012 Here, we investigated whether sensory nerves and Ca(v)3.2 are involved in the H(2)S-induced mucosal cytoprotection against 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats. Hydrogen Sulfide 78-83 caveolin 3 Rattus norvegicus 49-55 22460462-15 2012 Our findings suggest that luminal H(2)S causes excitation of sensory nerves most probably by activating Ca(v)3.2 T-type Ca(2+) channels that are upregulated in the early stage of colitis, leading to colonic mucosal cytoprotection in rats. Hydrogen Sulfide 34-39 caveolin 3 Rattus norvegicus 104-110 22036943-3 2012 H(2)S is produced by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulphurtransferase (MST). Hydrogen Sulfide 0-5 cystathionine beta-synthase Homo sapiens 21-48 22036943-3 2012 H(2)S is produced by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulphurtransferase (MST). Hydrogen Sulfide 0-5 cystathionine beta-synthase Homo sapiens 50-53 22036943-3 2012 H(2)S is produced by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulphurtransferase (MST). Hydrogen Sulfide 0-5 cystathionine gamma-lyase Homo sapiens 56-81 22036943-3 2012 H(2)S is produced by cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulphurtransferase (MST). Hydrogen Sulfide 0-5 cystathionine gamma-lyase Homo sapiens 83-86 22133671-9 2012 H(2)S precursor l-cysteine-induced relaxation in cerebral arteries was inhibited by cystathionine gamma-lyase (CSE) inhibitor dl-propargylglycine. Hydrogen Sulfide 0-5 cystathionine gamma-lyase Rattus norvegicus 84-109 22133671-9 2012 H(2)S precursor l-cysteine-induced relaxation in cerebral arteries was inhibited by cystathionine gamma-lyase (CSE) inhibitor dl-propargylglycine. Hydrogen Sulfide 0-5 cystathionine gamma-lyase Rattus norvegicus 111-114 22310774-0 2012 Characterization of hydrogen sulfide and its synthases, cystathionine beta-synthase and cystathionine gamma-lyase, in human prostatic tissue and cells. Hydrogen Sulfide 20-36 cystathionine beta-synthase Homo sapiens 56-83 22310774-1 2012 OBJECTIVE: To investigate hydrogen sulfide and its synthases, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), in human prostatic tissue and cells. Hydrogen Sulfide 26-42 cystathionine beta-synthase Homo sapiens 62-89 22310774-1 2012 OBJECTIVE: To investigate hydrogen sulfide and its synthases, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), in human prostatic tissue and cells. Hydrogen Sulfide 26-42 cystathionine beta-synthase Homo sapiens 91-94 22455639-1 2012 OBJECTIVE: To investigate the impact of sodium nitroprusside (a nitric oxide donor) in the ductus arteriosus in preterm rabbits on hydrogen sulfide (H(2)S)-cystathionine-gamma-lyase (CSE) system. Hydrogen Sulfide 131-147 cystathionine gamma-lyase Oryctolagus cuniculus 156-181 22015639-10 2012 H(2)S-induced expression of IL-6, IL-8 and COX-2 was completely blocked by specific inhibitors of p38 and ERK1/2 MAPK and NF-kappaB. Hydrogen Sulfide 0-5 interleukin 6 Homo sapiens 28-32 22015639-10 2012 H(2)S-induced expression of IL-6, IL-8 and COX-2 was completely blocked by specific inhibitors of p38 and ERK1/2 MAPK and NF-kappaB. Hydrogen Sulfide 0-5 C-X-C motif chemokine ligand 8 Homo sapiens 34-38 22015639-10 2012 H(2)S-induced expression of IL-6, IL-8 and COX-2 was completely blocked by specific inhibitors of p38 and ERK1/2 MAPK and NF-kappaB. Hydrogen Sulfide 0-5 mitochondrially encoded cytochrome c oxidase II Homo sapiens 43-48 22015639-10 2012 H(2)S-induced expression of IL-6, IL-8 and COX-2 was completely blocked by specific inhibitors of p38 and ERK1/2 MAPK and NF-kappaB. Hydrogen Sulfide 0-5 mitogen-activated protein kinase 1 Homo sapiens 98-101 22015639-10 2012 H(2)S-induced expression of IL-6, IL-8 and COX-2 was completely blocked by specific inhibitors of p38 and ERK1/2 MAPK and NF-kappaB. Hydrogen Sulfide 0-5 mitogen-activated protein kinase 3 Homo sapiens 106-112 22232681-3 2012 In this cascade, hypoxia elicits cerebral vasodilation via the coordinate actions of H(2)S formed by cystathionine beta-synthase (CBS) and CO generated by heme oxygenase (HO)-2. Hydrogen Sulfide 85-90 cystathionine beta-synthase Mus musculus 101-128 22232681-3 2012 In this cascade, hypoxia elicits cerebral vasodilation via the coordinate actions of H(2)S formed by cystathionine beta-synthase (CBS) and CO generated by heme oxygenase (HO)-2. Hydrogen Sulfide 85-90 cystathionine beta-synthase Mus musculus 130-133 21950347-8 2012 Physiological concentrations of H2S abrogated peroxynitrite-induced cell damage as demonstrated by the: (i) inhibition of apoptosis and necrosis caused by peroxynitrite; (ii) prevention of protein nitration; and (iii) inhibition of PARP-1 [poly(ADP-ribose) polymerase 1] activation in cellular models, implying that a major part of the cytoprotective effects of hydrogen sulfide may be mediated by modulation of peroxynitrite chemistry, in particular under inflammatory conditions. Hydrogen Sulfide 32-35 poly(ADP-ribose) polymerase 1 Homo sapiens 232-238 21950347-8 2012 Physiological concentrations of H2S abrogated peroxynitrite-induced cell damage as demonstrated by the: (i) inhibition of apoptosis and necrosis caused by peroxynitrite; (ii) prevention of protein nitration; and (iii) inhibition of PARP-1 [poly(ADP-ribose) polymerase 1] activation in cellular models, implying that a major part of the cytoprotective effects of hydrogen sulfide may be mediated by modulation of peroxynitrite chemistry, in particular under inflammatory conditions. Hydrogen Sulfide 32-35 poly(ADP-ribose) polymerase 1 Homo sapiens 240-269 22120434-9 2012 During hypoxia there were concurrent increases in H(2)S production, which could be prevented by CBS inhibitor, indicating the endogenous source of the gas. Hydrogen Sulfide 50-55 cystathionine beta-synthase Homo sapiens 96-99 22120434-12 2012 In conclusion, hypoxia activates H(2)S endogenous production through the CBS-H(2)S pathway in the AVPO, having a cryogenic effect. Hydrogen Sulfide 33-38 cystathionine beta-synthase Homo sapiens 73-76 22120434-12 2012 In conclusion, hypoxia activates H(2)S endogenous production through the CBS-H(2)S pathway in the AVPO, having a cryogenic effect. Hydrogen Sulfide 77-82 cystathionine beta-synthase Homo sapiens 73-76 22074719-4 2012 Western blots performed in lung tissue identified the presence of the H(2)S-synthesizing enzymes, cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfur transferase (3-MST), but not cystathionine beta-synthase (CBS). Hydrogen Sulfide 70-75 cystathionine gamma-lyase Rattus norvegicus 98-123 22074719-4 2012 Western blots performed in lung tissue identified the presence of the H(2)S-synthesizing enzymes, cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfur transferase (3-MST), but not cystathionine beta-synthase (CBS). Hydrogen Sulfide 70-75 cystathionine gamma-lyase Rattus norvegicus 125-128 22074719-4 2012 Western blots performed in lung tissue identified the presence of the H(2)S-synthesizing enzymes, cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfur transferase (3-MST), but not cystathionine beta-synthase (CBS). Hydrogen Sulfide 70-75 cystathionine beta synthase Rattus norvegicus 189-216 22244329-2 2012 We show that the antiapoptotic actions of NF-kappaB are mediated by hydrogen sulfide (H(2)S) synthesized by cystathionine gamma-lyase (CSE). Hydrogen Sulfide 68-84 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 42-51 22244329-2 2012 We show that the antiapoptotic actions of NF-kappaB are mediated by hydrogen sulfide (H(2)S) synthesized by cystathionine gamma-lyase (CSE). Hydrogen Sulfide 68-84 cystathionase (cystathionine gamma-lyase) Mus musculus 108-133 22244329-2 2012 We show that the antiapoptotic actions of NF-kappaB are mediated by hydrogen sulfide (H(2)S) synthesized by cystathionine gamma-lyase (CSE). Hydrogen Sulfide 68-84 cystathionase (cystathionine gamma-lyase) Mus musculus 135-138 22244329-2 2012 We show that the antiapoptotic actions of NF-kappaB are mediated by hydrogen sulfide (H(2)S) synthesized by cystathionine gamma-lyase (CSE). Hydrogen Sulfide 86-91 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 42-51 22244329-2 2012 We show that the antiapoptotic actions of NF-kappaB are mediated by hydrogen sulfide (H(2)S) synthesized by cystathionine gamma-lyase (CSE). Hydrogen Sulfide 86-91 cystathionase (cystathionine gamma-lyase) Mus musculus 108-133 22244329-2 2012 We show that the antiapoptotic actions of NF-kappaB are mediated by hydrogen sulfide (H(2)S) synthesized by cystathionine gamma-lyase (CSE). Hydrogen Sulfide 86-91 cystathionase (cystathionine gamma-lyase) Mus musculus 135-138 22244329-6 2012 H(2)S acts by sulfhydrating the p65 subunit of NF-kappaB at cysteine-38, which promotes its binding to the coactivator ribosomal protein S3 (RPS3). Hydrogen Sulfide 0-5 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 32-35 22244329-6 2012 H(2)S acts by sulfhydrating the p65 subunit of NF-kappaB at cysteine-38, which promotes its binding to the coactivator ribosomal protein S3 (RPS3). Hydrogen Sulfide 0-5 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 47-56 22244329-6 2012 H(2)S acts by sulfhydrating the p65 subunit of NF-kappaB at cysteine-38, which promotes its binding to the coactivator ribosomal protein S3 (RPS3). Hydrogen Sulfide 0-5 ribosomal protein S3 Mus musculus 119-139 22244329-6 2012 H(2)S acts by sulfhydrating the p65 subunit of NF-kappaB at cysteine-38, which promotes its binding to the coactivator ribosomal protein S3 (RPS3). Hydrogen Sulfide 0-5 ribosomal protein S3 Mus musculus 141-145 21866187-1 2012 BACKGROUND: Hydrogen sulfide (H(2)S), an endogenous vasoactive agent, is produced by cystathionine gamma-lyase (CGL) and cystathionine beta-synthase (CBS) enzymes. Hydrogen Sulfide 12-28 cystathionine gamma-lyase Rattus norvegicus 85-110 23080150-4 2012 The purpose of this article is to review recent studies addressing the role of H2S in carotid body.Cystathionine gamma-lyase (CSE) and cystathionine beta synthase (CBS) are the two major enzymes that catalyze the formation of endogenous H2S. Hydrogen Sulfide 79-82 cystathionase (cystathionine gamma-lyase) Mus musculus 99-124 23080150-4 2012 The purpose of this article is to review recent studies addressing the role of H2S in carotid body.Cystathionine gamma-lyase (CSE) and cystathionine beta synthase (CBS) are the two major enzymes that catalyze the formation of endogenous H2S. Hydrogen Sulfide 79-82 cystathionase (cystathionine gamma-lyase) Mus musculus 126-129 23080150-4 2012 The purpose of this article is to review recent studies addressing the role of H2S in carotid body.Cystathionine gamma-lyase (CSE) and cystathionine beta synthase (CBS) are the two major enzymes that catalyze the formation of endogenous H2S. Hydrogen Sulfide 79-82 cystathionine beta-synthase Mus musculus 135-162 23080150-4 2012 The purpose of this article is to review recent studies addressing the role of H2S in carotid body.Cystathionine gamma-lyase (CSE) and cystathionine beta synthase (CBS) are the two major enzymes that catalyze the formation of endogenous H2S. Hydrogen Sulfide 237-240 cystathionase (cystathionine gamma-lyase) Mus musculus 99-124 23080150-4 2012 The purpose of this article is to review recent studies addressing the role of H2S in carotid body.Cystathionine gamma-lyase (CSE) and cystathionine beta synthase (CBS) are the two major enzymes that catalyze the formation of endogenous H2S. Hydrogen Sulfide 237-240 cystathionase (cystathionine gamma-lyase) Mus musculus 126-129 23080150-4 2012 The purpose of this article is to review recent studies addressing the role of H2S in carotid body.Cystathionine gamma-lyase (CSE) and cystathionine beta synthase (CBS) are the two major enzymes that catalyze the formation of endogenous H2S. Hydrogen Sulfide 237-240 cystathionine beta-synthase Mus musculus 135-162 22120434-13 2012 Moreover, the present data are consistent with the notion that the two gaseous molecules, H(2)S and NO, play a key role in mediating the drop in Tb caused by hypoxia and that a fine-balanced interplay between NOS-NO and CBS-H(2)S pathways takes place in the AVPO of rats exposed to hypoxia. Hydrogen Sulfide 90-95 cystathionine beta synthase Rattus norvegicus 220-223 21866187-1 2012 BACKGROUND: Hydrogen sulfide (H(2)S), an endogenous vasoactive agent, is produced by cystathionine gamma-lyase (CGL) and cystathionine beta-synthase (CBS) enzymes. Hydrogen Sulfide 12-28 cystathionine gamma-lyase Rattus norvegicus 112-115 21866187-1 2012 BACKGROUND: Hydrogen sulfide (H(2)S), an endogenous vasoactive agent, is produced by cystathionine gamma-lyase (CGL) and cystathionine beta-synthase (CBS) enzymes. Hydrogen Sulfide 12-28 cystathionine beta synthase Rattus norvegicus 121-148 21866187-1 2012 BACKGROUND: Hydrogen sulfide (H(2)S), an endogenous vasoactive agent, is produced by cystathionine gamma-lyase (CGL) and cystathionine beta-synthase (CBS) enzymes. Hydrogen Sulfide 30-35 cystathionine gamma-lyase Rattus norvegicus 85-110 21866187-1 2012 BACKGROUND: Hydrogen sulfide (H(2)S), an endogenous vasoactive agent, is produced by cystathionine gamma-lyase (CGL) and cystathionine beta-synthase (CBS) enzymes. Hydrogen Sulfide 30-35 cystathionine gamma-lyase Rattus norvegicus 112-115 21866187-1 2012 BACKGROUND: Hydrogen sulfide (H(2)S), an endogenous vasoactive agent, is produced by cystathionine gamma-lyase (CGL) and cystathionine beta-synthase (CBS) enzymes. Hydrogen Sulfide 30-35 cystathionine beta synthase Rattus norvegicus 121-148 21940660-0 2012 Hydrogen sulfide regulates cAMP homeostasis and renin degranulation in As4.1 and rat renin-rich kidney cells. Hydrogen Sulfide 0-16 renin Rattus norvegicus 48-53 23080150-7 2012 CSE knockout mice displayed absence of hypoxia-evoked H2S generation and severely impaired sensory excitation by low O2. Hydrogen Sulfide 54-57 cystathionase (cystathionine gamma-lyase) Mus musculus 0-3 21940660-0 2012 Hydrogen sulfide regulates cAMP homeostasis and renin degranulation in As4.1 and rat renin-rich kidney cells. Hydrogen Sulfide 0-16 renin Rattus norvegicus 85-90 21940660-1 2012 The present study aims to investigate the regulatory effect of hydrogen sulfide (H(2)S) on cAMP homeostasis and renin degranulation in As4.1 and rat renin-rich kidney cells. Hydrogen Sulfide 63-79 renin Rattus norvegicus 149-154 21940660-1 2012 The present study aims to investigate the regulatory effect of hydrogen sulfide (H(2)S) on cAMP homeostasis and renin degranulation in As4.1 and rat renin-rich kidney cells. Hydrogen Sulfide 81-86 renin Rattus norvegicus 149-154 23539901-2 2012 Cystathionine gamma-lyase (CSE)/H2S pathway has been implicated in scavenging reactive oxygen species (ROS) in the mammalian cells. Hydrogen Sulfide 32-35 cystathionine gamma-lyase Homo sapiens 0-25 21998138-1 2012 Focus on "Hydrogen sulfide regulates cAMP homeostasis and renin degranulation in As4.1 and rat renin-rich kidney cell". Hydrogen Sulfide 10-26 renin Rattus norvegicus 58-63 21998138-1 2012 Focus on "Hydrogen sulfide regulates cAMP homeostasis and renin degranulation in As4.1 and rat renin-rich kidney cell". Hydrogen Sulfide 10-26 renin Rattus norvegicus 95-100 22680638-2 2012 H(2)S is biosynthesized in mammalian tissues by both non-enzymatic processes and several enzymatic pathways ensured by cystathionine-beta-synthase and cystathionine-gamma-lyase. Hydrogen Sulfide 0-5 cystathionine beta-synthase Homo sapiens 119-146 22680638-2 2012 H(2)S is biosynthesized in mammalian tissues by both non-enzymatic processes and several enzymatic pathways ensured by cystathionine-beta-synthase and cystathionine-gamma-lyase. Hydrogen Sulfide 0-5 cystathionine gamma-lyase Homo sapiens 151-176 21940660-4 2012 We continued to study whether H(2)S may mediate cAMP-dependent renin degranulaion in As4.1 cells. Hydrogen Sulfide 30-35 renin Rattus norvegicus 63-68 21940660-7 2012 RT-PCR showed that cystathionine-gamma-lyase is the main enzyme to produce endogenous H(2)S in As4.1 cells. Hydrogen Sulfide 86-91 cystathionase (cystathionine gamma-lyase) Mus musculus 19-44 21940660-8 2012 Overexpression of cystathionine-gamma-lyase increased endogenous H(2)S production and suppressed isoproterenol-induced renin release, suggesting that endogenous H(2)S may also inhibit renin release from As4.1 cells. Hydrogen Sulfide 65-70 cystathionase (cystathionine gamma-lyase) Mus musculus 18-43 21940660-8 2012 Overexpression of cystathionine-gamma-lyase increased endogenous H(2)S production and suppressed isoproterenol-induced renin release, suggesting that endogenous H(2)S may also inhibit renin release from As4.1 cells. Hydrogen Sulfide 161-166 cystathionase (cystathionine gamma-lyase) Mus musculus 18-43 21940660-8 2012 Overexpression of cystathionine-gamma-lyase increased endogenous H(2)S production and suppressed isoproterenol-induced renin release, suggesting that endogenous H(2)S may also inhibit renin release from As4.1 cells. Hydrogen Sulfide 161-166 renin Rattus norvegicus 184-189 21940660-9 2012 We also tested whether H(2)S has a similar effect in renin-rich kidney cells. Hydrogen Sulfide 23-28 renin Rattus norvegicus 53-58 21940660-13 2012 Our findings suggest that H(2)S plays a critical role in regulation of renin degranulation in As4.1 and rat renin-rich kidney cells. Hydrogen Sulfide 26-31 renin Rattus norvegicus 71-76 21940660-13 2012 Our findings suggest that H(2)S plays a critical role in regulation of renin degranulation in As4.1 and rat renin-rich kidney cells. Hydrogen Sulfide 26-31 renin Rattus norvegicus 108-113 23539901-2 2012 Cystathionine gamma-lyase (CSE)/H2S pathway has been implicated in scavenging reactive oxygen species (ROS) in the mammalian cells. Hydrogen Sulfide 32-35 cystathionine gamma-lyase Homo sapiens 27-30 22419888-2 2012 We previously reported that H2S inhibits antiangiogenic factors such, as endostatin and angiostatin, but a little is known about its effect on parstatin (a fragment of proteinase-activated receptor-1, PAR-1). Hydrogen Sulfide 28-31 collagen, type XVIII, alpha 1 Mus musculus 73-83 22419888-2 2012 We previously reported that H2S inhibits antiangiogenic factors such, as endostatin and angiostatin, but a little is known about its effect on parstatin (a fragment of proteinase-activated receptor-1, PAR-1). Hydrogen Sulfide 28-31 plasminogen Mus musculus 88-99 22419888-3 2012 We hypothesize that H2S inhibits parstatin formation and promotes VEGF activation, thus promoting angiogenesis and significantly limiting the extent of MI injury. Hydrogen Sulfide 20-23 vascular endothelial growth factor A Mus musculus 66-70 22724330-2 2012 Using immunocytochemical method to detect cystathionine beta-synthase, the presence of H2S+ neurons was demonstrated in the nuclei studied of Wistar rats (n = 16). Hydrogen Sulfide 87-90 cystathionine beta synthase Rattus norvegicus 42-69 22785020-0 2012 Colonic hydrogen sulfide-induced visceral pain and referred hyperalgesia involve activation of both Ca(v)3.2 and TRPA1 channels in mice. Hydrogen Sulfide 8-24 calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus 100-108 22785020-0 2012 Colonic hydrogen sulfide-induced visceral pain and referred hyperalgesia involve activation of both Ca(v)3.2 and