ライフサイエンスコーパス: H2S

1 H2S molecules specifically triggered the release of repo

2 H2S regulates a wide range of physiological processes, n

3 H2S separation processes using reactive and non-reactive

4 H2S-DOXOs 10 and 11 emerged as the most interesting memb

5 ing doses of homocysteine or Na2S/GYY4137, a H2S donor, and measured the levels of CBS and CSE.

6 K2 overexpression reduced eNOS activity in a H2S-reversible manner.

7 ne, wet coating helps the trapping of acidic H2S gas and its reaction with Bi(III) species, forming c

8 Mitochondria can be both an H2S source and sink, and many of the biological effects

9 od following a sulfurization treatment in an H2S atmosphere.

10 system containing Cu(2+), tartaric acid, and H2S.

11 vations demonstrate that dysregulated CO and H2S signaling in the CB leads to apneas and suggest that

12 to poisoning by small reactive gases (CO and H2S) that may interact with embedded metallic sites.

13 steine persulfide (Cys-SSH) from cystine and H2S from cysteine and/or homocysteine.

14 cluding acetone and ethanol for diabetes and H2S for cardiovascular diseases.

15 hione persulfide, glutathione disulfide, and H2S.

16 erts methanethiol to H2O2, formaldehyde, and H2S, an activity not previously known to exist in humans

17 We hypothesize that homocysteine and H2S regulate CBS and CSE expressions in a dose dependent

18 sly formed in high concentration when NO and H2S gases are mixed at room temperature in the presence

19 hted the cross-talk between nitric oxide and H2S in several bilogical contexts.

20 ration were measured as a function of pH and H2S addition, suggesting the type of complexes formed ma

21 donation, we report here the preparation and H2S release kinetics from a series of isomeric caged-car

22 , the sigL mutant produced less pyruvate and H2S than the wild-type strain.

23 Release is predominant for reds and H2S, while at 50 degrees C, de novo formation dominates

24 H 7, although nonselectively over thiols and H2S.

25 yl (HNO) over nitric oxide (NO), thiols, and H2S in metal-based fluorescent probes, we investigated f

26 dative stress via l-cysteine utilization and H2S-mediated sequestration of free iron necessary for th

27 The performance of AgNRs as H2S gas sensor is investigated by its sensing ability of

28 used as experimental models, and GYY4137 as H2S donor.

29 containing 4-hydroxythiobenzamide moiety as H2S donor, were selected for further in vivo evaluation.

30 pendent on hydrogen/electron donors, such as H2S, NH3, organic acids and Fe(2+), that were in limited

31 le to catalyse the formation of VSCs such as H2S.

32 action sequence for sulfide oxidation being: H2S --> glutathione persulfide --> sulfite --> sulfate,

33 The reaction between H2S gas and the current sensor produces a visible color

34 enriched in the brain, was reported to bind H2S tightly and was postulated to play a role in modulat

35 ry into investigations focused on biological H2S.

36 od H2S, and LPS-induced attenuation of blood H2S (~60%) was prevented by Sul-121.

37 rophilia was inversely correlated with blood H2S, and LPS-induced attenuation of blood H2S (~60%) was

38 Relevant increases of BR-H2S suggest that those wines contained other H2S precurs

39 er doses could induce the accumulation of BR-H2S.

40 y, we investigated the regulation of CFTR by H2S.

41 Ferric neuroglobin is slowly reduced by H2S and catalyzes its inefficient oxidative conversion t

42 Signaling by H2S is proposed to occur via persulfidation, a posttrans

43 fluorescence response and also release caged H2S, thus addressing challenges of analyte homeostasis i

44 However, it is unknown whether the CBS/H2S axis plays a role in colorectal carcinogenesis.

45 results establish that activation of the CBS/H2S axis promotes colon carcinogenesis.

46 In conclusion, increasing cellular H2S is associated with significant antiviral activity ag

47 N2, Ar, CH4, Kr, Xe, C2H4, C2H6, CH3F, CO2, H2S, CH3Cl, CH3OCH3, CH3Br, CH3SH, CH3CH2Cl, CH2Cl2, CH3

48 f magnitude more sensitive than a commercial H2S test paper based on Pb(II)(acetate)2.

49 ellular H2S distributions provided by common H2S donor molecules AP39, ADT-OH, GYY4137, and diallyltr

50 into the subcellular distribution of common H2S donors and a useful tool for investigating H2S bioch

51 hat this approach can be coupled with common H2S-sensing motifs to generate scaffolds which, upon rea

52 fluorometric detection of highly competitive H2S and cyanide ion in aqueous DMSO media.