TRPA1 channels in mice. Hydrogen Sulfide 8-24 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 113-118 22785020-5 2012 These findings demonstrate that H(2)S-induced colonic pain and referred hyperalgesia require activation of both Ca(v)3.2 and TRPA1 channels in mice. Hydrogen Sulfide 32-37 calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus 112-120 22785020-5 2012 These findings demonstrate that H(2)S-induced colonic pain and referred hyperalgesia require activation of both Ca(v)3.2 and TRPA1 channels in mice. Hydrogen Sulfide 32-37 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 125-130 21879311-0 2012 Nitric oxide synthase inhibition abrogates hydrogen sulfide-induced cardioprotection in mice. Hydrogen Sulfide 43-59 nitric oxide synthase 1, neuronal Mus musculus 0-21 21879311-7 2012 However, co-administration of N-nitro-L-arginine methyl ester, a nitric oxide synthase (NOS) inhibitor, and Celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor along with NaHS and ISO abrogated the beneficial effect of H(2)S differentially. Hydrogen Sulfide 225-230 prostaglandin-endoperoxide synthase 2 Mus musculus 149-154 21879311-10 2012 Our results revealed that H(2)S provides myocardial protection through interaction with NOS and COX-2 pathway and inhibition of NOS completely abrogates the hydrogen sulfide-induced cardioprotection in mice. Hydrogen Sulfide 26-31 prostaglandin-endoperoxide synthase 2 Mus musculus 96-101 23285278-9 2012 Treatment of aortic rings with NaHS, a fast releasing H2S donor, enhanced phosphorylation of vasodilator-stimulated phosphoprotein in a time-dependent manner, suggesting that cGMP-dependent protein kinase (PKG) is activated after exposure to H2S. Hydrogen Sulfide 242-245 protein kinase cGMP-dependent 1 Homo sapiens 206-209 23285261-2 2012 This study was designed to determine the role for the endogenous H2S producing enzyme cystathionine beta-synthetase (CBS) and cystathionine gamma-lyase (CSE) in a validated rat model of visceral hyperalgesia (VH). Hydrogen Sulfide 65-68 cystathionine beta synthase Rattus norvegicus 86-115 23285261-2 2012 This study was designed to determine the role for the endogenous H2S producing enzyme cystathionine beta-synthetase (CBS) and cystathionine gamma-lyase (CSE) in a validated rat model of visceral hyperalgesia (VH). Hydrogen Sulfide 65-68 cystathionine beta synthase Rattus norvegicus 117-120 23285261-2 2012 This study was designed to determine the role for the endogenous H2S producing enzyme cystathionine beta-synthetase (CBS) and cystathionine gamma-lyase (CSE) in a validated rat model of visceral hyperalgesia (VH). Hydrogen Sulfide 65-68 cystathionine gamma-lyase Rattus norvegicus 153-156 23285261-12 2012 To further confirm the role for CBS-H2S signaling, NaHS was used to mimic the production of H2S by CBS. Hydrogen Sulfide 36-39 cystathionine beta synthase Rattus norvegicus 32-35 23285261-12 2012 To further confirm the role for CBS-H2S signaling, NaHS was used to mimic the production of H2S by CBS. Hydrogen Sulfide 92-95 cystathionine beta synthase Rattus norvegicus 99-102 23285278-12 2012 Dilatory responses to NaHS and L-cysteine (a substrate for H2S production) were reduced in vessels of PKG-I knockout mice (PKG-I-/-). Hydrogen Sulfide 59-62 protein kinase cGMP-dependent 1 Homo sapiens 102-105 23285278-12 2012 Dilatory responses to NaHS and L-cysteine (a substrate for H2S production) were reduced in vessels of PKG-I knockout mice (PKG-I-/-). Hydrogen Sulfide 59-62 protein kinase cGMP-dependent 1 Homo sapiens 123-126 23071662-0 2012 TRPA1 has a key role in the somatic pro-nociceptive actions of hydrogen sulfide. Hydrogen Sulfide 63-79 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 0-5 23071662-8 2012 The sensitizing effects of L-cysteine in wild-type mice were inhibited by a cystathionine beta-synthase inhibitor, D,L-propargylglycine (PAG), which inhibits H(2)S formation. Hydrogen Sulfide 158-163 cystathionine beta-synthase Mus musculus 76-103 23071662-3 2012 A H(2)S donor, NaHS, activated TRPA1 expressed in CHO cells and stimulated DRG neurons isolated from Trpa1(+/+) but not Trpa1(-/-) mice. Hydrogen Sulfide 2-7 transient receptor potential cation channel subfamily A member 1 Homo sapiens 31-36 23071662-3 2012 A H(2)S donor, NaHS, activated TRPA1 expressed in CHO cells and stimulated DRG neurons isolated from Trpa1(+/+) but not Trpa1(-/-) mice. Hydrogen Sulfide 2-7 LOW QUALITY PROTEIN: transient receptor potential cation channel subfamily A member 1 Cricetulus griseus 101-106 23071662-9 2012 Mechanical hypersensitivity evoked by intraplantar injections of LPS was prevented by PAG and the TRPA1 antagonist AP-18 and was absent in Trpa1(-/-) mice, indicating that H(2)S mediated stimulation of TRPA1 is necessary for the local pronociceptive effects of LPS. Hydrogen Sulfide 172-177 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 98-103 23071662-9 2012 Mechanical hypersensitivity evoked by intraplantar injections of LPS was prevented by PAG and the TRPA1 antagonist AP-18 and was absent in Trpa1(-/-) mice, indicating that H(2)S mediated stimulation of TRPA1 is necessary for the local pronociceptive effects of LPS. Hydrogen Sulfide 172-177 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 202-207 23071662-13 2012 In electrophysiological studies, the depolarizing actions of H(2)S on isolated DRG neurons were inhibited by AP-18, but not by mibefradil indicating that the primary excitatory effect of H(2)S on DRG neurons is TRPA1 mediated depolarization. Hydrogen Sulfide 61-66 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 211-216 22970259-0 2012 PI3K p110alpha isoform-dependent Rho GTPase Rac1 activation mediates H2S-promoted endothelial cell migration via actin cytoskeleton reorganization. Hydrogen Sulfide 69-72 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 5-14 22970259-0 2012 PI3K p110alpha isoform-dependent Rho GTPase Rac1 activation mediates H2S-promoted endothelial cell migration via actin cytoskeleton reorganization. Hydrogen Sulfide 69-72 Rac family small GTPase 1 Homo sapiens 44-48 22970259-3 2012 Pharmacologic inhibiting vascular endothelial growth factor receptor (VEGFR) and phosphoinositide 3-kinase (PI3K) both blunted the activation of Rac1 and the promotion of cell migration induced by H(2)S. Hydrogen Sulfide 197-202 kinase insert domain receptor Homo sapiens 25-68 22970259-3 2012 Pharmacologic inhibiting vascular endothelial growth factor receptor (VEGFR) and phosphoinositide 3-kinase (PI3K) both blunted the activation of Rac1 and the promotion of cell migration induced by H(2)S. Hydrogen Sulfide 197-202 kinase insert domain receptor Homo sapiens 70-75 22970259-3 2012 Pharmacologic inhibiting vascular endothelial growth factor receptor (VEGFR) and phosphoinositide 3-kinase (PI3K) both blunted the activation of Rac1 and the promotion of cell migration induced by H(2)S. Hydrogen Sulfide 197-202 Rac family small GTPase 1 Homo sapiens 145-149 22970259-4 2012 Moreover, H(2)S-induced Rac1 activation was selectively dependent on the presence of the PI3K p110alpha isoform. Hydrogen Sulfide 10-15 Rac family small GTPase 1 Homo sapiens 24-28 22970259-4 2012 Moreover, H(2)S-induced Rac1 activation was selectively dependent on the presence of the PI3K p110alpha isoform. Hydrogen Sulfide 10-15 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 94-103 22970259-5 2012 Activated Rac1 by H(2)S thus in turn resulted in the phosphorylation of the F-actin polymerization modulator, cofilin. Hydrogen Sulfide 18-23 Rac family small GTPase 1 Homo sapiens 10-14 22970259-5 2012 Activated Rac1 by H(2)S thus in turn resulted in the phosphorylation of the F-actin polymerization modulator, cofilin. Hydrogen Sulfide 18-23 cofilin 1 Homo sapiens 110-117 22970259-6 2012 Additionally, inhibiting of extracellular signal-regulated kinase (ERK) decreased the augmented cell migration rate by H(2)S, but had no effect on Rac1 activation. Hydrogen Sulfide 119-124 mitogen-activated protein kinase 1 Homo sapiens 28-65 22970259-6 2012 Additionally, inhibiting of extracellular signal-regulated kinase (ERK) decreased the augmented cell migration rate by H(2)S, but had no effect on Rac1 activation. Hydrogen Sulfide 119-124 mitogen-activated protein kinase 1 Homo sapiens 67-70 22970259-7 2012 These results indicate that Rac1 conveys the H(2)S signal to microfilaments inducing rearrangements of actin cytoskeleton that regulates cell migration. Hydrogen Sulfide 45-50 Rac family small GTPase 1 Homo sapiens 28-32 22970259-9 2012 ERK was also shown to be involved in the action of H(2)S on endothelial cell migration, but independently of Rac1. Hydrogen Sulfide 51-56 mitogen-activated protein kinase 1 Homo sapiens 0-3 22396778-1 2012 Hydrogen sulfide (H(2)S), a novel gaseous messenger, is synthesized endogenously from L-cysteine by two pyridoxal-5"-phosphate-dependent enzymes, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine beta-synthase Mus musculus 146-173 22870237-1 2012 Hydrogen sulfide (H(2)S) can be endogenously generated from cystathionine gamma-lyase (CSE) in cardiovascular system, offering a cardiovascular protection. Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 60-85 22870237-1 2012 Hydrogen sulfide (H(2)S) can be endogenously generated from cystathionine gamma-lyase (CSE) in cardiovascular system, offering a cardiovascular protection. Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 87-90 22870237-1 2012 Hydrogen sulfide (H(2)S) can be endogenously generated from cystathionine gamma-lyase (CSE) in cardiovascular system, offering a cardiovascular protection. Hydrogen Sulfide 18-23 cystathionase (cystathionine gamma-lyase) Mus musculus 60-85 22870237-1 2012 Hydrogen sulfide (H(2)S) can be endogenously generated from cystathionine gamma-lyase (CSE) in cardiovascular system, offering a cardiovascular protection. Hydrogen Sulfide 18-23 cystathionase (cystathionine gamma-lyase) Mus musculus 87-90 22870237-10 2012 These results suggest that H(2)S mediates estrogen-inhibited proliferation of SMCs via selective activation of ERalpha/cyclin D1 pathways. Hydrogen Sulfide 27-32 estrogen receptor 1 (alpha) Mus musculus 111-118 22870237-10 2012 These results suggest that H(2)S mediates estrogen-inhibited proliferation of SMCs via selective activation of ERalpha/cyclin D1 pathways. Hydrogen Sulfide 27-32 cyclin D1 Mus musculus 119-128 22870268-0 2012 Differential effects of cystathionine-gamma-lyase-dependent vasodilatory H2S in periadventitial vasoregulation of rat and mouse aortas. Hydrogen Sulfide 73-76 cystathionine gamma-lyase Rattus norvegicus 24-49 22870268-16 2012 The present study provides novel insight into the interaction of CSE-H(2)S and perivascular adipose tissue. Hydrogen Sulfide 69-74 cystathionine gamma-lyase Rattus norvegicus 65-68 22815945-6 2012 Overexpression of cystathionine gamma-lyase (CSE), an enzyme that catalyzes H(2)S biosynthesis resulted in a significant reduction in CX3CR1 and CX3CL1 expression as well as CX3CR1-mediated chemotaxis in stimulated macrophages. Hydrogen Sulfide 76-81 cystathionase (cystathionine gamma-lyase) Mus musculus 18-43 22815945-6 2012 Overexpression of cystathionine gamma-lyase (CSE), an enzyme that catalyzes H(2)S biosynthesis resulted in a significant reduction in CX3CR1 and CX3CL1 expression as well as CX3CR1-mediated chemotaxis in stimulated macrophages. Hydrogen Sulfide 76-81 cystathionase (cystathionine gamma-lyase) Mus musculus 45-48 22815945-6 2012 Overexpression of cystathionine gamma-lyase (CSE), an enzyme that catalyzes H(2)S biosynthesis resulted in a significant reduction in CX3CR1 and CX3CL1 expression as well as CX3CR1-mediated chemotaxis in stimulated macrophages. Hydrogen Sulfide 76-81 chemokine (C-X3-C motif) receptor 1 Mus musculus 134-140 22815945-7 2012 The inhibitory effect of H(2)S on CX3CR1 and CX3CL1 expression was mediated by modulation of proliferators-activated receptor-gamma (PPAR-gamma) and NF-kappaB pathway. Hydrogen Sulfide 25-30 chemokine (C-X3-C motif) receptor 1 Mus musculus 34-40 22815945-7 2012 The inhibitory effect of H(2)S on CX3CR1 and CX3CL1 expression was mediated by modulation of proliferators-activated receptor-gamma (PPAR-gamma) and NF-kappaB pathway. Hydrogen Sulfide 25-30 chemokine (C-X3-C motif) ligand 1 Mus musculus 45-51 22815945-7 2012 The inhibitory effect of H(2)S on CX3CR1 and CX3CL1 expression was mediated by modulation of proliferators-activated receptor-gamma (PPAR-gamma) and NF-kappaB pathway. Hydrogen Sulfide 25-30 peroxisome proliferator activated receptor gamma Mus musculus 133-143 22815945-11 2012 However, inhibition of H(2)S formation by PAG increased aortic CX3CR1 and CX3CL1 expression and exacerbated the extent of atherosclerosis. Hydrogen Sulfide 23-28 chemokine (C-X3-C motif) receptor 1 Mus musculus 63-69 22815945-11 2012 However, inhibition of H(2)S formation by PAG increased aortic CX3CR1 and CX3CL1 expression and exacerbated the extent of atherosclerosis. Hydrogen Sulfide 23-28 chemokine (C-X3-C motif) ligand 1 Mus musculus 74-80 22679478-5 2012 The anti-mitogenic effect of H(2)S was accompanied by G(1)-phase cell cycle arrest and the induction of the cyclin-dependent kinase inhibitor p21(Cip). Hydrogen Sulfide 29-34 H3 histone pseudogene 16 Homo sapiens 142-145 22679478-5 2012 The anti-mitogenic effect of H(2)S was accompanied by G(1)-phase cell cycle arrest and the induction of the cyclin-dependent kinase inhibitor p21(Cip). Hydrogen Sulfide 29-34 adenylate kinase 6 Homo sapiens 146-149 22679478-6 2012 Moreover, exposure to H(2)S led to features characteristic of autophagy, including increased formation of LC3B(+) autophagic vacuoles and acidic vesicular organelles as determined by immunofluorescence and acridine orange staining, respectively. Hydrogen Sulfide 22-27 microtubule associated protein 1 light chain 3 beta Homo sapiens 106-110 22679478-7 2012 Abolition of autophagy by RNA interference targeting Vps34 or Atg7 enhanced the anti-proliferative effect of H(2)S. Hydrogen Sulfide 109-114 phosphatidylinositol 3-kinase catalytic subunit type 3 Homo sapiens 53-58 22679478-7 2012 Abolition of autophagy by RNA interference targeting Vps34 or Atg7 enhanced the anti-proliferative effect of H(2)S. Hydrogen Sulfide 109-114 autophagy related 7 Homo sapiens 62-66 22679478-8 2012 Further mechanistic investigation revealed that H(2)S stimulated the phosphorylation of AMP-activated protein kinase (AMPK) and inhibited the phosphorylation of mammalian target of rapamycin (mTOR) and S6 kinase. Hydrogen Sulfide 48-53 mechanistic target of rapamycin kinase Homo sapiens 161-190 22679478-8 2012 Further mechanistic investigation revealed that H(2)S stimulated the phosphorylation of AMP-activated protein kinase (AMPK) and inhibited the phosphorylation of mammalian target of rapamycin (mTOR) and S6 kinase. Hydrogen Sulfide 48-53 mechanistic target of rapamycin kinase Homo sapiens 192-196 23133623-15 2012 CONCLUSIONS: The down regulation of endogenous H(2)S biosynthesis is related to over expression of TNF-alpha in obstructed small intestine. Hydrogen Sulfide 47-52 tumor necrosis factor Mus musculus 99-108 22396778-1 2012 Hydrogen sulfide (H(2)S), a novel gaseous messenger, is synthesized endogenously from L-cysteine by two pyridoxal-5"-phosphate-dependent enzymes, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 184-209 22396778-1 2012 Hydrogen sulfide (H(2)S), a novel gaseous messenger, is synthesized endogenously from L-cysteine by two pyridoxal-5"-phosphate-dependent enzymes, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 211-214 22396778-1 2012 Hydrogen sulfide (H(2)S), a novel gaseous messenger, is synthesized endogenously from L-cysteine by two pyridoxal-5"-phosphate-dependent enzymes, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 18-23 cystathionine beta-synthase Mus musculus 146-173 22396778-1 2012 Hydrogen sulfide (H(2)S), a novel gaseous messenger, is synthesized endogenously from L-cysteine by two pyridoxal-5"-phosphate-dependent enzymes, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 18-23 cystathionase (cystathionine gamma-lyase) Mus musculus 184-209 22396778-1 2012 Hydrogen sulfide (H(2)S), a novel gaseous messenger, is synthesized endogenously from L-cysteine by two pyridoxal-5"-phosphate-dependent enzymes, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE). Hydrogen Sulfide 18-23 cystathionase (cystathionine gamma-lyase) Mus musculus 211-214 22815945-0 2012 Hydrogen sulfide inhibits the development of atherosclerosis with suppressing CX3CR1 and CX3CL1 expression. Hydrogen Sulfide 0-16 chemokine (C-X3-C motif) receptor 1 Mus musculus 78-84 22396778-2 2012 S-propargyl-cysteine (SPRC) is a slow H(2)S releasing drug that provides cysteine, a substrate of CSE. Hydrogen Sulfide 38-43 cystathionase (cystathionine gamma-lyase) Mus musculus 98-101 22815945-0 2012 Hydrogen sulfide inhibits the development of atherosclerosis with suppressing CX3CR1 and CX3CL1 expression. Hydrogen Sulfide 0-16 chemokine (C-X3-C motif) ligand 1 Mus musculus 89-95 22787557-2 2012 We assert that hydrogen sulfide plays an important role in regulating macrophage function in response to subsequent inflammatory stimuli, promoting clearance of leukocyte infiltrate and reducing TNF-alpha levels in vivo following zymosan-challenge. Hydrogen Sulfide 15-31 tumor necrosis factor Homo sapiens 195-204 22253933-1 2012 DDT1 MF-2 hamster ductus deferens cells are resistant to hypothermia due to serotonin secretion from secretory vesicles and subsequent cystathionine beta synthase (CBS) mediated formation of H2S. Hydrogen Sulfide 191-194 cystathionine beta synthase Rattus norvegicus 164-167 22253933-6 2012 Cooled VTSMAC produced up to 10 fold higher concentrations of H2S, and were protected from hypothermia, as shown by a 50% reduction of caspase 3/7 activity and 4 times higher survival compared to SMAC. Hydrogen Sulfide 62-65 diablo, IAP-binding mitochondrial protein Rattus norvegicus 9-13 22253933-8 2012 In VTkidney slices, expression of CBS was 3 fold increased in cold preserved kidney tissue, with two-fold increase in H2S concentration. Hydrogen Sulfide 118-121 cystathionine beta synthase Rattus norvegicus 34-37 22253933-11 2012 The vesicular serotonergic phenotype protects against hypothermic damage through re-uptake of serotonin inducing CBS mediated H2S production both in cells and kidney slices. Hydrogen Sulfide 126-129 cystathionine beta synthase Rattus norvegicus 113-116 22730684-0 2012 [Effect of ulinastatin on oxidative stress and nuclear factor E2-related factor 2 expression in the lung tissues of acute hydrogen sulfide intoxicated rats]. Hydrogen Sulfide 122-138 alpha-1-microglobulin/bikunin precursor Rattus norvegicus 11-22 22186034-7 2012 The mechanisms contributing to the beneficial effects of H(2)S on MSCs were associated with increased levels of phosphorylated Akt (pAkt), phosphorylated Erk1/2 (pErk1/2) and phosphorylated glycogen synthase kinase-3beta (pGSK-3beta) in MSCs. Hydrogen Sulfide 57-62 AKT serine/threonine kinase 1 Rattus norvegicus 127-130 22186034-7 2012 The mechanisms contributing to the beneficial effects of H(2)S on MSCs were associated with increased levels