53 Complementing H2S modulation techniques, we also highlight current str

54 ping probes that do not irreversibly consume H2S.

55 pathway operates in mitochondria, converting H2S to thiosulfate and sulfate.

56 rhodanese, and sulfite oxidase and converts H2S to thiosulfate and sulfate.

57 quinone oxidoreductase (SQR), which converts H2S to a persulfide and transfers electrons to coenzyme

58 by structural modifications, and compare COS/H2S release rates and efficiencies from isomeric core st

59 also demonstrate the H2O2 dose-dependent COS/H2S release from each donor core, establish that release

60 s into the potential energy surfaces for COS/H2S release from each platform.

61 As a whole, the insights on COS/H2S release gained from these investigations provide a f

62 Each donor is designed to release COS/H2S after the activation of a trigger by activation by h

63 nsion of the emerging area of responsive COS/H2S donor systems.

64 We conclude that decrease H2S diminishes miR-194, induces collagen deposition and

65 d the TUNEL assay, we show that 3MST-derived H2S protects chromosomal DNA from oxidative damage.

66 A new approach in detecting H2S by the reduction of an azide to a triazene intermedi

67 zyme pathway in the mitochondrion detoxifies H2S by converting it to thiosulfate and sulfate.

68 ying hydrogen sulfide (hs-MB) with different H2S/C3F8 ratios (4/0, 3/1, 2/2, 1/3, 0/4) and determined

69 this detection platform to image endogenous H2S in Chinese hamster ovary (CHO) cells and use the dev

70 Although a transient increase in endogenous H2S production provides cytoprotection, its chronic incr

71 re, we demonstrate that increased endogenous H2S production or its exogenous administration modulates

72 ase (3MST) is the major source of endogenous H2S in Escherichia coli Cellular resistance to H2O2 stro

73 electrochemical quantification of endogenous H2S in living cells, thus hold great promise in the anal

74 monitoring and quantification of endogenous H2S production in E. coli were successfully accomplished

75 hers often use H2S donors to mimic enzymatic H2S synthesis or to provide increased H2S levels under s

76 ection of iminothioethers (ITEs), exhibiting H2S-releasing properties and producing vasorelaxing effe

77 or H2S imaging, we report here a fluorescent H2S detection platform (HSN2-BG) that is compatible with

78 ion in vivo Although a number of fluorescent H2S probes have been developed these are best suited to

79 of detection (LOD for NO = 0.16 ppm and for H2S = 0.23 ppm), these constitute the best textile-suppo

80 pid detection has also been demonstrated for H2S emission from aged wool fabric.

81 onclusion, we revealed a novel mechanism for H2S-mediated regulation of homocysteine metabolism in ca

82 ew broad and easily modifiable platforms for H2S donation, we report here the preparation and H2S rel

83 es, we also highlight current strategies for H2S detection and quantification.

84 Here we report a new strategy for H2S donation based on self-immolation of benzyl thiocarb

85 ite materials; and membrane technologies for H2S removal.

86 l signaling molecule, and chemical tools for H2S delivery and detection have emerged as important inv

87 To provide new chemical tools for H2S imaging, we report here a fluorescent H2S detection

88 After 7weeks of anoxia levels of free H2S and MeSH were high and similar regardless of the cop

89 ts: 1) immediate decrease the levels of free H2S and methanethiol (MeSH); 2) slow the rate at which f

90 thiol (MeSH); 2) slow the rate at which free H2S (not MeSH) increases during anoxic storage.

91 terize these more complex VSCs produced from H2S, we performed fermentations in synthetic grape juice

92 al conditions of increased levels of gaseous H2S and the concrete type.

93 l epithelial cells; the two gasotransmitters H2S and NO and their interaction may serve as therapeuti

94 s, including Escherichia (E.) coli, generate H2S and encounter high H2S levels particularly in the hu

95 key primary producers on Earth, use H2O, H2, H2S and other reduced inorganic compounds as electron do

96 a (E.) coli, generate H2S and encounter high H2S levels particularly in the human gut, herein we test

97 n wild-type animals exposed to lethally high H2S or in hif-1(ia04) mutants that die when exposed to l

98 al ratio to prepare stable hs-MB with higher H2S loading capability.