of phosphorylated Akt (pAkt), phosphorylated Erk1/2 (pErk1/2) and phosphorylated glycogen synthase kinase-3beta (pGSK-3beta) in MSCs. Hydrogen Sulfide 57-62 mitogen activated protein kinase 3 Rattus norvegicus 154-160 22186034-7 2012 The mechanisms contributing to the beneficial effects of H(2)S on MSCs were associated with increased levels of phosphorylated Akt (pAkt), phosphorylated Erk1/2 (pErk1/2) and phosphorylated glycogen synthase kinase-3beta (pGSK-3beta) in MSCs. Hydrogen Sulfide 57-62 glycogen synthase kinase 3 beta Rattus norvegicus 190-220 22730684-1 2012 OBJECTIVE: To investigate the dynamic changes of oxidative stress and nuclear factor-E2 related factor 2 (Nrf2) expression in the lung tissues of acute hydrogen sulfide (H2S) intoxicated rats and intervention effects of ulinastatin (UTI). Hydrogen Sulfide 152-168 NFE2 like bZIP transcription factor 2 Rattus norvegicus 106-110 22730684-1 2012 OBJECTIVE: To investigate the dynamic changes of oxidative stress and nuclear factor-E2 related factor 2 (Nrf2) expression in the lung tissues of acute hydrogen sulfide (H2S) intoxicated rats and intervention effects of ulinastatin (UTI). Hydrogen Sulfide 152-168 alpha-1-microglobulin/bikunin precursor Rattus norvegicus 220-231 22730684-1 2012 OBJECTIVE: To investigate the dynamic changes of oxidative stress and nuclear factor-E2 related factor 2 (Nrf2) expression in the lung tissues of acute hydrogen sulfide (H2S) intoxicated rats and intervention effects of ulinastatin (UTI). Hydrogen Sulfide 170-173 NFE2 like bZIP transcription factor 2 Rattus norvegicus 106-110 22730684-1 2012 OBJECTIVE: To investigate the dynamic changes of oxidative stress and nuclear factor-E2 related factor 2 (Nrf2) expression in the lung tissues of acute hydrogen sulfide (H2S) intoxicated rats and intervention effects of ulinastatin (UTI). Hydrogen Sulfide 170-173 alpha-1-microglobulin/bikunin precursor Rattus norvegicus 220-231 22730684-7 2012 RESULTS: Compared with control group, the pulmonary SOD, CAT and GSH levels at 2,6 and 12 h after exposure and the pulmonary GSH-Px levels at 2, 6, 12 and 24 h after exposure in H2S-intoxicated model group significantly decreased (P < 0.05 or P < 0.01). Hydrogen Sulfide 178-181 catalase Rattus norvegicus 57-60 22730684-10 2012 The expression levels of Nrf2 mRNA at 2, 6, 12, 24 h after exposure in H2S-intoxicated model group were 0.314 +/- 0.011, 0.269 +/- 0.010, 0.246 +/- 0.011 and 0.221 +/- 0.018, respectively, which were significantly higher than those (0.149 +/- 0.012) in control group (P < 0.01). Hydrogen Sulfide 71-74 NFE2 like bZIP transcription factor 2 Rattus norvegicus 25-29 22730684-14 2012 CONCLUSION: Oxidative stress and Nrf2 activation may be the important factors in rat lung injury induced by H2S-intoxicated, UTI may reduce the rat lung injury and protect the rat lung from damage induced by H2S by inhibiting ROS, improving the imbalance in redox and up-regulating Nrf2 mRNA expression. Hydrogen Sulfide 108-111 NFE2 like bZIP transcription factor 2 Rattus norvegicus 33-37 22730684-14 2012 CONCLUSION: Oxidative stress and Nrf2 activation may be the important factors in rat lung injury induced by H2S-intoxicated, UTI may reduce the rat lung injury and protect the rat lung from damage induced by H2S by inhibiting ROS, improving the imbalance in redox and up-regulating Nrf2 mRNA expression. Hydrogen Sulfide 108-111 NFE2 like bZIP transcription factor 2 Rattus norvegicus 282-286 22730684-14 2012 CONCLUSION: Oxidative stress and Nrf2 activation may be the important factors in rat lung injury induced by H2S-intoxicated, UTI may reduce the rat lung injury and protect the rat lung from damage induced by H2S by inhibiting ROS, improving the imbalance in redox and up-regulating Nrf2 mRNA expression. Hydrogen Sulfide 208-211 NFE2 like bZIP transcription factor 2 Rattus norvegicus 282-286 22047765-2 2011 Western blotting and immunocytochemistry were used to determine expression levels of the H2S-producing enzymes cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) in gastric tissues and cultured smooth muscle cells. Hydrogen Sulfide 89-92 cystathionine beta-synthase Mus musculus 111-138 22834328-1 2012 Immunocytochemical method in Wistar rats in 6 nuclei of the medulla oblongata, related to the cardiovascular center, identified nerve cells (H2S-neurons) with a positive reaction to cystathionine beta-synthase (CBS)--an enzyme involved in the synthesis of hydrogen sulfide in the brain. Hydrogen Sulfide 141-144 cystathionine beta synthase Rattus norvegicus 182-209 22834328-1 2012 Immunocytochemical method in Wistar rats in 6 nuclei of the medulla oblongata, related to the cardiovascular center, identified nerve cells (H2S-neurons) with a positive reaction to cystathionine beta-synthase (CBS)--an enzyme involved in the synthesis of hydrogen sulfide in the brain. Hydrogen Sulfide 141-144 cystathionine beta synthase Rattus norvegicus 211-214 22834328-1 2012 Immunocytochemical method in Wistar rats in 6 nuclei of the medulla oblongata, related to the cardiovascular center, identified nerve cells (H2S-neurons) with a positive reaction to cystathionine beta-synthase (CBS)--an enzyme involved in the synthesis of hydrogen sulfide in the brain. Hydrogen Sulfide 256-272 cystathionine beta synthase Rattus norvegicus 182-209 22194727-0 2011 Hydrogen sulfide increases nitric oxide production from endothelial cells by an akt-dependent mechanism. Hydrogen Sulfide 0-16 AKT serine/threonine kinase 1 Homo sapiens 80-83 22194727-4 2011 H(2)S stimulated a twofold increase in NO production from endothelial nitric oxide synthase (eNOS), which was maximal 30 min after exposure to 25-150 muM H(2)S. Hydrogen Sulfide 0-5 nitric oxide synthase 3 Homo sapiens 58-91 22194727-6 2011 Pharmacological inhibition of Akt, the kinase responsible for Ser 1177 phosphorylation, attenuated the stimulatory effect of H(2)S on NO production. Hydrogen Sulfide 125-130 AKT serine/threonine kinase 1 Homo sapiens 30-33 24278674-1 2012 Hydrogen sulfide (H2S) is a well-known toxic gas that is synthesized in the human body from the amino acids cystathionine, homocysteine, and cysteine by the action of at least two distinct enzymes: cystathionine-gamma-lyase and cystathionine-beta-synthase. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 198-223 24278674-1 2012 Hydrogen sulfide (H2S) is a well-known toxic gas that is synthesized in the human body from the amino acids cystathionine, homocysteine, and cysteine by the action of at least two distinct enzymes: cystathionine-gamma-lyase and cystathionine-beta-synthase. Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 228-255 24278674-1 2012 Hydrogen sulfide (H2S) is a well-known toxic gas that is synthesized in the human body from the amino acids cystathionine, homocysteine, and cysteine by the action of at least two distinct enzymes: cystathionine-gamma-lyase and cystathionine-beta-synthase. Hydrogen Sulfide 18-21 cystathionine gamma-lyase Homo sapiens 198-223 24278674-1 2012 Hydrogen sulfide (H2S) is a well-known toxic gas that is synthesized in the human body from the amino acids cystathionine, homocysteine, and cysteine by the action of at least two distinct enzymes: cystathionine-gamma-lyase and cystathionine-beta-synthase. Hydrogen Sulfide 18-21 cystathionine beta-synthase Homo sapiens 228-255 22067608-2 2011 The pathway metabolizing H2S probably involves three mitochondrial enzymes, one of which is sulfide-quinone oxidoreductase (SQR), known as sulfide-quinone reductase-like protein (SQRDL) in vertebrates. Hydrogen Sulfide 25-28 sulfide quinone oxidoreductase Homo sapiens 139-177 22067608-2 2011 The pathway metabolizing H2S probably involves three mitochondrial enzymes, one of which is sulfide-quinone oxidoreductase (SQR), known as sulfide-quinone reductase-like protein (SQRDL) in vertebrates. Hydrogen Sulfide 25-28 sulfide quinone oxidoreductase Homo sapiens 179-184 22047765-2 2011 Western blotting and immunocytochemistry were used to determine expression levels of the H2S-producing enzymes cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) in gastric tissues and cultured smooth muscle cells. Hydrogen Sulfide 89-92 cystathionase (cystathionine gamma-lyase) Mus musculus 149-174 22047765-2 2011 Western blotting and immunocytochemistry were used to determine expression levels of the H2S-producing enzymes cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) in gastric tissues and cultured smooth muscle cells. Hydrogen Sulfide 89-92 cystathionase (cystathionine gamma-lyase) Mus musculus 176-179 22005276-7 2011 H(2)S production in prostate tissues from CSE knockout mice was only 20% of that from wild-type mice, suggesting CSE is a major H(2)S-producing enzyme in prostate. Hydrogen Sulfide 0-5 cystathionase (cystathionine gamma-lyase) Mus musculus 42-45 21767667-0 2011 "Hydrogen sulfide oxidation and the arterial chemoreflex: effect of methemoglobin" by Haouzi et al. Hydrogen Sulfide 1-17 hemoglobin subunit gamma 2 Homo sapiens 68-81 22005276-7 2011 H(2)S production in prostate tissues from CSE knockout mice was only 20% of that from wild-type mice, suggesting CSE is a major H(2)S-producing enzyme in prostate. Hydrogen Sulfide 128-133 cystathionase (cystathionine gamma-lyase) Mus musculus 113-116 22005276-8 2011 CSE overexpression enhanced H(2)S production and inhibited cell viability in PC-3 cells. Hydrogen Sulfide 28-33 cystathionase (cystathionine gamma-lyase) Mus musculus 0-3 22005276-11 2011 Suppression of both p38 MAPK and JNK reversed H(2)S- or SFN-reduced viability of PC-3 cells. Hydrogen Sulfide 46-51 mitogen-activated protein kinase 14 Homo sapiens 20-23 22005276-11 2011 Suppression of both p38 MAPK and JNK reversed H(2)S- or SFN-reduced viability of PC-3 cells. Hydrogen Sulfide 46-51 mitogen-activated protein kinase 8 Homo sapiens 33-36 21564085-8 2011 FXR(-/-) mice were more prone to develop severe gastric and intestinal injury in response to ASA and NSAIDs and showed a severe reduction in the gastrointestinal expression of cystathionine-gamma-lyase (CSE), an enzyme required for generation of hydrogen sulphide. Hydrogen Sulfide 246-263 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-3 22169477-0 2011 H2S-Induced sulfhydration of the phosphatase PTP1B and its role in the endoplasmic reticulum stress response. Hydrogen Sulfide 0-3 protein tyrosine phosphatase non-receptor type 1 Homo sapiens 45-50 22169477-4 2011 Here, we report that PTP1B was reversibly inactivated by H(2)S, in vitro and in cells, through sulfhydration of the active-site cysteine residue. Hydrogen Sulfide 57-62 protein tyrosine phosphatase non-receptor type 1 Homo sapiens 21-26 22169477-6 2011 Sulfhydration of PTP1B in cells required the presence of cystathionine gamma-lyase (CSE), a critical enzyme in H(2)S production, and resulted in inhibition of phosphatase activity. Hydrogen Sulfide 111-116 protein tyrosine phosphatase non-receptor type 1 Homo sapiens 17-22 22169477-6 2011 Sulfhydration of PTP1B in cells required the presence of cystathionine gamma-lyase (CSE), a critical enzyme in H(2)S production, and resulted in inhibition of phosphatase activity. Hydrogen Sulfide 111-116 cystathionine gamma-lyase Homo sapiens 57-82 22169477-6 2011 Sulfhydration of PTP1B in cells required the presence of cystathionine gamma-lyase (CSE), a critical enzyme in H(2)S production, and resulted in inhibition of phosphatase activity. Hydrogen Sulfide 111-116 cystathionine gamma-lyase Homo sapiens 84-87 22169477-7 2011 Suppression of CSE decreased H(2)S production and decreased the phosphorylation of tyrosine-619 in PERK [protein kinase-like endoplasmic reticulum (ER) kinase], thus reducing its activation in response to ER stress. Hydrogen Sulfide 29-34 cystathionine gamma-lyase Homo sapiens 15-18 22169477-10 2011 These effects of suppressing H(2)S production on the response to ER stress were abrogated by a small-molecule inhibitor of PTP1B. Hydrogen Sulfide 29-34 protein tyrosine phosphatase non-receptor type 1 Homo sapiens 123-128 22169477-11 2011 Together, these data define a signaling function for H(2)S in inhibiting PTP1B activity and thereby promoting PERK activity during the response to ER stress. Hydrogen Sulfide 53-58 protein tyrosine phosphatase non-receptor type 1 Homo sapiens 73-78 22169477-11 2011 Together, these data define a signaling function for H(2)S in inhibiting PTP1B activity and thereby promoting PERK activity during the response to ER stress. Hydrogen Sulfide 53-58 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 110-114 22210043-7 2011 Moreover, exogenous H(2)S not only increased cellular H(2)S and the cystathionine-beta-synthase protein level activity but also significantly improved heroin-induced oxidative stress. Hydrogen Sulfide 20-25 cystathionine beta synthase Rattus norvegicus 68-95 22210043-8 2011 Protein expression of cleaved caspase-3 and Bax decreased, whereas Bcl-2 protein levels in hippocampus increased with exogenous H(2)S. Hydrogen Sulfide 128-133 BCL2, apoptosis regulator Rattus norvegicus 67-72 21564085-8 2011 FXR(-/-) mice were more prone to develop severe gastric and intestinal injury in response to ASA and NSAIDs and showed a severe reduction in the gastrointestinal expression of cystathionine-gamma-lyase (CSE), an enzyme required for generation of hydrogen sulphide. Hydrogen Sulfide 246-263 cystathionase (cystathionine gamma-lyase) Mus musculus 176-201 21564085-8 2011 FXR(-/-) mice were more prone to develop severe gastric and intestinal injury in response to ASA and NSAIDs and showed a severe reduction in the gastrointestinal expression of cystathionine-gamma-lyase (CSE), an enzyme required for generation of hydrogen sulphide. Hydrogen Sulfide 246-263 cystathionase (cystathionine gamma-lyase) Mus musculus 203-206 21857260-13 2011 The simultaneous reduction in cystathionine-beta synthase and cystathionine-gamma lyase expression supports the role of H2S-generating enzymes as an adaptive response during stress states. Hydrogen Sulfide 120-123 cystathionine beta-synthase Mus musculus 30-57 21850523-0 2011 Increased oxidative stress and cytotoxicity by hydrogen sulfide in HepG2 cells overexpressing cytochrome P450 2E1. Hydrogen Sulfide 47-63 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 94-113 21850523-1 2011 The main objectives of this work were to evaluate the effects of hydrogen sulfide on oxidative stress and cytotoxicity parameters in HepG2 cells and to assess the extent to which cytochrome P450 2E1 (CYP2E1) activity modulates the effects of hydrogen sulfide on oxidative stress and cytotoxicity. Hydrogen Sulfide 242-258 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 179-198 21850523-1 2011 The main objectives of this work were to evaluate the effects of hydrogen sulfide on oxidative stress and cytotoxicity parameters in HepG2 cells and to assess the extent to which cytochrome P450 2E1 (CYP2E1) activity modulates the effects of hydrogen sulfide on oxidative stress and cytotoxicity. Hydrogen Sulfide 242-258 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 200-206 21850523-8 2011 These data suggest that CYP2E1 enhances H(2)S-dependent cytotoxicity in HepG2 cells through the generation of iron-dependent oxidative stress and lipid peroxidation. Hydrogen Sulfide 40-45 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 24-30 21857260-13 2011 The simultaneous reduction in cystathionine-beta synthase and cystathionine-gamma lyase expression supports the role of H2S-generating enzymes as an adaptive response during stress states. Hydrogen Sulfide 120-123 cystathionase (cystathionine gamma-lyase) Mus musculus 62-87 21937432-2 2011 Cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) are well-known as H(2)S-producing enzymes. Hydrogen Sulfide 88-93 cystathionine beta-synthase Homo sapiens 0-27 22333058-0 2011 [Effects of hydrogen sulfide on the expressions of nuclear factor-kappaB and intercellular adhesion molecule 1 in pulmonary tissue of rats with acute lung injury]. Hydrogen Sulfide 12-28 intercellular adhesion molecule 1 Rattus norvegicus 77-110 22333058-1 2011 OBJECTIVE: To explore the potential effects of hydrogen sulfide (H(2)S) on nuclear factor kappa B (NF-kappaB) and intercellular adhesion molecule 1 (ICAM-1) in lung tissue with oleic acid (OA)-induced acute lung injury (ALI) in rats. Hydrogen Sulfide 47-63 intercellular adhesion molecule 1 Rattus norvegicus 99-147 21967893-10 2011 Immunization of H2s-congenic C57BL/6 mice (B6.SJL-H2s) led to Th1 polarization in dLN and clinical disease. Hydrogen Sulfide 16-19 negative elongation factor complex member C/D, Th1l Mus musculus 62-65 21967893-10 2011 Immunization of H2s-congenic C57BL/6 mice (B6.SJL-H2s) led to Th1 polarization in dLN and clinical disease. Hydrogen Sulfide 50-53 negative elongation factor complex member C/D, Th1l Mus musculus 62-65 21953448-0 2011 Hydrogen sulfide and L-cysteine increase phosphatidylinositol 3,4,5-trisphosphate (PIP3) and glucose utilization by inhibiting phosphatase and tensin homolog (PTEN) protein and activating phosphoinositide 3-kinase (PI3K)/serine/threonine protein kinase (AKT)/protein kinase Czeta/lambda (PKCzeta/lambda) in 3T3l1 adipocytes. Hydrogen Sulfide 0-16 phosphatase and tensin homolog Homo sapiens 159-163 21953448-0 2011 Hydrogen sulfide and L-cysteine increase phosphatidylinositol 3,4,5-trisphosphate (PIP3) and glucose utilization by inhibiting phosphatase and tensin homolog (PTEN) protein and activating phosphoinositide 3-kinase (PI3K)/serine/threonine protein kinase (AKT)/protein kinase Czeta/lambda (PKCzeta/lambda) in 3T3l1 adipocytes. Hydrogen Sulfide 0-16 AKT serine/threonine kinase 1 Homo sapiens 254-257 21953448-0 2011 Hydrogen sulfide and L-cysteine increase phosphatidylinositol 3,4,5-trisphosphate (PIP3) and glucose utilization by inhibiting phosphatase and tensin homolog (PTEN) protein and activating phosphoinositide 3-kinase (PI3K)/serine/threonine protein kinase (AKT)/protein kinase Czeta/lambda (PKCzeta/lambda) in 3T3l1 adipocytes. Hydrogen Sulfide 0-16 protein kinase C zeta Homo sapiens 288-295 21953448-3 2011 Both LC and H(2)S treatments caused an increase in phosphatidylinositol-3,4,5 trisphosphate (PIP3), AKT phosphorylation, and glucose utilization in HG-treated cells. Hydrogen Sulfide 12-17 AKT serine/threonine kinase 1 Homo sapiens 100-103 21953448-7 2011 Treatment with LC, H(2)S, or PIP3 increased the phosphorylation of IRS1, AKT, and PKCzeta/lambda as well as GLUT4 activation and glucose utilization in HG-treated cells. Hydrogen Sulfide 19-24 insulin receptor substrate 1 Homo sapiens 67-71 21953448-7 2011 Treatment with LC, H(2)S, or PIP3 increased the phosphorylation of IRS1, AKT, and PKCzeta/lambda as well as GLUT4 activation and glucose utilization in HG-treated cells. Hydrogen Sulfide 19-24 AKT serine/threonine kinase 1 Homo sapiens 73-76 21953448-7 2011 Treatment with LC, H(2)S, or PIP3 increased the phosphorylation of IRS1, AKT, and PKCzeta/lambda as well as GLUT4 activation and glucose utilization in HG-treated cells. Hydrogen Sulfide 19-24 protein kinase C zeta Homo sapiens 82-89 21953448-7 2011 Treatment with LC, H(2)S, or PIP3 increased the phosphorylation of IRS1, AKT, and PKCzeta/lambda as well as GLUT4 activation and glucose utilization in HG-treated cells. Hydrogen Sulfide 19-24 solute carrier family 2 member 4 Homo sapiens 108-113 21953448-9 2011 Comparative signal silencing studies with siAKT2 or siPKCzeta revealed that PKCzeta phosphorylation is more effective for the GLUT4 activation and glucose utilization in LC-, H(2)S-, or PIP3-treated cells exposed to HG. Hydrogen Sulfide 175-180 solute carrier family 2 member 4 Homo sapiens 126-131 21953448-12 2011 This study provides evidence for a molecular mechanism by which H(2)S or LC can up-regulate the insulin-signaling pathways essential for maintenance of glucose metabolism. Hydrogen Sulfide 64-69 insulin Homo sapiens 96-103 21937432-2 2011 Cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) are well-known as H(2)S-producing enzymes. Hydrogen Sulfide 88-93 cystathionine gamma-lyase Homo sapiens 38-63 21937432-2 2011 Cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) are well-known as H(2)S-producing enzymes. Hydrogen Sulfide 88-93 cystathionine gamma-lyase Homo sapiens 65-68 21937432-3 2011 We recently demonstrated that 3-mercaptopyruvate sulfurtransferase (3MST) along with cysteine aminotransferase (CAT) produces H(2)S in the brain and in vascular endothelium. Hydrogen Sulfide 126-131 mercaptopyruvate sulfurtransferase Homo sapiens 30-66 21980127-3 2011 Hydrogen sulfide (H(2)S) is a prominent EDRF, since mice lacking its biosynthetic enzyme, cystathionine gamma-lyase (CSE), display pronounced hypertension with deficient vasorelaxant responses to acetylcholine. Hydrogen Sulfide 0-16 alpha hemoglobin stabilizing protein Mus musculus 40-44 22001931-0 2011 Involvement of ERK in NMDA receptor-independent cortical neurotoxicity of hydrogen sulfide. Hydrogen Sulfide 74-90 mitogen-activated protein kinase 1 Homo sapiens 15-18 21980127-3 2011 Hydrogen sulfide (H(2)S) is a prominent EDRF, since mice lacking its biosynthetic enzyme, cystathionine gamma-lyase (CSE), display pronounced hypertension with deficient vasorelaxant responses to acetylcholine. Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 90-115 21980127-3 2011 Hydrogen sulfide (H(2)S) is a prominent EDRF, since mice lacking its biosynthetic enzyme, cystathionine gamma-lyase (CSE), display pronounced hypertension with deficient vasorelaxant responses to acetylcholine. Hydrogen Sulfide 0-16 cystathionase (cystathionine gamma-lyase) Mus musculus 117-120 21980127-3 2011 Hydrogen sulfide (H(2)S) is a prominent EDRF, since mice lacking its biosynthetic enzyme, cystathionine gamma-lyase (CSE), display pronounced hypertension with deficient vasorelaxant responses to acetylcholine. Hydrogen Sulfide 18-23 alpha hemoglobin stabilizing protein Mus musculus 40-44 21980127-3 2011 Hydrogen sulfide (H(2)S) is a prominent EDRF, since mice lacking its biosynthetic enzyme, cystathionine gamma-lyase (CSE), display pronounced hypertension with deficient vasorelaxant responses to acetylcholine. Hydrogen Sulfide 18-23 cystathionase (cystathionine gamma-lyase) Mus musculus 90-115 21980127-3 2011 Hydrogen sulfide (H(2)S) is a prominent EDRF, since mice lacking its biosynthetic enzyme, cystathionine gamma-lyase (CSE), display pronounced hypertension with deficient vasorelaxant responses to acetylcholine. Hydrogen Sulfide 18-23 cystathionase (cystathionine gamma-lyase) Mus musculus 117-120 21980127-5 2011 METHODS AND RESULTS: We now show that H(2)S is a major EDHF because in blood vessels of CSE-deleted mice, hyperpolarization is virtually abolished. Hydrogen Sulfide 38-43 cystathionase (cystathionine gamma-lyase) Mus musculus 88-91 22001931-1 2011 Hydrogen sulfide (H(2)S), a gasotransmitter, exerts both neurotoxicity and neuroprotection, and targets multiple molecules including NMDA receptors, T-type calcium channels and NO synthase (NOS) that might affect neuronal viability. Hydrogen Sulfide 0-16 nitric oxide synthase 2 Homo sapiens 177-188 22001931-1 2011 Hydrogen sulfide (H(2)S), a gasotransmitter, exerts both neurotoxicity and neuroprotection, and targets multiple molecules including NMDA receptors, T-type calcium channels and NO synthase (NOS) that might affect neuronal viability. Hydrogen Sulfide 18-23 nitric oxide synthase 2 Homo sapiens 177-188 21912243-6 2011 Inhalation of 1 or 5 ppm H2S during HVT ventilation did not alter lung injury, but inhalation of 60 ppm H2S accelerated the development of ventilator-induced lung injury and enhanced the pulmonary expression of the chemoattractant CXCL-2 and the leukocyte adhesion molecules CD11b and L-selectin. Hydrogen Sulfide 104-107 chemokine (C-X-C motif) ligand 2 Mus musculus 231-237 21912243-6 2011 Inhalation of 1 or 5 ppm H2S during HVT ventilation did not alter lung injury, but inhalation of 60 ppm H2S accelerated the development of ventilator-induced lung injury and enhanced the pulmonary expression of the chemoattractant CXCL-2 and the leukocyte adhesion molecules CD11b and L-selectin. Hydrogen Sulfide 104-107 integrin alpha M Mus musculus 275-280 21912243-6 2011 Inhalation of 1 or 5 ppm H2S during HVT ventilation did not alter lung injury, but inhalation of 60 ppm H2S accelerated the development of ventilator-induced lung injury and enhanced the pulmonary expression of the chemoattractant CXCL-2 and the leukocyte adhesion molecules CD11b and L-selectin. Hydrogen Sulfide 104-107 selectin, lymphocyte Mus musculus 285-295 21732914-0 2011 Thioredoxin and dihydrolipoic acid are required for 3-mercaptopyruvate sulfurtransferase to produce hydrogen sulfide. Hydrogen Sulfide 100-116 thioredoxin Homo sapiens 0-11 21732914-0 2011 Thioredoxin and dihydrolipoic acid are required for 3-mercaptopyruvate sulfurtransferase to produce hydrogen sulfide. Hydrogen Sulfide 100-116 mercaptopyruvate sulfurtransferase Homo sapiens 52-88 21732914-2 2011 We recently demonstrated that 3MST (3-mercaptopyruvate sulfurtransferase) produces H2S from 3MP (3-mercaptopyruvate). Hydrogen Sulfide 83-86 mercaptopyruvate sulfurtransferase Homo sapiens 36-72 21732914-4 2011 In the present study we show that Trx (thioredoxin) and DHLA (dihydrolipoic acid) associate with 3MST to release H2S. Hydrogen Sulfide 113-116 thioredoxin Homo sapiens 34-37 21732914-4 2011 In the present study we show that Trx (thioredoxin) and DHLA (dihydrolipoic acid) associate with 3MST to release H2S. Hydrogen Sulfide 113-116 thioredoxin Homo sapiens 39-50 22340226-9 2011 Stepwise regression analysis showed that erythrocytic H(2)S production was correlated with sBP, TG, HDL-C, low density lipoprotein cholesterol (LDL-C) and blood urea nitrogen (BUN) and serum H(2)S was correlated with dBP and TG. Hydrogen Sulfide 54-59 selenium binding protein 1 Homo sapiens 91-94 22340157-2 2011 We investigated the possible role of endogenous hydrogen sulfide (H(2)S) of cerebrospinal fluid (CSF) in predicting CNSL. Hydrogen Sulfide 48-64 colony stimulating factor 2 Homo sapiens 97-100 22340157-2 2011 We investigated the possible role of endogenous hydrogen sulfide (H(2)S) of cerebrospinal fluid (CSF) in predicting CNSL. Hydrogen Sulfide 66-71 colony stimulating factor 2 Homo sapiens 97-100 22340157-10 2011 Compared with the leukemia group, CSF H(2)S content of the CNSL group was significantly high (P < 0.01). Hydrogen Sulfide 38-43 colony stimulating factor 2 Homo sapiens 34-37 22340157-11 2011 Meanwhile, in contrast to the non-leukemia group, CSF H(2)S contents of the CNSL and leukemia groups were both significantly increased (P < 0.01). Hydrogen Sulfide 54-59 colony stimulating factor 2 Homo sapiens 50-53 22340159-19 2011 CONCLUSION: H(2)S plays a regulatory role in aortic ERS and reduces atherosclerotic lesions in apoE(-/-) mice fed with a Western type diet. Hydrogen Sulfide 12-17 apolipoprotein E Mus musculus 95-99 22340180-7 2011 H(2)S offers anti-oxidant, anti-inflammatory and anti-apoptotic effects, as well as activates ATP-sensitive potassium channels and cystic fibrosis transmembrane conductance regulator Cl- channels. Hydrogen Sulfide 0-5 CF transmembrane conductance regulator Homo sapiens 131-182 22340226-7 2011 The erythrocytic H(2)S production was associated with increased systolic blood pressure (sBP), diastolic blood pressure (dBP), age, BMI, level of C-reactive protein (CRP), as well as triglycerides (TG) and high density lipoprotein cholesterol (HDL-C). Hydrogen Sulfide 17-22 selenium binding protein 1 Homo sapiens 89-92 22340226-7 2011 The erythrocytic H(2)S production was associated with increased systolic blood pressure (sBP), diastolic blood pressure (dBP), age, BMI, level of C-reactive protein (CRP), as well as triglycerides (TG) and high density lipoprotein cholesterol (HDL-C). Hydrogen Sulfide 17-22 C-reactive protein Homo sapiens 146-164 21957141-9 2011 H(2)S augmented COX-2 and PGEM production in sepsis-evoked ALI by a TRPV1 channel-dependent mechanism. Hydrogen Sulfide 0-5 prostaglandin-endoperoxide synthase 2 Mus musculus 16-21 22340226-7 2011 The erythrocytic H(2)S production was associated with increased systolic blood pressure (sBP), diastolic blood pressure (dBP), age, BMI, level of C-reactive protein (CRP), as well as triglycerides (TG) and high density lipoprotein cholesterol (HDL-C). Hydrogen Sulfide 17-22 C-reactive protein Homo sapiens 166-169 22340157-16 2011 Therefore, we speculated that H(2)S levels of CSF would predict CNSL in ALL children. Hydrogen Sulfide 30-35 colony stimulating factor 2 Homo sapiens 46-49 22340158-11 2011 Endogenous H(2)S may be generated by CSE and act as an important regulator of electrophysiological properties in human atrial fibers. Hydrogen Sulfide 11-16 choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity) Homo sapiens 37-40 22340159-0 2011 Hydrogen sulfide regulates vascular endoplasmic reticulum stress in apolipoprotein E knockout mice. Hydrogen Sulfide 0-16 apolipoprotein E Mus musculus 68-84 22340159-14 2011 Compared with apoE(-/-) mice, H(2)S donor-treated apoE(-/-) mice showed a decreased plasma LDL level, lessened plaque necrosis and attenuated aortic ultra-structural disorder. Hydrogen Sulfide 30-35 apolipoprotein E Homo sapiens 50-54 22340159-15 2011 H(2)S donor-treatment induced GRP78 expression but suppressed caspase-12 expression in aortic lesions. Hydrogen Sulfide 0-5 heat shock protein family A (Hsp70) member 5 Homo sapiens 30-35 22340159-15 2011 H(2)S donor-treatment induced GRP78 expression but suppressed caspase-12 expression in aortic lesions. Hydrogen Sulfide 0-5 caspase 12 Rattus norvegicus 62-72 21957141-0 2011 Hydrogen sulfide upregulates cyclooxygenase-2 and prostaglandin E metabolite in sepsis-evoked acute lung injury via transient receptor potential vanilloid type 1 channel activation. Hydrogen Sulfide 0-16 prostaglandin-endoperoxide synthase 2 Mus musculus 29-45 21957141-0 2011 Hydrogen sulfide upregulates cyclooxygenase-2 and prostaglandin E metabolite in sepsis-evoked acute lung injury via transient receptor potential vanilloid type 1 channel activation. Hydrogen Sulfide 0-16 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 116-161 21957141-1 2011 Hydrogen sulfide (H(2)S) has been shown to promote transient receptor potential vanilloid type 1 (TRPV1)-mediated neurogenic inflammation in sepsis and its associated multiple organ failure, including acute lung injury (ALI). Hydrogen Sulfide 0-16 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 51-96 21957141-9 2011 H(2)S augmented COX-2 and PGEM production in sepsis-evoked ALI by a TRPV1 channel-dependent mechanism. Hydrogen Sulfide 0-5 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 68-73 21957141-1 2011 Hydrogen sulfide (H(2)S) has been shown to promote transient receptor potential vanilloid type 1 (TRPV1)-mediated neurogenic inflammation in sepsis and its associated multiple organ failure, including acute lung injury (ALI). Hydrogen Sulfide 0-16 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 98-103 21957141-1 2011 Hydrogen sulfide (H(2)S) has been shown to promote transient receptor potential vanilloid type 1 (TRPV1)-mediated neurogenic inflammation in sepsis and its associated multiple organ failure, including acute lung injury (ALI). Hydrogen Sulfide 18-23 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 51-96 21957141-10 2011 COX-2 inhibition with parecoxib attenuated H(2)S-augmented lung PGEM production, neutrophil infiltration, edema, proinflammatory cytokines, chemokines, and adhesion molecules levels, restored lung histoarchitecture, and protected against CLP-induced lethality. Hydrogen Sulfide 43-48 prostaglandin-endoperoxide synthase 2 Mus musculus 0-5 21957141-1 2011 Hydrogen sulfide (H(2)S) has been shown to promote transient receptor potential vanilloid type 1 (TRPV1)-mediated neurogenic inflammation in sepsis and its associated multiple organ failure, including acute lung injury (ALI). Hydrogen Sulfide 18-23 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 98-103 21957141-10 2011 COX-2 inhibition with parecoxib attenuated H(2)S-augmented lung PGEM production, neutrophil infiltration, edema, proinflammatory cytokines, chemokines, and adhesion molecules levels, restored lung histoarchitecture, and protected against CLP-induced lethality. Hydrogen Sulfide 43-48 hyaluronan and proteoglycan link protein 1 Mus musculus 238-241 21957141-4 2011 Therefore, the aim of this study was to investigate whether H(2)S would upregulate COX-2 and work in conjunction with it to instigate ALI in a murine model of polymicrobial sepsis. Hydrogen Sulfide 60-65 prostaglandin-endoperoxide synthase 2 Mus musculus 83-88 21865440-13 2011 In conclusion, this work demonstrated for the first time that H(2)S produced cardioprotection via the suppression of NHE-1 activity involving a PI3K/Akt/PKG-dependent mechanism. Hydrogen Sulfide 62-67 solute carrier family 9 member A1 Rattus norvegicus 117-122 21865440-13 2011 In conclusion, this work demonstrated for the first time that H(2)S produced cardioprotection via the suppression of NHE-1 activity involving a PI3K/Akt/PKG-dependent mechanism. Hydrogen Sulfide 62-67 AKT serine/threonine kinase 1 Rattus norvegicus 149-152 21865440-0 2011 Hydrogen sulfide regulates Na+/H+ exchanger activity via stimulation of phosphoinositide 3-kinase/Akt and protein kinase G pathways. Hydrogen Sulfide 0-16 AKT serine/threonine kinase 1 Rattus norvegicus 98-101 21986537-3 2011 Two cysteine desulfhydrases (CDes), L-cysteine desulfhydrase and D-cysteine desulfhydrase, were identified as being mainly responsible for the degradation of cysteine in order to generate H(2)S. Hydrogen Sulfide 188-193 Pyridoxal phosphate (PLP)-dependent transferases superfamily protein Arabidopsis thaliana 36-89 21748658-4 2011 We showed that ADMA prevented MPP+-induced inhibition of endogenous H2S generation through inhibiting the down-regulation of cystathionine-beta-synthetase (CBS, the major enzyme responsible for endogenous H2S generation in PC12 cells) expression and activity elicited by MPP+. Hydrogen Sulfide 68-71 cystathionine beta synthase Rattus norvegicus 156-159 21748658-4 2011 We showed that ADMA prevented MPP+-induced inhibition of endogenous H2S generation through inhibiting the down-regulation of cystathionine-beta-synthetase (CBS, the major enzyme responsible for endogenous H2S generation in PC12 cells) expression and activity elicited by MPP+. Hydrogen Sulfide 205-208 cystathionine beta synthase Rattus norvegicus 156-159 21784135-2 2011 In the present study, we examined the neuroprotective effects of S-aspirin, a hydrogen sulfide (H(2)S)-releasing aspirin, on Abeta-induced cell toxicity. Hydrogen Sulfide 96-101 histocompatibility 2, class II antigen A, beta 1 Mus musculus 125-130 21297080-0 2011 Hydrogen sulfide inhibits proliferation and release of IL-8 from human airway smooth muscle cells. Hydrogen Sulfide 0-16 C-X-C motif chemokine ligand 8 Homo sapiens 55-59 21297080-1 2011 Hydrogen sulfide (H(2)S) is synthesized intracellularly by the enzymes cystathionine-gamma-lyase and cystathionine-beta-synthase (CBS), and is proposed to be a gasotransmitter with effects in modulating inflammation and cellular proliferation. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 71-96 21297080-1 2011 Hydrogen sulfide (H(2)S) is synthesized intracellularly by the enzymes cystathionine-gamma-lyase and cystathionine-beta-synthase (CBS), and is proposed to be a gasotransmitter with effects in modulating inflammation and cellular proliferation. Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 101-128 21297080-1 2011 Hydrogen sulfide (H(2)S) is synthesized intracellularly by the enzymes cystathionine-gamma-lyase and cystathionine-beta-synthase (CBS), and is proposed to be a gasotransmitter with effects in modulating inflammation and cellular proliferation. Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 130-133 21297080-1 2011 Hydrogen sulfide (H(2)S) is synthesized intracellularly by the enzymes cystathionine-gamma-lyase and cystathionine-beta-synthase (CBS), and is proposed to be a gasotransmitter with effects in modulating inflammation and cellular proliferation. Hydrogen Sulfide 18-23 cystathionine gamma-lyase Homo sapiens 71-96 21297080-1 2011 Hydrogen sulfide (H(2)S) is synthesized intracellularly by the enzymes cystathionine-gamma-lyase and cystathionine-beta-synthase (CBS), and is proposed to be a gasotransmitter with effects in modulating inflammation and cellular proliferation. Hydrogen Sulfide 18-23 cystathionine beta-synthase Homo sapiens 101-128 21297080-1 2011 Hydrogen sulfide (H(2)S) is synthesized intracellularly by the enzymes cystathionine-gamma-lyase and cystathionine-beta-synthase (CBS), and is proposed to be a gasotransmitter with effects in modulating inflammation and cellular proliferation. Hydrogen Sulfide 18-23 cystathionine beta-synthase Homo sapiens 130-133 21297080-7 2011 Methemoglobin, a scavenger of endogenous H(2)S, increased DNA synthesis induced by FCS and IL-1beta. Hydrogen Sulfide 41-46 hemoglobin subunit gamma 2 Homo sapiens 0-13 21297080-7 2011 Methemoglobin, a scavenger of endogenous H(2)S, increased DNA synthesis induced by FCS and IL-1beta. Hydrogen Sulfide 41-46 interleukin 1 beta Homo sapiens 91-99 21297080-8 2011 In addition, methemoglobin increased IL-8 release induced by FCS, but not by IL-1beta, indicating a role for endogenous H(2)S in these systems. Hydrogen Sulfide 120-125 hemoglobin subunit gamma 2 Homo sapiens 13-26 21297080-9 2011 Inhibition of CBS, but not cystathionine-gamma-lyase, reversed the inhibitory effect of H(2)S on proliferation and IL-8 release, indicating that this is dependent on CBS. Hydrogen Sulfide 88-93 cystathionine beta-synthase Homo sapiens 14-17 21297080-9 2011 Inhibition of CBS, but not cystathionine-gamma-lyase, reversed the inhibitory effect of H(2)S on proliferation and IL-8 release, indicating that this is dependent on CBS. Hydrogen Sulfide 88-93 C-X-C motif chemokine ligand 8 Homo sapiens 115-119 21297080-9 2011 Inhibition of CBS, but not cystathionine-gamma-lyase, reversed the inhibitory effect of H(2)S on proliferation and IL-8 release, indicating that this is dependent on CBS. Hydrogen Sulfide 88-93 cystathionine beta-synthase Homo sapiens 166-169 21875066-1 2011 Human CBS is a PLP-dependent enzyme that clears homocysteine, gates the flow of sulfur into glutathione, and contributes to the biogenesis of H(2)S. Hydrogen Sulfide 142-147 cystathionine beta-synthase Homo sapiens 6-9 21875066-5 2011 These data provide a mechanism for cross talk between two gas-signaling systems, CO and H(2)S, via heme-mediated allosteric regulation of CBS. Hydrogen Sulfide 88-93 cystathionine beta-synthase Homo sapiens 138-141 21693692-0 2011 Knockout of the murine cysteine dioxygenase gene results in severe impairment in ability to synthesize taurine and an increased catabolism of cysteine to hydrogen sulfide. Hydrogen Sulfide 154-170 cysteine dioxygenase 1, cytosolic Mus musculus 23-43 21693692-10 2011 Control of cysteine levels by regulation of CDO may be necessary to maintain low H(2)S/sulfane sulfur levels and facilitate the use of H(2)S as a signaling molecule. Hydrogen Sulfide 81-86 cysteine dioxygenase 1, cytosolic Mus musculus 44-47 21693692-10 2011 Control of cysteine levels by regulation of CDO may be necessary to maintain low H(2)S/sulfane sulfur levels and facilitate the use of H(2)S as a signaling molecule. Hydrogen Sulfide 135-140 cysteine dioxygenase 1, cytosolic Mus musculus 44-47 21297080-10 2011 CBS mRNA and protein expression were inhibited by H(2)S donors, and were increased by methemoglobin, indicating that CBS is the main enzyme responsible for endogenous H(2)S production. Hydrogen Sulfide 50-55 cystathionine beta-synthase Homo sapiens 0-3 21297080-10 2011 CBS mRNA and protein expression were inhibited by H(2)S donors, and were increased by methemoglobin, indicating that CBS is the main enzyme responsible for endogenous H(2)S production. Hydrogen Sulfide 50-55 cystathionine beta-synthase Homo sapiens 117-120 22485212-4 2011 H(2)S-induced cell apoptosis was accompanied by activation of caspase-3 and caspase-9. Hydrogen Sulfide 0-5 caspase 3 Homo sapiens 62-71 21297080-10 2011 CBS mRNA and protein expression were inhibited by H(2)S donors, and were increased by methemoglobin, indicating that CBS is the main enzyme responsible for endogenous H(2)S production. Hydrogen Sulfide 167-172 cystathionine beta-synthase Homo sapiens 0-3 21297080-10 2011 CBS mRNA and protein expression were inhibited by H(2)S donors, and were increased by methemoglobin, indicating that CBS is the main enzyme responsible for endogenous H(2)S production. Hydrogen Sulfide 167-172 hemoglobin subunit gamma 2 Homo sapiens 86-99 21297080-10 2011 CBS mRNA and protein expression were inhibited by H(2)S donors, and were increased by methemoglobin, indicating that CBS is the main enzyme responsible for endogenous H(2)S production. Hydrogen Sulfide 167-172 cystathionine beta-synthase Homo sapiens 117-120 21297080-11 2011 Finally, we found that exogenous H(2)S inhibited the phosphorylation of extracellular signal-regulated kinase-1/2 and p38, which could represent a mechanism by which H(2)S inhibited cellular proliferation and IL-8 release. Hydrogen Sulfide 33-38 mitogen-activated protein kinase 3 Homo sapiens 72-113 21297080-11 2011 Finally, we found that exogenous H(2)S inhibited the phosphorylation of extracellular signal-regulated kinase-1/2 and p38, which could represent a mechanism by which H(2)S inhibited cellular proliferation and IL-8 release. Hydrogen Sulfide 33-38 mitogen-activated protein kinase 14 Homo sapiens 118-121 21297080-11 2011 Finally, we found that exogenous H(2)S inhibited the phosphorylation of extracellular signal-regulated kinase-1/2 and p38, which could represent a mechanism by which H(2)S inhibited cellular proliferation and IL-8 release. Hydrogen Sulfide 33-38 C-X-C motif chemokine ligand 8 Homo sapiens 209-213 21297080-11 2011 Finally, we found that exogenous H(2)S inhibited the phosphorylation of extracellular signal-regulated kinase-1/2 and p38, which could represent a mechanism by which H(2)S inhibited cellular proliferation and IL-8 release. Hydrogen Sulfide 166-171 mitogen-activated protein kinase 3 Homo sapiens 72-113 21297080-11 2011 Finally, we found that exogenous H(2)S inhibited the phosphorylation of extracellular signal-regulated kinase-1/2 and p38, which could represent a mechanism by which H(2)S inhibited cellular proliferation and IL-8 release. Hydrogen Sulfide 166-171 mitogen-activated protein kinase 14 Homo sapiens 118-121 21297080-11 2011 Finally, we found that exogenous H(2)S inhibited the phosphorylation of extracellular signal-regulated kinase-1/2 and p38, which could represent a mechanism by which H(2)S inhibited cellular proliferation and IL-8 release. Hydrogen Sulfide 166-171 C-X-C motif chemokine ligand 8 Homo sapiens 209-213 21297080-12 2011 In summary, H(2)S production provides a novel mechanism for regulation of ASM proliferation and IL-8 release. Hydrogen Sulfide 12-17 C-X-C motif chemokine ligand 8 Homo sapiens 96-100 21198548-1 2011 In vascular tissues, hydrogen sulphide (H(2)S) is mainly produced from L-cysteine by the cystathionine gamma-lyase (CSE) enzyme. Hydrogen Sulfide 21-38 cystathionine gamma-lyase Gallus gallus 89-114 21198548-1 2011 In vascular tissues, hydrogen sulphide (H(2)S) is mainly produced from L-cysteine by the cystathionine gamma-lyase (CSE) enzyme. Hydrogen Sulfide 21-38 cystathionine gamma-lyase Gallus gallus 116-119 21198548-1 2011 In vascular tissues, hydrogen sulphide (H(2)S) is mainly produced from L-cysteine by the cystathionine gamma-lyase (CSE) enzyme. Hydrogen Sulfide 40-46 cystathionine gamma-lyase Gallus gallus 89-114 21198548-1 2011 In vascular tissues, hydrogen sulphide (H(2)S) is mainly produced from L-cysteine by the cystathionine gamma-lyase (CSE) enzyme. Hydrogen Sulfide 40-46 cystathionine gamma-lyase Gallus gallus 116-119 22485212-4 2011 H(2)S-induced cell apoptosis was accompanied by activation of caspase-3 and caspase-9. Hydrogen Sulfide 0-5 caspase 9 Homo sapiens 76-85 22038352-4 2011 We examined hippocampal H(2)S synthesis and the expression of cystathionine-beta-synthetase (CBS), a major enzyme involved in the H(2)S synthesis in hippocampus. Hydrogen Sulfide 130-135 cystathionine beta synthase Rattus norvegicus 62-91 21840852-5 2011 The H2S-oxidation pathway requires two distinct enzymes important for the oxidation of H2S: the sulfide:quinone reductase sqrd-1 and the dioxygenase ethe-1. Hydrogen Sulfide 4-7 Pyr_redox_2 domain-containing protein Caenorhabditis elegans 122-128 21840852-5 2011 The H2S-oxidation pathway requires two distinct enzymes important for the oxidation of H2S: the sulfide:quinone reductase sqrd-1 and the dioxygenase ethe-1. Hydrogen Sulfide 87-90 Pyr_redox_2 domain-containing protein Caenorhabditis elegans 122-128 21840852-7 2011 A low dose of either H2S or HCN can activate hypoxia-inducible factor 1 (HIF-1), which is required for C. elegans to respond to either gas. Hydrogen Sulfide 21-24 Hypoxia-inducible factor 1 Caenorhabditis elegans 45-71 21840852-7 2011 A low dose of either H2S or HCN can activate hypoxia-inducible factor 1 (HIF-1), which is required for C. elegans to respond to either gas. Hydrogen Sulfide 21-24 Hypoxia-inducible factor 1 Caenorhabditis elegans 73-78 21840852-8 2011 sqrd-1 and cysl-2 represent the entry points in the H2S-oxidation and HCN-assimilation pathways, respectively, and expression of both of these enzymes is highly induced by HIF-1 in response to both H2S and HCN. Hydrogen Sulfide 52-55 Pyr_redox_2 domain-containing protein Caenorhabditis elegans 0-6 21840852-8 2011 sqrd-1 and cysl-2 represent the entry points in the H2S-oxidation and HCN-assimilation pathways, respectively, and expression of both of these enzymes is highly induced by HIF-1 in response to both H2S and HCN. Hydrogen Sulfide 52-55 Bifunctional L-3-cyanoalanine synthase/cysteine synthase Caenorhabditis elegans 11-17 21840852-8 2011 sqrd-1 and cysl-2 represent the entry points in the H2S-oxidation and HCN-assimilation pathways, respectively, and expression of both of these enzymes is highly induced by HIF-1 in response to both H2S and HCN. Hydrogen Sulfide 52-55 Hypoxia-inducible factor 1 Caenorhabditis elegans 172-177 21840852-8 2011 sqrd-1 and cysl-2 represent the entry points in the H2S-oxidation and HCN-assimilation pathways, respectively, and expression of both of these enzymes is highly induced by HIF-1 in response to both H2S and HCN. Hydrogen Sulfide 198-201 Pyr_redox_2 domain-containing protein Caenorhabditis elegans 0-6 21840852-8 2011 sqrd-1 and cysl-2 represent the entry points in the H2S-oxidation and HCN-assimilation pathways, respectively, and expression of both of these enzymes is highly induced by HIF-1 in response to both H2S and HCN. Hydrogen Sulfide 198-201 Bifunctional L-3-cyanoalanine synthase/cysteine synthase Caenorhabditis elegans 11-17 21840852-8 2011 sqrd-1 and cysl-2 represent the entry points in the H2S-oxidation and HCN-assimilation pathways, respectively, and expression of both of these enzymes is highly induced by HIF-1 in response to both H2S and HCN. Hydrogen Sulfide 198-201 Hypoxia-inducible factor 1 Caenorhabditis elegans 172-177 21840852-9 2011 In addition to their role in appropriately responding to H2S and HCN, we found that cysl-1 and cysl-2 are both essential mediators of innate immunity against fast paralytic killing by Pseudomonas. Hydrogen Sulfide 57-60 Cysteine synthase 1 Caenorhabditis elegans 84-90 21840852-9 2011 In addition to their role in appropriately responding to H2S and HCN, we found that cysl-1 and cysl-2 are both essential mediators of innate immunity against fast paralytic killing by Pseudomonas. Hydrogen Sulfide 57-60 Bifunctional L-3-cyanoalanine synthase/cysteine synthase Caenorhabditis elegans 95-101 21840852-11 2011 Our results suggest the hypoxia-independent hif-1 response in C. elegans evolved to respond to the naturally occurring small molecules H2S and HCN. Hydrogen Sulfide 135-138 Hypoxia-inducible factor 1 Caenorhabditis elegans 44-49 21618058-1 2011 AIMS/HYPOTHESIS: Cystathionine gamma-lyase (CSE) catalyses the endogenous production of hydrogen sulphide (H(2)S) in pancreatic beta cells, and H(2)S has been shown to inhibit insulin release from these cells. Hydrogen Sulfide 88-105 cystathionine gamma-lyase Rattus norvegicus 17-42 21618058-1 2011 AIMS/HYPOTHESIS: Cystathionine gamma-lyase (CSE) catalyses the endogenous production of hydrogen sulphide (H(2)S) in pancreatic beta cells, and H(2)S has been shown to inhibit insulin release from these cells. Hydrogen Sulfide 88-105 cystathionine gamma-lyase Rattus norvegicus 44-47 21618058-1 2011 AIMS/HYPOTHESIS: Cystathionine gamma-lyase (CSE) catalyses the endogenous production of hydrogen sulphide (H(2)S) in pancreatic beta cells, and H(2)S has been shown to inhibit insulin release from these cells. Hydrogen Sulfide 107-112 cystathionine gamma-lyase Rattus norvegicus 17-42 21618058-1 2011 AIMS/HYPOTHESIS: Cystathionine gamma-lyase (CSE) catalyses the endogenous production of hydrogen sulphide (H(2)S) in pancreatic beta cells, and H(2)S has been shown to inhibit insulin release from these cells. Hydrogen Sulfide 107-112 cystathionine gamma-lyase Rattus norvegicus 44-47 21618058-12 2011 Inhibited H(2)S production through glucose-mediated CSE activity and production alterations may be involved in the fine control of glucose-induced insulin secretion. Hydrogen Sulfide 10-15 cystathionine gamma-lyase Rattus norvegicus 52-55 21716261-2 2011 Hydrogen sulfide (H(2)S) is a gas endogenously produced by cystathionine gamma-lyase in VSMC. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 59-84 21716261-2 2011 Hydrogen sulfide (H(2)S) is a gas endogenously produced by cystathionine gamma-lyase in VSMC. Hydrogen Sulfide 18-23 cystathionine gamma-lyase Homo sapiens 59-84 21716261-4 2011 Hydrogen sulfide was found to inhibit calcium deposition in the extracellular matrix and to suppress the induction of the genes involved in osteoblastic transformation of VSMC: alkaline phosphatase, osteocalcin, and Cbfa1. Hydrogen Sulfide 0-16 bone gamma-carboxyglutamate protein Homo sapiens 199-210 21716261-4 2011 Hydrogen sulfide was found to inhibit calcium deposition in the extracellular matrix and to suppress the induction of the genes involved in osteoblastic transformation of VSMC: alkaline phosphatase, osteocalcin, and Cbfa1. Hydrogen Sulfide 0-16 RUNX family transcription factor 2 Homo sapiens 216-221 21716261-5 2011 Moreover, phosphate uptake and phosphate-triggered upregulation of the sodium-dependent phosphate cotransporter (Pit-1) were also prevented by H(2)S. Hydrogen Sulfide 143-148 POU class 1 homeobox 1 Homo sapiens 113-118 21716261-6 2011 Reduction of endogenous production of H(2)S by inhibition of cystathionine gamma-lyase activity resulted in increased osteoblastic transformation and mineralization. Hydrogen Sulfide 38-43 cystathionine gamma-lyase Homo sapiens 61-86 21716261-7 2011 Low plasma levels of H(2)S, associated with decreased cystathionine gamma-lyase enzyme activity, were found in patients with chronic kidney disease receiving hemodialysis. Hydrogen Sulfide 21-26 cystathionine gamma-lyase Homo sapiens 54-79 21734104-3 2011 In the central nervous system, hydrogen sulfide (H2S) is a gasotransmitter generated primarily by the enzyme cystathionine-beta-synthase (CBS). Hydrogen Sulfide 31-47 cystathionine beta-synthase Homo sapiens 109-136 22038352-4 2011 We examined hippocampal H(2)S synthesis and the expression of cystathionine-beta-synthetase (CBS), a major enzyme involved in the H(2)S synthesis in hippocampus. Hydrogen Sulfide 130-135 cystathionine beta synthase Rattus norvegicus 93-96 21734104-3 2011 In the central nervous system, hydrogen sulfide (H2S) is a gasotransmitter generated primarily by the enzyme cystathionine-beta-synthase (CBS). Hydrogen Sulfide 49-52 cystathionine beta-synthase Homo sapiens 109-136 21603936-6 2011 Exogenous H(2)S enhanced synaptic plasticity in the hippocampus of brain-ischemic rats, inhibited the edema around pyramidal neurons and the nuclear shrink induced by ischemia, and promoted the expression of growth-associated protein-43 (GAP-43) in the CA1 region of hippocampus post ischemia. Hydrogen Sulfide 10-15 growth associated protein 43 Rattus norvegicus 208-236 21603936-6 2011 Exogenous H(2)S enhanced synaptic plasticity in the hippocampus of brain-ischemic rats, inhibited the edema around pyramidal neurons and the nuclear shrink induced by ischemia, and promoted the expression of growth-associated protein-43 (GAP-43) in the CA1 region of hippocampus post ischemia. Hydrogen Sulfide 10-15 growth associated protein 43 Rattus norvegicus 238-244 21603936-6 2011 Exogenous H(2)S enhanced synaptic plasticity in the hippocampus of brain-ischemic rats, inhibited the edema around pyramidal neurons and the nuclear shrink induced by ischemia, and promoted the expression of growth-associated protein-43 (GAP-43) in the CA1 region of hippocampus post ischemia. Hydrogen Sulfide 10-15 carbonic anhydrase 1 Rattus norvegicus 253-256 22309020-2 2011 In the vascular system, H2S is synthesized from cysteine by cystathionine-gamma-lyase (CSE) in smooth muscle cells (SMC) and 3- mercaptopyruvate sulfuresterase (3MST) and CSE in the endothelial cells. Hydrogen Sulfide 24-27 cystathionine gamma-lyase Homo sapiens 60-85 21723961-0 2011 Protective action of endogenously generated H2S on hypoxia-induced respiratory suppression and its relation to antioxidation and down-regulation of c-fos mRNA in medullary slices of neonatal rats. Hydrogen Sulfide 44-47 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 148-153 21723961-2 2011 The protective action of endogenous H(2)S and its relation to antioxidation and down-regulation of c-fos mRNA were investigated in the present study. Hydrogen Sulfide 36-41 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 99-104 21723961-7 2011 These results indicate that endogenously generated H(2)S was involved in protection of the medullary respiratory centers against hypoxic injury partly via antioxidation and down-regulation of c-fos. Hydrogen Sulfide 51-56 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 192-197 21235456-7 2011 The basal production of H2S is determined by the activity of, at least, three constitutively expressed enzymes (CBS, CSE, and 3-MPT) with tissue specificity for CBS and CSE in the central nervous and cardiovascular system, respectively. Hydrogen Sulfide 24-27 cystathionase (cystathionine gamma-lyase) Mus musculus 117-120 21235456-7 2011 The basal production of H2S is determined by the activity of, at least, three constitutively expressed enzymes (CBS, CSE, and 3-MPT) with tissue specificity for CBS and CSE in the central nervous and cardiovascular system, respectively. Hydrogen Sulfide 24-27 cystathionase (cystathionine gamma-lyase) Mus musculus 169-172 21235456-8 2011 The assumption of a pivotal role of H2S in regulating physiological function is supported by the demonstration that reduced production of this gaseous molecule by CSE induces hypertension in mice. Hydrogen Sulfide 36-39 cystathionase (cystathionine gamma-lyase) Mus musculus 163-166 21470138-11 2011 These data provide the first evidence that H2S may stimulate Ca2+ influx into ECs by recruiting the reverse-mode of NCX and KATP channels. Hydrogen Sulfide 43-46 solute carrier family 8 member A1 Rattus norvegicus 116-119 21527544-2 2011 We demonstrated in 1996 that cystathionine beta-synthase can produce H(2)S in the brain and that H(2)S facilitates the induction of hippocampal long-term potentiation by enhancing the activity of NMDA receptors. Hydrogen Sulfide 69-74 cystathionine beta-synthase Homo sapiens 29-56 21527544-3 2011 The following year, we showed that another H(2)S-producing enzyme, cystathionine gamma-lyase, is expressed in the thoracic aorta, portal vein and ileum and that H(2)S relaxes these tissues. Hydrogen Sulfide 43-48 cystathionine gamma-lyase Homo sapiens 67-92 21527544-3 2011 The following year, we showed that another H(2)S-producing enzyme, cystathionine gamma-lyase, is expressed in the thoracic aorta, portal vein and ileum and that H(2)S relaxes these tissues. Hydrogen Sulfide 161-166 cystathionine gamma-lyase Homo sapiens 67-92 21527544-7 2011 We recently demonstrated that a third H(2)S-producing enzyme, 3-mercaptopyruvate sulfurtransferase (3MST), is expressed in neurons and vascular endothelium. Hydrogen Sulfide 38-43 mercaptopyruvate sulfurtransferase Homo sapiens 62-98 21941511-3 2011 In the present study we have demonstrated the presence of the H(2)S-producing enzyme, cystathionine-beta-synthase (CBS) in the rostral ventrolateral medulla (RVLM), and the hypothalamic paraventricular nucleus (PVN), brain regions with key cardiovascular regulatory functions. Hydrogen Sulfide 62-67 cystathionine beta synthase Rattus norvegicus 86-113 21941511-3 2011 In the present study we have demonstrated the presence of the H(2)S-producing enzyme, cystathionine-beta-synthase (CBS) in the rostral ventrolateral medulla (RVLM), and the hypothalamic paraventricular nucleus (PVN), brain regions with key cardiovascular regulatory functions. Hydrogen Sulfide 62-67 cystathionine beta synthase Rattus norvegicus 115-118 21519787-5 2011 Exogenous administration of NaHS (a donor of H2S) augmented not only HSP90 expression under normal conditions, but also CoCl2-induced overexpression of HSP90. Hydrogen Sulfide 45-48 heat shock protein 90 alpha family class A member 1 Homo sapiens 69-74 21519787-5 2011 Exogenous administration of NaHS (a donor of H2S) augmented not only HSP90 expression under normal conditions, but also CoCl2-induced overexpression of HSP90. Hydrogen Sulfide 45-48 heat shock protein 90 alpha family class A member 1 Homo sapiens 152-157 21519787-9 2011 We also provide novel evidence that HSP90 mediates the cardioprotection of H2S against CoCl2-induced injuries by its antioxidant effect and preservation of mitochondrial function in H9c2 cells. Hydrogen Sulfide 75-78 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 36-41 21506909-14 2011 CONCLUSIONS: Onion extract exerted a marked antiatherogenic effect in association with the up-regulation of the endogenous CSE/H2S pathway but down-regulation of the ADM/CRLR family in atherosclerotic rats. Hydrogen Sulfide 127-130 cystathionine gamma-lyase Rattus norvegicus 123-126 21666033-3 2011 The biosynthesis of H(2)S has been attributed to three endogenous enzymes: cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CGL or CSE) and 3-mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 20-25 cystathionine beta-synthase Homo sapiens 75-102 21666033-3 2011 The biosynthesis of H(2)S has been attributed to three endogenous enzymes: cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CGL or CSE) and 3-mercaptopyruvate sulfurtransferase (3-MST). Hydrogen Sulfide 20-25 cystathionine gamma-lyase Homo sapiens 110-135 21666034-3 2011 Hydrogen sulfide can be produced in the lung and airway tissues via the actions of two H(2)S-generating enzymes, cystathionine beta-synthase (CBS) and/or cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 113-140 21666034-3 2011 Hydrogen sulfide can be produced in the lung and airway tissues via the actions of two H(2)S-generating enzymes, cystathionine beta-synthase (CBS) and/or cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 154-179 21666034-3 2011 Hydrogen sulfide can be produced in the lung and airway tissues via the actions of two H(2)S-generating enzymes, cystathionine beta-synthase (CBS) and/or cystathionine gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 181-184 21666034-8 2011 Major challenges for establishing the diagnostic and treatment values of H(2)S include the differential expression of CSE and CBS along the airway and their changes during asthma, the effects of H(2)S on bronchoconstriction and airway remodelling, as well as the underlying mechanisms, and the detection of the changes in H(2)S levels in airway tissues and in exhaled air. Hydrogen Sulfide 73-78 cystathionine gamma-lyase Homo sapiens 118-121 21519787-0 2011 Novel insights into the role of HSP90 in cytoprotection of H2S against chemical hypoxia-induced injury in H9c2 cardiac myocytes. Hydrogen Sulfide 59-62 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 32-37 21519787-3 2011 The aim of this study was to investigate the role of heat shock protein 90 (HSP90) in cardioprotection of H2S in H9c2 cells. Hydrogen Sulfide 106-109 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 53-74 21519787-3 2011 The aim of this study was to investigate the role of heat shock protein 90 (HSP90) in cardioprotection of H2S in H9c2 cells. Hydrogen Sulfide 106-109 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 76-81 22309020-2 2011 In the vascular system, H2S is synthesized from cysteine by cystathionine-gamma-lyase (CSE) in smooth muscle cells (SMC) and 3- mercaptopyruvate sulfuresterase (3MST) and CSE in the endothelial cells. Hydrogen Sulfide 24-27 cystathionine gamma-lyase Homo sapiens 87-90 22309020-2 2011 In the vascular system, H2S is synthesized from cysteine by cystathionine-gamma-lyase (CSE) in smooth muscle cells (SMC) and 3- mercaptopyruvate sulfuresterase (3MST) and CSE in the endothelial cells. Hydrogen Sulfide 24-27 cystathionine gamma-lyase Homo sapiens 171-174 22309020-6 2011 H2S contracts SMC through a reduction in nitric oxide (NO) availability by reacting with NO forming a nitrosothiol compound and through an inhibitory effect on endothelial nitric oxide synthase (eNOS) as well as a reduction in SMC cyclic AMP concentration. Hydrogen Sulfide 0-3 nitric oxide synthase 3 Homo sapiens 160-193 21104457-4 2011 We show that homocysteine inhibits the generation of endogenous H(2)S and the expression and activity of cystathionine-beta-synthetase (CBS), the main enzyme responsible for the generation of H(2)S in PC12 cells. Hydrogen Sulfide 192-197 cystathionine beta synthase Rattus norvegicus 105-134 21104457-4 2011 We show that homocysteine inhibits the generation of endogenous H(2)S and the expression and activity of cystathionine-beta-synthetase (CBS), the main enzyme responsible for the generation of H(2)S in PC12 cells. Hydrogen Sulfide 192-197 cystathionine beta synthase Rattus norvegicus 136-139 21104457-5 2011 S-Adenosylmethionine, an activator of CBS, not only prevents homocysteine-induced inhibition of endogenous H(2)S production but also attenuates homocysteine-triggered cytotoxicity and accumulation of ROS. Hydrogen Sulfide 107-112 cystathionine beta synthase Rattus norvegicus 38-41 21104457-6 2011 We find that activation of ERK1/2 occurs in homocysteine-treated PC12 cells and blockade of ERK1/2 with U0126 abolished the homocysteine-induced cytotoxicity and inhibitory effect on endogenous H(2)S generation. Hydrogen Sulfide 194-199 mitogen activated protein kinase 3 Rattus norvegicus 27-33 21104457-6 2011 We find that activation of ERK1/2 occurs in homocysteine-treated PC12 cells and blockade of ERK1/2 with U0126 abolished the homocysteine-induced cytotoxicity and inhibitory effect on endogenous H(2)S generation. Hydrogen Sulfide 194-199 mitogen activated protein kinase 3 Rattus norvegicus 92-98 21104457-7 2011 These results indicate that homocysteine neurotoxicity involves reduction of H(2)S production, which is caused by inhibition of CBS and mediated by activation of ERK1/2. Hydrogen Sulfide 77-82 cystathionine beta synthase Rattus norvegicus 128-131 21104457-7 2011 These results indicate that homocysteine neurotoxicity involves reduction of H(2)S production, which is caused by inhibition of CBS and mediated by activation of ERK1/2. Hydrogen Sulfide 77-82 mitogen activated protein kinase 3 Rattus norvegicus 162-168 21984157-0 2011 [Effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase expression during myocardial ischemia-reperfusion in rats]. Hydrogen Sulfide 11-27 hematopoietic prostaglandin D synthase Rattus norvegicus 63-88 21984157-1 2011 OBJECTIVE: To investigate the effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase (GST) expression during myocardial ischemia-reperfusion in rats. Hydrogen Sulfide 40-56 hematopoietic prostaglandin D synthase Rattus norvegicus 92-117 21984157-1 2011 OBJECTIVE: To investigate the effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase (GST) expression during myocardial ischemia-reperfusion in rats. Hydrogen Sulfide 40-56 hematopoietic prostaglandin D synthase Rattus norvegicus 119-122 21984157-11 2011 CONCLUSION: The hydrogen sulfide-induced delayed preconditioning attenuates myocardial IR injury possibly through up-regulating glutathione S-transferase expression in rats. Hydrogen Sulfide 16-32 hematopoietic prostaglandin D synthase Rattus norvegicus 128-153 21659522-1 2011 Cystathionine gamma-lyase (CSE) is the major enzyme in vascular smooth muscle cells (SMCs) that catalyzes the endogenous production of H(2)S. Hydrogen Sulfide 135-140 cystathionine gamma-lyase Homo sapiens 0-25 21718679-2 2011 Cystathionine gamma-lyase (CSE) is a major hydrogen sulfide (H(2)S)-producing enzyme in pancreatic beta cells. Hydrogen Sulfide 43-59 cystathionase (cystathionine gamma-lyase) Mus musculus 0-25 21718679-2 2011 Cystathionine gamma-lyase (CSE) is a major hydrogen sulfide (H(2)S)-producing enzyme in pancreatic beta cells. Hydrogen Sulfide 43-59 cystathionase (cystathionine gamma-lyase) Mus musculus 27-30 21718679-2 2011 Cystathionine gamma-lyase (CSE) is a major hydrogen sulfide (H(2)S)-producing enzyme in pancreatic beta cells. Hydrogen Sulfide 61-67 cystathionase (cystathionine gamma-lyase) Mus musculus 0-25 21718679-2 2011 Cystathionine gamma-lyase (CSE) is a major hydrogen sulfide (H(2)S)-producing enzyme in pancreatic beta cells. Hydrogen Sulfide 61-67 cystathionase (cystathionine gamma-lyase) Mus musculus 27-30 22097720-11 2011 Plasma level of H2S, the activity of H2S generating enzymes, CSE mRNA each was closely positively related to Al while inversely related to mPAP and Bcl-2/Bax (all P < 0.01). Hydrogen Sulfide 37-40 BCL2 associated X, apoptosis regulator Rattus norvegicus 154-157 22097720-13 2011 The depression of the H2S/CSE system in HHPH may help increase the ratio of Bcl-2/Bax, inhibit apoptosis of pulmonary artery smooth muscle cells and finally result in the formation of pulmonary hypertension. Hydrogen Sulfide 22-25 cystathionine gamma-lyase Rattus norvegicus 26-29 22097720-13 2011 The depression of the H2S/CSE system in HHPH may help increase the ratio of Bcl-2/Bax, inhibit apoptosis of pulmonary artery smooth muscle cells and finally result in the formation of pulmonary hypertension. Hydrogen Sulfide 22-25 BCL2, apoptosis regulator Rattus norvegicus 76-81 22097720-13 2011 The depression of the H2S/CSE system in HHPH may help increase the ratio of Bcl-2/Bax, inhibit apoptosis of pulmonary artery smooth muscle cells and finally result in the formation of pulmonary hypertension. Hydrogen Sulfide 22-25 BCL2 associated X, apoptosis regulator Rattus norvegicus 82-85 21658433-0 2011 Time- and concentration-dependent activation of TRPA1 by hydrogen sulfide in rat DRG neurons. Hydrogen Sulfide 57-73 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 48-53 21658433-9 2011 These results suggest that H(2)S stimulates sensory neurons via activation of TRPA1. Hydrogen Sulfide 27-32 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 78-83 21658433-10 2011 Endogenous H(2)S may be involved in physiological processes through TRPA1. Hydrogen Sulfide 11-16 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 68-73 21555999-0 2011 Hydrogen sulfide inhibits IL-8 expression in human keratinocytes via MAP kinase signaling. Hydrogen Sulfide 0-16 C-X-C motif chemokine ligand 8 Homo sapiens 26-30 21555999-5 2011 Here, we demonstrate both in vitro and in vivo on primary psoriatic lesions that pharmacological inhibitors of ERKs as well as hydrogen sulfide not only reduce the basal expression and secretion of IL-8, but also interfere with IL-17- and IL-22-induced IL-8 production. Hydrogen Sulfide 127-143 C-X-C motif chemokine ligand 8 Homo sapiens 198-202 21555999-5 2011 Here, we demonstrate both in vitro and in vivo on primary psoriatic lesions that pharmacological inhibitors of ERKs as well as hydrogen sulfide not only reduce the basal expression and secretion of IL-8, but also interfere with IL-17- and IL-22-induced IL-8 production. Hydrogen Sulfide 127-143 interleukin 17A Homo sapiens 228-233 21555999-5 2011 Here, we demonstrate both in vitro and in vivo on primary psoriatic lesions that pharmacological inhibitors of ERKs as well as hydrogen sulfide not only reduce the basal expression and secretion of IL-8, but also interfere with IL-17- and IL-22-induced IL-8 production. Hydrogen Sulfide 127-143 interleukin 22 Homo sapiens 239-244 21555999-5 2011 Here, we demonstrate both in vitro and in vivo on primary psoriatic lesions that pharmacological inhibitors of ERKs as well as hydrogen sulfide not only reduce the basal expression and secretion of IL-8, but also interfere with IL-17- and IL-22-induced IL-8 production. Hydrogen Sulfide 127-143 C-X-C motif chemokine ligand 8 Homo sapiens 253-257 21659522-1 2011 Cystathionine gamma-lyase (CSE) is the major enzyme in vascular smooth muscle cells (SMCs) that catalyzes the endogenous production of H(2)S. Hydrogen Sulfide 135-140 cystathionine gamma-lyase Homo sapiens 27-30 21254839-1 2011 The enzymes of the transsulfuration pathway, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), are important for the endogenous production of hydrogen sulfide (H(2)S), a gaseous signaling molecule. Hydrogen Sulfide 163-179 cystathionine beta-synthase Mus musculus 45-72 20812865-2 2011 The main consequence of the absence of Ethe1-SDO is the accumulation of sulfide (H(2)S) in critical tissues, including colonic mucosa, liver, muscle, and brain. Hydrogen Sulfide 81-86 ETHE1 persulfide dioxygenase Homo sapiens 39-44 21254839-1 2011 The enzymes of the transsulfuration pathway, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), are important for the endogenous production of hydrogen sulfide (H(2)S), a gaseous signaling molecule. Hydrogen Sulfide 163-179 cystathionine beta-synthase Mus musculus 74-77 20812865-5 2011 The accumulation of H(2)S over time causes progressive COX deficiency in animal tissues and human cells, which is associated with reduced amount of COX holoenzyme, and of several COX subunits, including mitochondrially encoded cytochrome c oxidase 1 (MTCO1), MTCO2, COX4, and COX5A. Hydrogen Sulfide 20-25 cytochrome c oxidase subunit 4I1 Homo sapiens 266-270 21254839-1 2011 The enzymes of the transsulfuration pathway, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), are important for the endogenous production of hydrogen sulfide (H(2)S), a gaseous signaling molecule. Hydrogen Sulfide 163-179 cystathionase (cystathionine gamma-lyase) Mus musculus 83-108 21254839-1 2011 The enzymes of the transsulfuration pathway, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), are important for the endogenous production of hydrogen sulfide (H(2)S), a gaseous signaling molecule. Hydrogen Sulfide 163-179 cystathionase (cystathionine gamma-lyase) Mus musculus 110-113 20812865-5 2011 The accumulation of H(2)S over time causes progressive COX deficiency in animal tissues and human cells, which is associated with reduced amount of COX holoenzyme, and of several COX subunits, including mitochondrially encoded cytochrome c oxidase 1 (MTCO1), MTCO2, COX4, and COX5A. Hydrogen Sulfide 20-25 cytochrome c oxidase subunit 5A Homo sapiens 276-281 20812865-5 2011 The accumulation of H(2)S over time causes progressive COX deficiency in animal tissues and human cells, which is associated with reduced amount of COX holoenzyme, and of several COX subunits, including mitochondrially encoded cytochrome c oxidase 1 (MTCO1), MTCO2, COX4, and COX5A. Hydrogen Sulfide 20-25 cytochrome c oxidase subunit 5A Homo sapiens 55-58 21254839-1 2011 The enzymes of the transsulfuration pathway, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), are important for the endogenous production of hydrogen sulfide (H(2)S), a gaseous signaling molecule. Hydrogen Sulfide 181-186 cystathionine beta-synthase Mus musculus 45-72 20812865-5 2011 The accumulation of H(2)S over time causes progressive COX deficiency in animal tissues and human cells, which is associated with reduced amount of COX holoenzyme, and of several COX subunits, including mitochondrially encoded cytochrome c oxidase 1 (MTCO1), MTCO2, COX4, and COX5A. Hydrogen Sulfide 20-25 cytochrome c oxidase subunit 5A Homo sapiens 148-151 20812865-5 2011 The accumulation of H(2)S over time causes progressive COX deficiency in animal tissues and human cells, which is associated with reduced amount of COX holoenzyme, and of several COX subunits, including mitochondrially encoded cytochrome c oxidase 1 (MTCO1), MTCO2, COX4, and COX5A. Hydrogen Sulfide 20-25 cytochrome c oxidase subunit 5A Homo sapiens 148-151 20812865-5 2011 The accumulation of H(2)S over time causes progressive COX deficiency in animal tissues and human cells, which is associated with reduced amount of COX holoenzyme, and of several COX subunits, including mitochondrially encoded cytochrome c oxidase 1 (MTCO1), MTCO2, COX4, and COX5A. Hydrogen Sulfide 20-25 mitochondrially encoded cytochrome c oxidase I Homo sapiens 251-256 20812865-5 2011 The accumulation of H(2)S over time causes progressive COX deficiency in animal tissues and human cells, which is associated with reduced amount of COX holoenzyme, and of several COX subunits, including mitochondrially encoded cytochrome c oxidase 1 (MTCO1), MTCO2, COX4, and COX5A. Hydrogen Sulfide 20-25 mitochondrially encoded cytochrome c oxidase II Homo sapiens 259-264 20812865-7 2011 Tissue-specific ablation of Ethe1 causes COX deficiency in targeted organs, suggesting that failure in neutralizing endogenous, tissue-specific production of H(2)S is sufficient to cause the biochemical defect but neither to determine a clinical impact nor to induce the biomarker profile typical of EE. Hydrogen Sulfide 158-163 ETHE1 persulfide dioxygenase Homo sapiens 28-33 20812865-8 2011 The mechanism by which H(2)S causes COX deficiency consists of rapid heme a inhibition and accelerated long-term degradation of COX subunits. Hydrogen Sulfide 23-28 cytochrome c oxidase subunit 5A Homo sapiens 36-39 20812865-8 2011 The mechanism by which H(2)S causes COX deficiency consists of rapid heme a inhibition and accelerated long-term degradation of COX subunits. Hydrogen Sulfide 23-28 cytochrome c oxidase subunit 5A Homo sapiens 128-131 20812865-9 2011 However, the pleiotropic devastating effects of H(2)S accumulation in EE cannot be fully explained by the sole defect of COX in critical tissues, but are likely consequent to several toxic actions on a number of enzymatic activities in different tissues, including endothelial lining of the small vessels, leading to multiorgan failure. Hydrogen Sulfide 48-53 cytochrome c oxidase subunit 5A Homo sapiens 121-124 21254839-1 2011 The enzymes of the transsulfuration pathway, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), are important for the endogenous production of hydrogen sulfide (H(2)S), a gaseous signaling molecule. Hydrogen Sulfide 181-186 cystathionine beta-synthase Mus musculus 74-77 21254839-1 2011 The enzymes of the transsulfuration pathway, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), are important for the endogenous production of hydrogen sulfide (H(2)S), a gaseous signaling molecule. Hydrogen Sulfide 181-186 cystathionase (cystathionine gamma-lyase) Mus musculus 83-108 21254839-1 2011 The enzymes of the transsulfuration pathway, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), are important for the endogenous production of hydrogen sulfide (H(2)S), a gaseous signaling molecule. Hydrogen Sulfide 181-186 cystathionase (cystathionine gamma-lyase) Mus musculus 110-113 21254839-3 2011 In this study, we report quantification of CBS and CSE in murine liver and kidney and their contribution to H(2)S generation in these tissues and in brain at saturating substrate concentrations. Hydrogen Sulfide 108-113 cystathionine beta-synthase Mus musculus 43-46 21254839-3 2011 In this study, we report quantification of CBS and CSE in murine liver and kidney and their contribution to H(2)S generation in these tissues and in brain at saturating substrate concentrations. Hydrogen Sulfide 108-113 cystathionase (cystathionine gamma-lyase) Mus musculus 51-54 21254839-6 2011 At high