99 We speculate that SQRD-1 activity in H2S may coordinate proteostasis responses in multiple ce

100 icular, mitochondrial proteins implicated in H2S detoxification are downregulated, while the relative

101 GSH) were associated with small increases in H2S concentrations, with a maximum yield of 0.18% and 1.

102 sors, was associated with large increases in H2S in Shiraz wines.

103 ein is a highly conserved enzyme involved in H2S metabolism.

104 eview focuses on the recent progress made in H2S signaling that affects mechanistic and functional as

105 required to maintain protein translation in H2S.

106 ymatic H2S synthesis or to provide increased H2S levels under specific circumstances.

107 cystathionine, the product of CBS, inhibits H2S synthesis by the second enzyme, CSE.

108 l tools, as well as effective and innovative H2S donors for cardiovascular drug discovery.

109 Carbonic anhydrase converts COS into H2S, allowing NTAs to serve as either COS or H2S donors,

110 S donors and a useful tool for investigating H2S biochemistry.

111 The small volume of 1.35-L H2S is important, as the commercial Pb(II)(acetate)2-bas

112 teine and glutathione lower pH produced less H2S.

113 unds (OSCs) in the presence of percent-level H2S.

114 1(ia04) mutants that die when exposed to low H2S.

115 Decreased CSE-mediated H2S bioavailability is an underlying source of BMC dysfu

116 Ag2S formation, resulting from CSE-mediated H2S production in microglia, sequesters Ag(+) ions relea

117 the interplay between l-cysteine metabolism, H2S production, and oxidative stress, in which 3MST prot

118 n be used to assess changes in mitochondrial H2S levels in vivo As a proof of principle we used MitoA

119 to assess relative changes in mitochondrial H2S levels in vivo MitoA comprises a lipophilic tripheny

120 an indication of the levels of mitochondrial H2S in vivo Both compounds can be detected sensitively b

121 However, the significance of mitochondrial H2S is uncertain, in part due to the difficulty of asses

122 Experimental methods for modulating H2S levels, including enzymatic knockout, RNA silencing,

123 ymatic inhibition, and use of small molecule H2S donors are highlighted.

124 The sensor was employed to monitor H2S released from a mini-scale wastewater treatment tank

125 Moreover, H2S elicits cytoprotective effects against stressors in

126 Moreover, H2S promoted PYK2 sulfhydration and inhibited its activi

127 ifferentiate important gaseous analytes (NO, H2S, and H2O) at ppm levels and maintain their chemiresi

128 nt toxic chemicals, including NH3, SO2, NO2, H2S, and some volatile organic compounds, with particula

129 Our results unravel the existence of a novel H2S-NO interaction and identify PYK2 as a crucial target

130 We investigated the ability of H2S to relieve PYK2-mediated eNOS inhibition and evaluat

131 wnregulated, while the relative abundance of H2S microbial producers is increased.

132 Administration of H2S donor diallyl trisulfide (DATS) or overexpression of

133 Alteration of H2S metabolism may affect multiple signaling pathways an

134 d great promise in the analytical aspects of H2S.

135 residue to alanine promotes rapid binding of H2S and its efficient conversion to oxidized products.

136 scuss the biologically relevant chemistry of H2S and the enzymatic routes for its production and oxid

137 enzyme, might be due to the concentration of H2S by myoglobin in this tissue.

138 S release and increased the concentration of H2S in the myocardium and lung.

139 We hypothesized that delivery of H2S by ultrasound targeted microbubble destruction atten

140 fusion injury, however, systemic delivery of H2S may cause unwanted side effects.

141 Delivery of H2S to the myocardium by ultrasound targeted hs-MB destr

142 el approach for selective rapid detection of H2S gas using silver nanorods (AgNRs) arrays on glass su

143 monitor real-time colorimetric detection of H2S.

144 latforms were developed for the detection of H2S.

145 ble sensors for the in situ determination of H2S in a variety of environments.

146 robes are successful in the determination of H2S spiked in whole human blood, fetal bovine serum, and

147 The quantitative determination of H2S was based on the quenching of fluorescence intensity

148 the processes involved in the development of H2S and methanethiol (MeSH) along anoxic storage of wine

149 S but, lacking organelles, cannot dispose of H2S via the mitochondrial sulfide oxidation pathway.

150 However, effect of H2S or homocysteine on CBS and CSE expression, and cross

151 sink, and many of the biological effects of H2S relate to its interactions with mitochondria.