substrate concentrations (20 mM each cysteine and homocysteine), the capacity for liver H(2)S production is approximately equal for CBS and CSE, whereas in kidney and brain, CBS constitutes the major source of H(2)S, accounting for ~80% and ~95%, respectively, of the total output. Hydrogen Sulfide 96-101 cystathionine beta-synthase Mus musculus 140-143 21254839-6 2011 At high substrate concentrations (20 mM each cysteine and homocysteine), the capacity for liver H(2)S production is approximately equal for CBS and CSE, whereas in kidney and brain, CBS constitutes the major source of H(2)S, accounting for ~80% and ~95%, respectively, of the total output. Hydrogen Sulfide 96-101 cystathionase (cystathionine gamma-lyase) Mus musculus 148-151 21254839-6 2011 At high substrate concentrations (20 mM each cysteine and homocysteine), the capacity for liver H(2)S production is approximately equal for CBS and CSE, whereas in kidney and brain, CBS constitutes the major source of H(2)S, accounting for ~80% and ~95%, respectively, of the total output. Hydrogen Sulfide 218-223 cystathionine beta-synthase Mus musculus 182-185 21254839-7 2011 At physiologically relevant concentrations of substrate, and adjusting for the differences in CBS versus CSE levels, we estimate that CBS accounts for only 3% of H(2)S production by the transsulfuration pathway enzymes in liver. Hydrogen Sulfide 162-167 cystathionine beta-synthase Mus musculus 134-137 21671682-3 2011 Sulfidefluor-1 (SF1) and Sulfidefluor-2 (SF2) respond to H(2)S by a turn-on fluorescence signal enhancement and display high selectivity for H(2)S over other biologically relevant reactive sulfur, oxygen, and nitrogen species. Hydrogen Sulfide 57-62 splicing factor 1 Homo sapiens 16-19 21671682-3 2011 Sulfidefluor-1 (SF1) and Sulfidefluor-2 (SF2) respond to H(2)S by a turn-on fluorescence signal enhancement and display high selectivity for H(2)S over other biologically relevant reactive sulfur, oxygen, and nitrogen species. Hydrogen Sulfide 57-62 serine and arginine rich splicing factor 1 Homo sapiens 41-44 21671682-3 2011 Sulfidefluor-1 (SF1) and Sulfidefluor-2 (SF2) respond to H(2)S by a turn-on fluorescence signal enhancement and display high selectivity for H(2)S over other biologically relevant reactive sulfur, oxygen, and nitrogen species. Hydrogen Sulfide 141-146 splicing factor 1 Homo sapiens 16-19 21671682-3 2011 Sulfidefluor-1 (SF1) and Sulfidefluor-2 (SF2) respond to H(2)S by a turn-on fluorescence signal enhancement and display high selectivity for H(2)S over other biologically relevant reactive sulfur, oxygen, and nitrogen species. Hydrogen Sulfide 141-146 serine and arginine rich splicing factor 1 Homo sapiens 41-44 21671682-4 2011 In addition, SF1 and SF2 can be used to detect H(2)S in both water and live cells, providing a potentially powerful approach for probing H(2)S chemistry in biological systems. Hydrogen Sulfide 47-52 splicing factor 1 Homo sapiens 13-16 21671682-4 2011 In addition, SF1 and SF2 can be used to detect H(2)S in both water and live cells, providing a potentially powerful approach for probing H(2)S chemistry in biological systems. Hydrogen Sulfide 47-52 serine and arginine rich splicing factor 1 Homo sapiens 21-24 21671682-4 2011 In addition, SF1 and SF2 can be used to detect H(2)S in both water and live cells, providing a potentially powerful approach for probing H(2)S chemistry in biological systems. Hydrogen Sulfide 137-142 splicing factor 1 Homo sapiens 13-16 21671682-4 2011 In addition, SF1 and SF2 can be used to detect H(2)S in both water and live cells, providing a potentially powerful approach for probing H(2)S chemistry in biological systems. Hydrogen Sulfide 137-142 serine and arginine rich splicing factor 1 Homo sapiens 21-24 21208996-10 2011 Administration of NaHS, a H(2)S donor, reversed the increases in TGF-beta1 and collagen IV in diabetic rats. Hydrogen Sulfide 26-31 transforming growth factor beta 1 Homo sapiens 65-74 21208996-16 2011 Reduction of endogenous H(2)S generation by DL-propargylglycine, a CSE inhibitor, produced similar cellular effects as high glucose, including increases in cell proliferation, TGF-beta1 and collagen IV expressions and ROS generation. Hydrogen Sulfide 24-29 cystathionine gamma-lyase Rattus norvegicus 67-70 21208996-16 2011 Reduction of endogenous H(2)S generation by DL-propargylglycine, a CSE inhibitor, produced similar cellular effects as high glucose, including increases in cell proliferation, TGF-beta1 and collagen IV expressions and ROS generation. Hydrogen Sulfide 24-29 transforming growth factor, beta 1 Rattus norvegicus 176-185 21208996-17 2011 CONCLUSION: Suppressed CSE-catalyzed endogenous H(2)S production in the kidney by hyperglycemia may play an important role in the pathogenesis of DN. Hydrogen Sulfide 48-53 cystathionine gamma-lyase Rattus norvegicus 23-26 20135153-2 2011 The best characterized Str is bovine rhodanese (EC 2.8.1.1) which catalyses in vitro the transfer of a sulfane sulfur atom from thiosulfate to cyanide, leading to the formation of sulfite and thiocyanate. Hydrogen Sulfide 103-110 thiosulfate sulfurtransferase Bos taurus 37-46 21417705-1 2011 OBJECT: Cystathionine beta-synthase (CBS) is an enzyme that metabolizes homocysteine to form H(2)S in the brain. Hydrogen Sulfide 93-98 cystathionine beta-synthase Homo sapiens 8-35 21417705-1 2011 OBJECT: Cystathionine beta-synthase (CBS) is an enzyme that metabolizes homocysteine to form H(2)S in the brain. Hydrogen Sulfide 93-98 cystathionine beta-synthase Homo sapiens 37-40 21417705-3 2011 Given the myriad effects of H(2)S, the authors hypothesized that patients possessing gain-of-function polymorphisms of the CBS gene will experience a decreased incidence of delayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage (aSAH). Hydrogen Sulfide 28-33 cystathionine beta-synthase Homo sapiens 123-126 21512160-3 2011 Hydrogen sulfide (H(2)S), a recently described endothelium-derived vasodilator, is produced by the enzyme cystathionine gamma-lyase (CSE) and acts by hyperpolarizing VSM. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Rattus norvegicus 106-131 21512160-3 2011 Hydrogen sulfide (H(2)S), a recently described endothelium-derived vasodilator, is produced by the enzyme cystathionine gamma-lyase (CSE) and acts by hyperpolarizing VSM. Hydrogen Sulfide 0-16 cystathionine gamma-lyase Rattus norvegicus 133-136 21512160-3 2011 Hydrogen sulfide (H(2)S), a recently described endothelium-derived vasodilator, is produced by the enzyme cystathionine gamma-lyase (CSE) and acts by hyperpolarizing VSM. Hydrogen Sulfide 18-23 cystathionine gamma-lyase Rattus norvegicus 106-131 21512160-3 2011 Hydrogen sulfide (H(2)S), a recently described endothelium-derived vasodilator, is produced by the enzyme cystathionine gamma-lyase (CSE) and acts by hyperpolarizing VSM. Hydrogen Sulfide 18-23 cystathionine gamma-lyase Rattus norvegicus 133-136 21512160-13 2011 CONCLUSIONS: IH appears to decrease endothelial CSE expression to reduce H(2)S production, depolarize VSM, and enhance myogenic tone. Hydrogen Sulfide 73-78 cystathionine gamma-lyase Rattus norvegicus 48-51 20414692-3 2011 It also affects the activity of two sulfurtransferases, 3-mercaptopyruvate sulfurtransferase and rhodanese, involved in the metabolism of sulfane sulfur-containing compounds and in consequence exerts an effect on the level of sulfane sulfur. Hydrogen Sulfide 138-145 mercaptopyruvate sulfurtransferase Homo sapiens 56-92 20414692-4 2011 Under conditions, in which the raised level of sulfane sulfur was accompanied by an elevated activity of 3-mercaptopyruvate sulfurtransferase, the proliferation of the human astrocytome U373 line was decreased. Hydrogen Sulfide 47-54 mercaptopyruvate sulfurtransferase Homo sapiens 105-141 21486070-4 2011 In this work, we utilize near-infrared cavity-enhanced optical absorption spectroscopy (off-axis ICOS) to quantify H(2)S in a JP-8 fuel reformer product stream. Hydrogen Sulfide 115-120 inducible T cell costimulator Homo sapiens 97-101 21421823-11 2011 Pinacidil- and H(2)S-induced vasodilations were smaller in arterioles of SUR2 null mice than in wild-type controls. Hydrogen Sulfide 15-20 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 Mus musculus 73-77 21308383-5 2011 The effects of SPRC were abolished by cystathionine gamma-lyase [CSE-an enzyme that synthesizes hydrogen sulfide (H(2)S)] inhibitor, DL: -propargylglycine (PAG), SPRC-induced Akt phosphorylation and TNF-alpha release was also abolished by the phosphoinositide 3-kinase (PI3K) inhibitor LY294002. Hydrogen Sulfide 96-112 cystathionine gamma-lyase Rattus norvegicus 38-63 21308383-5 2011 The effects of SPRC were abolished by cystathionine gamma-lyase [CSE-an enzyme that synthesizes hydrogen sulfide (H(2)S)] inhibitor, DL: -propargylglycine (PAG), SPRC-induced Akt phosphorylation and TNF-alpha release was also abolished by the phosphoinositide 3-kinase (PI3K) inhibitor LY294002. Hydrogen Sulfide 114-120 cystathionine gamma-lyase Rattus norvegicus 38-63 21393430-0 2011 Hydrogen sulfide is a partially redox-independent activator of the human jejunum Na+ channel, Nav1.5. Hydrogen Sulfide 0-16 sodium voltage-gated channel alpha subunit 5 Homo sapiens 94-100 21393430-4 2011 The aims of this study were to determine the effects of the H(2)S donor NaHS on Na(V)1.5, a voltage-dependent sodium channel expressed in the gastrointestinal tract in human jejunum smooth muscle cells and interstitial cells of Cajal, and to elucidate whether H(2)S acts on Na(V)1.5 by redox reactions. Hydrogen Sulfide 60-65 immunoglobulin lambda variable 2-18 Homo sapiens 80-88 21393430-4 2011 The aims of this study were to determine the effects of the H(2)S donor NaHS on Na(V)1.5, a voltage-dependent sodium channel expressed in the gastrointestinal tract in human jejunum smooth muscle cells and interstitial cells of Cajal, and to elucidate whether H(2)S acts on Na(V)1.5 by redox reactions. Hydrogen Sulfide 260-265 immunoglobulin lambda variable 2-18 Homo sapiens 80-88 21194352-7 2011 More importantly, enzymatic generation of H(2)S from recombinant cystathionine-gamma-lyase protein also interacted with endogenous NO generated from l-arginine to stimulate heart contraction. Hydrogen Sulfide 42-47 cystathionine gamma-lyase Homo sapiens 65-90 21354272-2 2011 To test a hypothesis that H(2)S might chelate and remove endogenous Zn(2+) that inhibits the Ca(v)3.2 isoform of T-type Ca(2+) channels, facilitating visceral nociception, we asked if intracolonic (i.col.) Hydrogen Sulfide 26-31 calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus 93-101 21354302-10 2011 Cell viability and Western blotting analysis demonstrated that the protective effects of H2S were mediated by p38 and ERK1/2 MAPKs. Hydrogen Sulfide 89-92 mitogen-activated protein kinase 14 Mus musculus 110-113 21354302-10 2011 Cell viability and Western blotting analysis demonstrated that the protective effects of H2S were mediated by p38 and ERK1/2 MAPKs. Hydrogen Sulfide 89-92 mitogen-activated protein kinase 3 Mus musculus 118-124 21354302-11 2011 In conclusion, H2S protects osteoblastic cells against oxidative stress-induced cell injury and suppression of proliferation and differentiation via a MAPK (p38 and ERK1/2)-dependent mechanism. Hydrogen Sulfide 15-18 mitogen-activated protein kinase 1 Mus musculus 151-155 21354302-11 2011 In conclusion, H2S protects osteoblastic cells against oxidative stress-induced cell injury and suppression of proliferation and differentiation via a MAPK (p38 and ERK1/2)-dependent mechanism. Hydrogen Sulfide 15-18 mitogen-activated protein kinase 14 Mus musculus 157-160 21354302-11 2011 In conclusion, H2S protects osteoblastic cells against oxidative stress-induced cell injury and suppression of proliferation and differentiation via a MAPK (p38 and ERK1/2)-dependent mechanism. Hydrogen Sulfide 15-18 mitogen-activated protein kinase 3 Mus musculus 165-171 21572963-0 2011 Hydrogen sulfide attenuated tumor necrosis factor-alpha-induced inflammatory signaling and dysfunction in vascular endothelial cells. Hydrogen Sulfide 0-16 tumor necrosis factor Homo sapiens 28-55 21354272-15 2011 Removal of luminal Zn(2+) by H(2)S and other Zn(2+) chelators thus produces colonic pain through activation of T-type Ca(2+) channels, most probably of the Ca(v)3.2 isoform. Hydrogen Sulfide 29-34 calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus 156-164 21467968-6 2011 In humans, both CBS and CSE are widely expressed on trabecular muscle, implying that the smooth muscle component is the major source of H(2)S. Hydrogen Sulfide 136-141 cystathionine beta-synthase Homo sapiens 16-19 21310231-3 2011 CSE-KO mice fed a cysteine-limited diet exhibited growth retardation; decreased levels of cysteine, glutathione, and H2S; and increased plasma homocysteine level. Hydrogen Sulfide 117-120 cystathionase (cystathionine gamma-lyase) Mus musculus 0-3 20945398-0 2011 Gene profiling reveals hydrogen sulphide recruits death signaling via the N-methyl-D-aspartate receptor identifying commonalities with excitotoxicity. Hydrogen Sulfide 23-40 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 74-103 20945398-3 2011 Moreover N-methyl-D-aspartate receptor (NMDAR) antagonists abolished the consequences of H(2) S-induced neuronal death. Hydrogen Sulfide 89-95 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 9-38 20945398-3 2011 Moreover N-methyl-D-aspartate receptor (NMDAR) antagonists abolished the consequences of H(2) S-induced neuronal death. Hydrogen Sulfide 89-95 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 40-45 20945398-4 2011 This study focuses on deciphering the downstream effects activation of NMDAR on H(2) S-mediated neuronal injury by analyzing the time-course of global gene profiling (5, 15, and 24 h) to provide a comprehensive description of the recruitment of NMDAR-mediated signaling. Hydrogen Sulfide 80-86 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 71-76 20945398-4 2011 This study focuses on deciphering the downstream effects activation of NMDAR on H(2) S-mediated neuronal injury by analyzing the time-course of global gene profiling (5, 15, and 24 h) to provide a comprehensive description of the recruitment of NMDAR-mediated signaling. Hydrogen Sulfide 80-86 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 245-250 21467968-2 2011 H(2)S is formed endogenously from L-cysteine or L-methionine by two enzymes, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), and normally circulates in blood. Hydrogen Sulfide 0-5 cystathionine beta-synthase Homo sapiens 77-104 21467968-2 2011 H(2)S is formed endogenously from L-cysteine or L-methionine by two enzymes, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), and normally circulates in blood. Hydrogen Sulfide 0-5 cystathionine beta-synthase Homo sapiens 106-109 21467968-2 2011 H(2)S is formed endogenously from L-cysteine or L-methionine by two enzymes, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), and normally circulates in blood. Hydrogen Sulfide 0-5 cystathionine gamma-lyase Homo sapiens 115-140 21467968-2 2011 H(2)S is formed endogenously from L-cysteine or L-methionine by two enzymes, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), and normally circulates in blood. Hydrogen Sulfide 0-5 cystathionine gamma-lyase Homo sapiens 142-145 21239532-6 2011 Exogenous H(2)S caused concentration-dependent apoptosis in RPASMC due to activation of ERK1/2 and p38, as well as downregulation of Bcl-2. Hydrogen Sulfide 10-15 mitogen activated protein kinase 3 Rattus norvegicus 88-94 21239532-6 2011 Exogenous H(2)S caused concentration-dependent apoptosis in RPASMC due to activation of ERK1/2 and p38, as well as downregulation of Bcl-2. Hydrogen Sulfide 10-15 mitogen activated protein kinase 14 Rattus norvegicus 99-102 21239532-6 2011 Exogenous H(2)S caused concentration-dependent apoptosis in RPASMC due to activation of ERK1/2 and p38, as well as downregulation of Bcl-2. Hydrogen Sulfide 10-15 BCL2, apoptosis regulator Rattus norvegicus 133-138 21239532-7 2011 Pretreatment with SNO-Alb reduced H(2)S-mediated apoptosis in a concentration-dependent manner that was associated with SNO-Alb-mediated inhibition of activation of ERK1/2 and p38. Hydrogen Sulfide 34-39 albumin Rattus norvegicus 22-25 21239532-7 2011 Pretreatment with SNO-Alb reduced H(2)S-mediated apoptosis in a concentration-dependent manner that was associated with SNO-Alb-mediated inhibition of activation of ERK1/2 and p38. Hydrogen Sulfide 34-39 albumin Rattus norvegicus 124-127 21239532-7 2011 Pretreatment with SNO-Alb reduced H(2)S-mediated apoptosis in a concentration-dependent manner that was associated with SNO-Alb-mediated inhibition of activation of ERK1/2 and p38. Hydrogen Sulfide 34-39 mitogen activated protein kinase 3 Rattus norvegicus 165-171 21239532-7 2011 Pretreatment with SNO-Alb reduced H(2)S-mediated apoptosis in a concentration-dependent manner that was associated with SNO-Alb-mediated inhibition of activation of ERK1/2 and p38. Hydrogen Sulfide 34-39 mitogen activated protein kinase 14 Rattus norvegicus 176-179 21239532-9 2011 Therefore, SNO-Alb is cytoprotective against models of oxidant-induced necrosis (tBH) and inhibitors of cellular respiration and apoptosis (H(2)S) in both pulmonary endothelium and smooth muscle, respectively, and a component of such protection can be attributed to a SH-Alb-mediated activation of constitutive NOS. Hydrogen Sulfide 140-146 albumin Rattus norvegicus 15-18 21275893-2 2011 In the vasculature, cystathionine-gamma-lyase (CSE) is the main enzyme responsible for H(2)S biosynthesis starting from the substrate e.g. L-cysteine. Hydrogen Sulfide 87-92 cystathionine gamma-lyase Homo sapiens 20-45 21275893-2 2011 In the vasculature, cystathionine-gamma-lyase (CSE) is the main enzyme responsible for H(2)S biosynthesis starting from the substrate e.g. L-cysteine. Hydrogen Sulfide 87-92 cystathionine gamma-lyase Homo sapiens 47-50 21275900-9 2011 This review focuses on the recent aspects of the molecular regulation of both CBS and CSE and highlights the possibility that members of the nuclear receptors superfamily might be involved in the regulation of hydrogen sulphide metabolism. Hydrogen Sulfide 210-227 cystathionine beta-synthase Homo sapiens 78-81 21275894-2 2011 H(2)S is generated by three enzymes, cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST). Hydrogen Sulfide 0-5 cystathionine beta-synthase Homo sapiens 37-64 21275900-9 2011 This review focuses on the recent aspects of the molecular regulation of both CBS and CSE and highlights the possibility that members of the nuclear receptors superfamily might be involved in the regulation of hydrogen sulphide metabolism. Hydrogen Sulfide 210-227 cystathionine gamma-lyase Homo sapiens 86-89 21275894-2 2011 H(2)S is generated by three enzymes, cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST). Hydrogen Sulfide 0-5 cystathionine beta-synthase Homo sapiens 66-69 21275894-2 2011 H(2)S is generated by three enzymes, cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST). Hydrogen Sulfide 0-5 cystathionine gamma-lyase Homo sapiens 72-97 21275894-2 2011 H(2)S is generated by three enzymes, cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST). Hydrogen Sulfide 0-5 cystathionine gamma-lyase Homo sapiens 99-102 21275894-2 2011 H(2)S is generated by three enzymes, cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST). Hydrogen Sulfide 0-5 mercaptopyruvate sulfurtransferase Homo sapiens 108-144 21275894-3 2011 In the CNS, H(2)S, generated mainly by CBS in astrocytes and 3MST in neurons, appears to participate in cognition, memory, regulation of the cardiopulmonary functions and neuroprotection. Hydrogen Sulfide 12-17 cystathionine beta-synthase Homo sapiens 39-42 21275895-3 2011 The production of H(2)S from L-cysteine is catalysed primarily by two enzymes, cystathionine gamma-lyase and cystathionine beta-synthase. Hydrogen Sulfide 18-23 cystathionine gamma-lyase Homo sapiens 79-104 21275895-3 2011 The production of H(2)S from L-cysteine is catalysed primarily by two enzymes, cystathionine gamma-lyase and cystathionine beta-synthase. Hydrogen Sulfide 18-23 cystathionine beta-synthase Homo sapiens 109-136 21275897-1 2011 Hydrogen sulfide (H(2)S) is a gas that can be formed by the action of two enzymes, cystathionine gamma lyase (CSE) and cystathionine beta synthase (CBS). Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 119-146 21275897-1 2011 Hydrogen sulfide (H(2)S) is a gas that can be formed by the action of two enzymes, cystathionine gamma lyase (CSE) and cystathionine beta synthase (CBS). Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 148-151 21275897-1 2011 Hydrogen sulfide (H(2)S) is a gas that can be formed by the action of two enzymes, cystathionine gamma lyase (CSE) and cystathionine beta synthase (CBS). Hydrogen Sulfide 18-23 cystathionine beta-synthase Homo sapiens 119-146 21275897-1 2011 Hydrogen sulfide (H(2)S) is a gas that can be formed by the action of two enzymes, cystathionine gamma lyase (CSE) and cystathionine beta synthase (CBS). Hydrogen Sulfide 18-23 cystathionine beta-synthase Homo sapiens 148-151 21275900-0 2011 Hydrogen sulfide generation in mammals: the molecular biology of cystathionine-beta- synthase (CBS) and cystathionine-gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 65-93 21275900-0 2011 Hydrogen sulfide generation in mammals: the molecular biology of cystathionine-beta- synthase (CBS) and cystathionine-gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine beta-synthase Homo sapiens 95-98 21275900-0 2011 Hydrogen sulfide generation in mammals: the molecular biology of cystathionine-beta- synthase (CBS) and cystathionine-gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 104-129 21275900-0 2011 Hydrogen sulfide generation in mammals: the molecular biology of cystathionine-beta- synthase (CBS) and cystathionine-gamma-lyase (CSE). Hydrogen Sulfide 0-16 cystathionine gamma-lyase Homo sapiens 131-134 21275900-1 2011 Cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) are two key enzymes involved in the synthesis of hydrogen sulphide (H(2)S). Hydrogen Sulfide 119-136 cystathionine beta-synthase Homo sapiens 0-27 21275900-1 2011 Cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) are two key enzymes involved in the synthesis of hydrogen sulphide (H(2)S). Hydrogen Sulfide 119-136 cystathionine beta-synthase Homo sapiens 29-32 21275900-1 2011 Cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) are two key enzymes involved in the synthesis of hydrogen sulphide (H(2)S). Hydrogen Sulfide 119-136 cystathionine gamma-lyase Homo sapiens 38-63 21275900-1 2011 Cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) are two key enzymes involved in the synthesis of hydrogen sulphide (H(2)S). Hydrogen Sulfide 119-136 cystathionine gamma-lyase Homo sapiens 65-68 21233344-9 2011 These results show that H2S by inducing MMP-2 promotes VEGF synthesis and angiogenesis while it suppresses MMP-9 and TIMP-3 levels, inhibits antiangiogenic factors, reduces intracardiac fibrosis, and mitigates transition from compensatory hypertrophy to heart failure. Hydrogen Sulfide 24-27 matrix metallopeptidase 2 Mus musculus 40-45 21122846-0 2011 Endogenous hydrogen sulfide as a mediator of vas deferens smooth muscle relaxation. Hydrogen Sulfide 11-27 arginine vasopressin Rattus norvegicus 45-48 21233344-9 2011 These results show that H2S by inducing MMP-2 promotes VEGF synthesis and angiogenesis while it suppresses MMP-9 and TIMP-3 levels, inhibits antiangiogenic factors, reduces intracardiac fibrosis, and mitigates transition from compensatory hypertrophy to heart failure. Hydrogen Sulfide 24-27 vascular endothelial growth factor A Mus musculus 55-59 21122846-2 2011 Endogenous H(2)S mediated vas deferens smooth muscle relaxation. Hydrogen Sulfide 11-16 arginine vasopressin Rattus norvegicus 26-29 21233344-3 2011 We hypothesize that H2S induces MMP-2 activation and inhibits MMP-9 activation, thus promoting angiogenesis, and mitigates transition from compensatory cardiac hypertrophy to heart failure. Hydrogen Sulfide 20-23 matrix metallopeptidase 2 Mus musculus 32-37 21233344-3 2011 We hypothesize that H2S induces MMP-2 activation and inhibits MMP-9 activation, thus promoting angiogenesis, and mitigates transition from compensatory cardiac hypertrophy to heart failure. Hydrogen Sulfide 20-23 matrix metallopeptidase 9 Mus musculus 62-67 21233344-9 2011 These results show that H2S by inducing MMP-2 promotes VEGF synthesis and angiogenesis while it suppresses MMP-9 and TIMP-3 levels, inhibits antiangiogenic factors, reduces intracardiac fibrosis, and mitigates transition from compensatory hypertrophy to heart failure. Hydrogen Sulfide 24-27 matrix metallopeptidase 9 Mus musculus 107-112 21233344-9 2011 These results show that H2S by inducing MMP-2 promotes VEGF synthesis and angiogenesis while it suppresses MMP-9 and TIMP-3 levels, inhibits antiangiogenic factors, reduces intracardiac fibrosis, and mitigates transition from compensatory hypertrophy to heart failure. Hydrogen Sulfide 24-27 tissue inhibitor of metalloproteinase 3 Mus musculus 117-123 21324981-2 2011 Although cystathionine beta-synthase and cystathionine gamma-lyase have been regarded as the main producers of H(2)S in many tissues including brain, liver and kidney, Kimura and his colleagues have recently communicated that 3-mercaptopyruvate sulphurtransferase coupled with cysteine (aspartate) aminotransferase is responsible for the production of H(2)S in the vascular endothelium of the thoracic aorta [Shibuya et al. Hydrogen Sulfide 111-116 cystathionine gamma-lyase Homo sapiens 41-66 21324981-2 2011 Although cystathionine beta-synthase and cystathionine gamma-lyase have been regarded as the main producers of H(2)S in many tissues including brain, liver and kidney, Kimura and his colleagues have recently communicated that 3-mercaptopyruvate sulphurtransferase coupled with cysteine (aspartate) aminotransferase is responsible for the production of H(2)S in the vascular endothelium of the thoracic aorta [Shibuya et al. Hydrogen Sulfide 352-357 cystathionine gamma-lyase Homo sapiens 41-66 21228064-12 2011 Our data indicate that H(2)S could activate PLA(2), which in turn releases arachidonic acid leading, initially, to vasoconstriction followed by vasodilation mediated by cytochrome P450-derived metabolites. Hydrogen Sulfide 23-28 phospholipase A2 group IB Rattus norvegicus 44-50 21336541-4 2011 H(2)S expression was examined by Western blot, and H(2)S production from CSE was assayed using a spectroscopic method. Hydrogen Sulfide 51-56 cystathionase (cystathionine gamma-lyase) Mus musculus 73-76 21336541-10 2011 The H(2)S-producing enzyme cystathionine-gamma-lyase (CSE) was expressed in mouse aorta and had activity of 7 +- 3 mumol H(2)S/g/min. Hydrogen Sulfide 4-9 cystathionase (cystathionine gamma-lyase) Mus musculus 54-57 21336541-14 2011 The L: -cysteine-CSE-H(2)S pathway contributes to vasorelaxation and appears to modulate basal vessel tone. Hydrogen Sulfide 21-26 cystathionase (cystathionine gamma-lyase) Mus musculus 17-20 20938376-4 2011 In the sham-operated animals, inhaled H2S and hypothermia alone comparably reduced the plasma chemokine and IL-6 levels, but combining hypothermia and inhaled H2S had no additional effect. Hydrogen Sulfide 38-41 interleukin 6 Mus musculus 108-112 20938376-8 2011 With or without sepsis, inhaled H2S and hypothermia alone comparably reduced the lung tissue heme oxygenase 1 expression, whereas inhaled H2S had no additional effect during hypothermia. Hydrogen Sulfide 32-35 heme oxygenase 1 Mus musculus 93-109 21473819-14 2011 CONCLUSION: The results suggested that intraperitoneal administration of H(2)S could reverse hyporesponsiveness of PARs to H(2)S induced by LPS, and the result might be related to an intensification of HO-1/CO system in pulmonary artery tissue. Hydrogen Sulfide 73-78 heme oxygenase 1 Rattus norvegicus 202-209 21289528-0 2011 Preprotachykinin-A gene deletion regulates hydrogen sulfide-induced toll-like receptor 4 signaling pathway in cerulein-treated pancreatic acinar cells. Hydrogen Sulfide 43-59 tachykinin 1 Mus musculus 0-18 21289528-0 2011 Preprotachykinin-A gene deletion regulates hydrogen sulfide-induced toll-like receptor 4 signaling pathway in cerulein-treated pancreatic acinar cells. Hydrogen Sulfide 43-59 toll-like receptor 4 Mus musculus 68-88 21289528-1 2011 OBJECTIVE: This study aimed to determine the effect of hydrogen sulfide (H2S) on Toll-like receptor 4 (TLR4)-mediated innate immune signaling in acute pancreatitis (AP) via substance P. Hydrogen Sulfide 55-71 toll-like receptor 4 Mus musculus 81-101 21289528-1 2011 OBJECTIVE: This study aimed to determine the effect of hydrogen sulfide (H2S) on Toll-like receptor 4 (TLR4)-mediated innate immune signaling in acute pancreatitis (AP) via substance P. Hydrogen Sulfide 55-71 toll-like receptor 4 Mus musculus 103-107 21289528-1 2011 OBJECTIVE: This study aimed to determine the effect of hydrogen sulfide (H2S) on Toll-like receptor 4 (TLR4)-mediated innate immune signaling in acute pancreatitis (AP) via substance P. Hydrogen Sulfide 55-71 tachykinin 1 Mus musculus 173-184 21289528-1 2011 OBJECTIVE: This study aimed to determine the effect of hydrogen sulfide (H2S) on Toll-like receptor 4 (TLR4)-mediated innate immune signaling in acute pancreatitis (AP) via substance P. Hydrogen Sulfide 73-76 toll-like receptor 4 Mus musculus 81-101 21289528-1 2011 OBJECTIVE: This study aimed to determine the effect of hydrogen sulfide (H2S) on Toll-like receptor 4 (TLR4)-mediated innate immune signaling in acute pancreatitis (AP) via substance P. Hydrogen Sulfide 73-76 toll-like receptor 4 Mus musculus 103-107 21289528-1 2011 OBJECTIVE: This study aimed to determine the effect of hydrogen sulfide (H2S) on Toll-like receptor 4 (TLR4)-mediated innate immune signaling in acute pancreatitis (AP) via substance P. Hydrogen Sulfide 73-76 tachykinin 1 Mus musculus 173-184 21289528-7 2011 RESULTS: The H2S inhibitor PAG eliminated TLR4, interleukin 1 receptor-associated kinase 4, tumor necrosis factor receptor-associated factor 6, and nuclear factor-kappaB (NF-kappaB) levels in in vitro and in vivo models of cerulein-induced AP. Hydrogen Sulfide 13-16 toll-like receptor 4 Mus musculus 42-46 21289528-7 2011 RESULTS: The H2S inhibitor PAG eliminated TLR4, interleukin 1 receptor-associated kinase 4, tumor necrosis factor receptor-associated factor 6, and nuclear factor-kappaB (NF-kappaB) levels in in vitro and in vivo models of cerulein-induced AP. Hydrogen Sulfide 13-16 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 171-180 21289528-9 2011 CONCLUSION: The present findings show for the first time that in AP, H2S may up-regulate the TLR4 pathway and NF-kappaB via substance P. Hydrogen Sulfide 69-72 toll-like receptor 4 Mus musculus 93-97 21289528-9 2011 CONCLUSION: The present findings show for the first time that in AP, H2S may up-regulate the TLR4 pathway and NF-kappaB via substance P. Hydrogen Sulfide 69-72 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 110-119 21289528-9 2011 CONCLUSION: The present findings show for the first time that in AP, H2S may up-regulate the TLR4 pathway and NF-kappaB via substance P. Hydrogen Sulfide 69-72 tachykinin 1 Mus musculus 124-135 20826746-12 2011 In addition, NS results in down-regulation of CBS which can curtail conversion of Hcy to cysteine and reduce production of H(2)S which is an important endogenous signalling molecule. Hydrogen Sulfide 123-128 cystathionine beta synthase Rattus norvegicus 46-49 21091646-12 2011 CONCLUSIONS AND IMPLICATIONS: H2S may prevent pancreatic beta-cells from cell apoptosis via an anti-oxidative mechanism and the activation of Akt signalling. Hydrogen Sulfide 30-33 thymoma viral proto-oncogene 1 Mus musculus 142-145 21195095-8 2011 However, exogenous H(2)S decreased the phosphorylation level of radiation-induced ATM. Hydrogen Sulfide 19-24 ATM serine/threonine kinase Homo sapiens 82-85 20967511-0 2011 H2S protects hippocampal neurons from anoxia-reoxygenation through cAMP-mediated PI3K/Akt/p70S6K cell-survival signaling pathways. Hydrogen Sulfide 0-3 AKT serine/threonine kinase 1 Rattus norvegicus 86-89 20967511-0 2011 H2S protects hippocampal neurons from anoxia-reoxygenation through cAMP-mediated PI3K/Akt/p70S6K cell-survival signaling pathways. Hydrogen Sulfide 0-3 ribosomal protein S6 kinase B1 Rattus norvegicus 90-96 20967511-1 2011 The study aims to investigate the effect of hydrogen sulfide (H(2)S) on the phosphatidylinositol 3-kinase (PI3K)/Akt/p70 ribosomal S6 kinase (p70S6K) signal transduction pathway after oxygen glucose deprivation/reoxygenation (OGD/R) in the rat hippocampus. Hydrogen Sulfide 44-60 phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma Rattus norvegicus 76-105 20967511-1 2011 The study aims to investigate the effect of hydrogen sulfide (H(2)S) on the phosphatidylinositol 3-kinase (PI3K)/Akt/p70 ribosomal S6 kinase (p70S6K) signal transduction pathway after oxygen glucose deprivation/reoxygenation (OGD/R) in the rat hippocampus. Hydrogen Sulfide 44-60 AKT serine/threonine kinase 1 Rattus norvegicus 113-116 20967511-1 2011 The study aims to investigate the effect of hydrogen sulfide (H(2)S) on the phosphatidylinositol 3-kinase (PI3K)/Akt/p70 ribosomal S6 kinase (p70S6K) signal transduction pathway after oxygen glucose deprivation/reoxygenation (OGD/R) in the rat hippocampus. Hydrogen Sulfide 44-60 ribosomal protein S6 kinase B1 Rattus norvegicus 142-148 20967511-1 2011 The study aims to investigate the effect of hydrogen sulfide (H(2)S) on the phosphatidylinositol 3-kinase (PI3K)/Akt/p70 ribosomal S6 kinase (p70S6K) signal transduction pathway after oxygen glucose deprivation/reoxygenation (OGD/R) in the rat hippocampus. Hydrogen Sulfide 62-67 phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma Rattus norvegicus 76-105 20967511-1 2011 The study aims to investigate the effect of hydrogen sulfide (H(2)S) on the phosphatidylinositol 3-kinase (PI3K)/Akt/p70 ribosomal S6 kinase (p70S6K) signal transduction pathway after oxygen glucose deprivation/reoxygenation (OGD/R) in the rat hippocampus. Hydrogen Sulfide 62-67 AKT serine/threonine kinase 1 Rattus norvegicus 113-116 20967511-1 2011 The study aims to investigate the effect of hydrogen sulfide (H(2)S) on the phosphatidylinositol 3-kinase (PI3K)/Akt/p70 ribosomal S6 kinase (p70S6K) signal transduction pathway after oxygen glucose deprivation/reoxygenation (OGD/R) in the rat hippocampus. Hydrogen Sulfide 62-67 ribosomal protein S6 kinase B1 Rattus norvegicus 142-148 20967511-10 2011 H(2)S acted via cAMP-mediated PI3K/Akt/p70S6K signal transduction pathways to inhibit hippocampal neuronal apoptosis and protect neurons from OGD/R-induced injury. Hydrogen Sulfide 0-5 AKT serine/threonine kinase 1 Rattus norvegicus 35-38 20967511-10 2011 H(2)S acted via cAMP-mediated PI3K/Akt/p70S6K signal transduction pathways to inhibit hippocampal neuronal apoptosis and protect neurons from OGD/R-induced injury. Hydrogen Sulfide 0-5 ribosomal protein S6 kinase B1 Rattus norvegicus 39-45 20858204-0 2011 Myoglobin as a new fluorescence probe to sense H2S. Hydrogen Sulfide 47-50 myoglobin Homo sapiens 0-9 21195095-10 2011 CSE, rather than CBS, may mainly responsible for the H(2)S production during this RAR which may also be mediated by ATM pathway. Hydrogen Sulfide 53-58 cystathionine gamma-lyase Homo sapiens 0-3 21131483-6 2011 L-cysteine, the substrate of the H2S-producing enzymes cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS), also dilated pial arterioles. Hydrogen Sulfide 33-36 cystathionine gamma-lyase Sus scrofa 55-80 21131483-6 2011 L-cysteine, the substrate of the H2S-producing enzymes cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS), also dilated pial arterioles. Hydrogen Sulfide 33-36 cystathionine gamma-lyase Sus scrofa 82-85 21131483-13 2011 These data show that H2S is a dilator of the newborn cerebral circulation and that endogenous CSE can produce sufficient H2S to decrease vascular tone. Hydrogen Sulfide 121-124 cystathionine gamma-lyase Sus scrofa 94-97 21375934-12 2011 However, activities of cNOS and iNOS in myocardium and the expression of eNOS mRNA were significantly decreased in H2S donor group (P<0.01), while the myocardial function significantly increased (P<0.05). Hydrogen Sulfide 115-118 nitric oxide synthase 3 Homo sapiens 23-27 21095213-0 2011 Hydrogen sulfide reduces mRNA and protein levels of beta-site amyloid precursor protein cleaving enzyme 1 in PC12 cells. Hydrogen Sulfide 0-16 beta-secretase 1 Rattus norvegicus 52-105 21141970-2 2011 Recently, we have reported a steady-state kinetic analysis of the three hydrogen sulfide (H(2)S)-generating reactions that are catalyzed by human and yeast CBS [Singh, S., et al. Hydrogen Sulfide 72-88 cystathionine beta-synthase Homo sapiens 156-159 21141970-2 2011 Recently, we have reported a steady-state kinetic analysis of the three hydrogen sulfide (H(2)S)-generating reactions that are catalyzed by human and yeast CBS [Singh, S., et al. Hydrogen Sulfide 90-95 cystathionine beta-synthase Homo sapiens 156-159 21375934-12 2011 However, activities of cNOS and iNOS in myocardium and the expression of eNOS mRNA were significantly decreased in H2S donor group (P<0.01), while the myocardial function significantly increased (P<0.05). Hydrogen Sulfide 115-118 nitric oxide synthase 2 Homo sapiens 32-36 21375934-12 2011 However, activities of cNOS and iNOS in myocardium and the expression of eNOS mRNA were significantly decreased in H2S donor group (P<0.01), while the myocardial function significantly increased (P<0.05). Hydrogen Sulfide 115-118 nitric oxide synthase 3 Homo sapiens 73-77 21591344-14 2011 Serum content of H2S in B group was respectively correlated with CSE activities of all organs (with r value from 0.639 to 0.894, P values all below 0.005) and serum contents of biochemical indexes (with r value from 0.301 to 0.585, P values all below 0.001). Hydrogen Sulfide 17-20 cystathionine gamma-lyase Rattus norvegicus 65-68 21591344-15 2011 CONCLUSIONS: H2S/CSE system may take part in pathophysiological process in rats with severe burn. Hydrogen Sulfide 13-16 cystathionine gamma-lyase Rattus norvegicus 17-20