152 crucial target for the protective effects of H2S under conditions of oxidative stress.

153 physiological and pharmacological effects of H2S.

154 ent at 435 nm after reaction with 1 equiv of H2S due to the inhibition of PET.

155 s to provide researchers new to the field of H2S chemical biology with practical considerations, pitf

156 ys mediating the cytoprotective functions of H2S is not well understood.

157 KRI-1, plays a key role in the generation of H2S and ROS.

158 l related to the intracellular generation of H2S.

159 iple role in the 3MST-mediated generation of H2S.

160 is the predominant endothelial generator of H2S, and recent evidence suggests that its transcription

161 metabolic switch for transient induction of H2S production in the trans-sulfuration pathway.

162 cytes to H2O2 or pharmacologic inhibition of H2S production increased PYK2 (Y402) and eNOS (Y656) pho

163 and declined further after the inhibition of H2S production.

164 Together, inhibition of H2S-producing enzymes sensitize lung adenocarcinoma cell

165 In addition, inhibition of H2S-producing enzymes suppresses critical bioenergetics

166 to H2O2 Furthermore, the endogenous level of H2S is reduced in fur or sodA sodB cells but restored af

167 ation of vascular tone via the modulation of H2S production.

168 toward the sulfurization, in the presence of H2S gas with a minimal concentration in ppm range.

169 y toward Hg(0) vapor even in the presence of H2S.

170 l and multicolor emission in the presence of H2S.

171 The production of H2S during fermentation has also been associated in the

172 orm in probe SNAN-3, a much broader range of H2S can be detected.

173 Release of H2S triggered by ultrasound was investigated.

174 ths where acids are generated as a result of H2S oxidation in waters mixed upward from the anoxic dep

175 active biomolecule, and cover basic roles of H2S biogenesis and action.

176 To investigate the expanding roles of H2S in biology, researchers often use H2S donors to mimi

177 d by sodium hydrosulfide (NaHS), a source of H2S.

178 iency of CBS leads to chronic stimulation of H2S production.

179 ate level regulation favors the synthesis of H2S over persulfides.

180 ysteine and/or homocysteine for synthesis of H2S, a signaling molecule.

181 igher microbial production and less usage of H2S in subjects with halitosis.

182 Greater yields of H2S were obtained from the combined Cys/GSH and copper t

183 The effects of pH and Cu(2+) on H2S formation from known precursor compounds were subseq

184 h concentrations of methane (95% v/v) and/or H2S (20% v/v) had no effect (within 0.5 per thousand) on

185 H2S, allowing NTAs to serve as either COS or H2S donors, depending on the availability of the enzyme.

186 e endogenously produced by the epithelium or H2S-generating microflora.

187 hyl sulphide and methanethiol) in euxinic or H2S-rich seawaters that were widespread in Proterozoic c

188 Analysis of the pseudo-first-order H2S release rate under biologically relevant conditions

189 H2S suggest that those wines contained other H2S precursors non-detectable by the brine dilution meth

190 ke hemoglobin and myoglobin can also oxidize H2S to thiosulfate and hydropolysulfides.

191 e concentrations, ferric hemoglobin oxidizes H2S to a mixture of thiosulfate and iron-bound polysulfi

192 In diabetic mice, plasma H2S levels were decreased while ROS and expression of it

193 brown, and the sensor responds to >/= 30 ppb H2S in a total volume of 1.35 L of gas, a typical volume

194 -based paper requires large volumes of 5 ppm H2S gas.

195 cted as representative of slow and fast rate H2S donors, respectively, produced a complete recovery o

196 s reveal that HSNO is formed by the reaction H2S + N2O3 --> HSNO + HNO2, where N2O3 is a product of N

197 queous cadmium acetate solution via reactive H2S generation from l-cysteine and controls nanocrystal

198 eloping donors that are triggered to release H2S in response to stimuli and developing probes that do

199 Their ability to release H2S in vivo was recorded using a new fully validated UPL

200 esearch of original moieties able to release H2S represents a timely issue for drug discovery.

201 able donors that can be triggered to release H2S.

202 ns into dithiocarbamate cores, which release H2S directly upon H2O2-mediated activation.

203 phur salt Na2S as well as the slow-releasing H2S-liberating compound GYY4137 increased transmembrane

204 nine to cysteine and/or homocysteine renders H2S synthesis by CSE responsive to the known modulators

205 ide (DATS) or overexpression of CSE restored H2S production and enhanced cell survival and migratory

206 hionine to cysteine, transiently stimulating H2S production.

207 been investigated for their ability to store H2S in vivo and as a line of defense against oxidative s

208 oped constructs to report on the subcellular H2S distributions provided by common H2S donor molecules

209 ombining the adenine nucleus with a suitable H2S slow-releasing moiety, coupled via a stable ether bo

210 the gaseous biotransmitter hydrogen sulfide (H2S) and disulfides (RSSR) and/or sulfenic acids (RSOH).

211 hase (CBS) and its product hydrogen sulfide (H2S) are aberrantly upregulated in colorectal cancers, w

212 ified the gaseous molecule hydrogen sulfide (H2S) as the major effector molecule driving apneas.

213 own-regulation of cellular hydrogen sulfide (H2S) by 50% and of glutathione (GSH) by 40%.

214 Hydrogen sulfide (H2S) elicits pleiotropic physiological effects ranging f

215 Hydrogen sulfide (H2S) exhibits beneficial effects in the cardiovascular s

216 process for the removal of hydrogen sulfide (H2S) from low pressure biogas, the need arose to broaden

217 ensor for the detection of hydrogen sulfide (H2S) gas has been developed to replace commercial lead(I

218 Hydrogen sulfide (H2S) has been recognized as a signalling molecule which

219 Hydrogen sulfide (H2S) has long been known as a toxic gas.

220 ion of the gasotransmitter hydrogen sulfide (H2S) has recently been proposed as a novel targeted anti

221 Because hydrogen sulfide (H2S) inhibits high glucose-induced matrix protein increa

222 Hydrogen sulfide (H2S) is a biologically important small gaseous molecule

223 Hydrogen sulfide (H2S) is a hazardous gas, which not only harms living bei

224 Hydrogen sulfide (H2S) is a signaling molecule that is toxic at elevated c

225 Hydrogen sulfide (H2S) is an attractive agent for myocardial ischemia-repe

226 Hydrogen sulfide (H2S) is an endogenously produced gaseous molecule with i

227 Hydrogen sulfide (H2S) is an essential biological signaling molecule in di

228 Hydrogen sulfide (H2S) is an important biological signaling molecule, and

229 The gasotransmitter hydrogen sulfide (H2S) is an important tuner of the cardiovascular homeost

230 Hydrogen sulfide (H2S) is produced by yeast during winemaking and possesse

231 Hydrogen sulfide (H2S) is produced endogenously in vivo and has multiple e

232 The gasotransmitter, hydrogen sulfide (H2S) is recognized as an important mediator of endotheli

233 Hydrogen sulfide (H2S) is the most recently accepted endogenously produced

234 Hydrogen sulfide (H2S) regulates various physiological processes, includin

235 Endogenous hydrogen sulfide (H2S) renders bacteria highly resistant to oxidative stre

236 Hydrogen sulfide (H2S) was discovered as a third gasotransmitter in biolog

237 dium thiophosphate (TP) to hydrogen sulfide (H2S) which in the presence Cd(2+) ions yields CdS semico

238 Hydrogen sulfide (H2S), a cardioprotective gas, is endogenously produced f

239 Hydrogen sulfide (H2S), a novel gasotransmitter, is endogenously synthesiz

240 te the signaling molecule, hydrogen sulfide (H2S), from the amino acids cysteine and homocysteine.

241 Precursors to hydrogen sulfide (H2S), methanethiol (MeSH), ethanethiol (EtSH), and dimet

242 associated with decreased hydrogen sulfide (H2S), methanethiol, dimethyl sulfide, and carbon disulfi

243 The relationship between hydrogen sulfide (H2S), microRNAs (miRs), matrix metalloproteinases (MMPs)

244 dynamics based on oxygen, hydrogen sulfide (H2S), pH, dissolved inorganic carbon and total alkalinit

245 Buildup of hydrogen sulfide (H2S), which functions as a signaling molecule but is tox

246 carbon monoxide (CO), and hydrogen sulfide (H2S).

247 Hydrogen sulphide (H2S)-related metabolic pathways suggested that there was

248 roglial expression of the hydrogen sulphide (H2S)-synthesizing enzyme cystathionine-gamma-lyase (CSE)

249 actor operation at which 80% of the supplied H2S (61 mM d(-1)) was biologically oxidized to elemental

250 these constitute the best textile-supported H2S and NO detectors reported and the best MOF-based che

251 Red blood cells can synthesize H2S but, lacking organelles, cannot dispose of H2S via t

252 ed we have developed a mitochondria-targeted H2S probe, MitoA, which can be used to assess relative c

253 We conclude that H2S relieves the inhibitory effect of PYK2 on eNOS, allo

254 thors discuss current emerging evidence that H2S regulates mesenchymal stem cell and T-cell functions

255 These data indicate that H2S activates CFTR in Xenopus oocytes by inhibiting phos

256 ecently, we made a critical observation that H2S also has a protective role in paramyxovirus infectio

257 patic substrate concentrations predicts that H2S rather than Cys-SSH is the primary product of the tr

258 roof of principle we used MitoA to show that H2S levels increase in vivo during myocardial ischemia.

259 We show that H2S transiently increases phosphorylation of eukaryotic

260 recently accumulated evidence suggests that H2S contributes to a variety of physiologic and patholog

261 The H2S release rate of the hybrids and their ability to inc

262 The H2S-forming sulphur salt Na2S as well as the slow-releas

263 The H2S-induced increase in eIF2alpha phosphorylation was me

264 The H2S/C3F8 ratio of 2/2 was found to be an optimal ratio t

265 c cysteine mutant (C127S-PP1c) abrogated the H2S effect on eIF2alpha phosphorylation.

266 ophysiology of diseases where a role for the H2S pathway has been proposed and the development of new

267 However, the H2S reactivity of the coordinately saturated heme in neu

268 iviral and anti-inflammatory activity of the H2S slow-releasing donor GYY4137 on enveloped RNA viruse

269 Genetic ablation of the H2S-synthesizing enzyme cystathionine-gamma-lyase (CSE)

270 hibition and evaluated the importance of the H2S/PYK2/eNOS axis on cardiomyocyte injury in vitro and

271 h a gas inlet and a valve that transfers the H2S to a thermal conductivity detector (TCD), enables a

272 Thus, H2S recruits iNOS to generate NO to inhibit high glucose

273 bonyl sulfide, which is rapidly converted to H2S by carbonic anhydrase.

274 ich release COS that is quickly converted to H2S by the ubiquitous enzyme carbonic anhydrase.

275 and l-Cys desulfhydrase that degrades Cys to H2S, NH3, and pyruvate.

276 hytes are enzymes that also degrade l-Cys to H2S.

277 In sqrd-1 mutant animals, exposure to H2S leads to phosphorylation of eIF2alpha and inhibition

278 thyl disulfide - increased proportionally to H2S.

279 ulfide donor and whether its relationship to H2S is as a product or precursor is controversial.

280 ay correspond to a pro-secretory response to H2S which may be endogenously produced by the epithelium

281 annel, 1 was found to be highly selective to H2S in 50% aqueous buffer (pH 7).

282 a role in modulating neuronal sensitivity to H2S in conditions such as stroke.

283 Thus, high sensing ability of AgNRs toward H2S gas may have potential applications in health monito

284 ty and selectivity of the array AgNRs toward H2S.

285 g the reactivity of human neuroglobin toward H2S.

286 nd in neuroglobin caps its reactivity toward H2S and identifies by cryo-mass spectrometry a range of

287 e "turn-on" type fluorescent response toward H2S.

288 rasound targeted hs-MB destruction triggered H2S release and increased the concentration of H2S in th

289 les of H2S in biology, researchers often use H2S donors to mimic enzymatic H2S synthesis or to provid

290 od are demonstrated on a gas sample (10% v/v H2S) that was produced by pyrolysis of sulfur-rich kerog

291 In vivo, H2S administration reduced reactive oxygen species level

292 nal fibrosis in diabetes kidney, and whether H2S ameliorates fibrosis.

293 ssion of NOX4 and matrix protein and whether H2S and NO pathways are integrated.

294 ing AMPK in renal cells, we examined whether H2S inhibits high glucose-induced expression of NOX4 and

295 n, a posttranslational modification by which H2S is postulated to signal.

296 growing number of diverse targets for which H2S serves as a gasotransmitter has been extensively rev

297 Our data support a model in which H2S exerts its cytoprotective effect on ISR signaling by

298 o suggest that further reaction of HSNO with H2S may form HNO and HSSH.

299 generate scaffolds which, upon reaction with H2S, generate a fluorescence response and also release c

300 vivo There, the aryl azido group reacts with H2S to form an aryl amine (MitoN).