Noncanonical transnitrosylation network contributes to synapse loss in Alzheimer’s disease

 [possibly in the form of nitrosonium cation (NO+)] reacts with 

 [or, more precisely, thiolate anion (R-S−, where R is a protein)].

Gasotransmitters in pregnancy: from conception to uterine involution†

 and sulfide also covalently modify target protein 

Role of sulfiredoxin as a peroxiredoxin-2 denitrosylase in human iPSC-derived dopaminergic neurons

Significance S-nitrosylation, addition of an

Nitric oxide may inhibit neointimal hyperplasia by decreasing isopeptidase T levels and activity in the vasculature.

 can cause S-nitrosylation of active-site 

, we hypothesize that NO inhibits isopeptidase T activity through S-nitrosylation.

Transport rather than diffusion-dependent route for nitric oxide gas activity in alveolar epithelium.

 uptake was also concentration dependent.

Hypoxia Enhances S-Nitrosylation-Mediated NMDA Receptor Inhibition via a Thiol Oxygen Sensor Motif

 inhibits NMDAR activity by reacting with the NR2A subunit C399 along with two additional 

 if their disulfide bonds are reduced to free thiol groups [NR1(C744,C798); NR2(C87,C320)].

Inducible NO Synthase–Dependent S-Nitrosylation and Activation of Arginase1 Contribute to Age-Related Endothelial Dysfunction

 exerts its effects is by posttranslational modification through S-nitrosylation of 

S-Nitrosylation and uncompetitive/fast off-rate (UFO) drug therapy in neurodegenerative disorders of protein misfolding

 groups to form S-nitrosothiols and thus change protein function.

Nitric oxide-induced persistent inhibition and nitrosylation of active site cysteine residues of mitochondrial cytochrome-c oxidase in lung endothelial cells.

These results demonstrate for the first time that

 of complex IV, which is associated with persistent inhibition of complex IV.

Design and synthesis of 3'- and 5'-O-(3-benzenesulfonylfuroxan-4-yl)-2'-deoxyuridines: biological evaluation as hybrid nitric oxide donor-nucleoside anticancer agents.

 donor-nucleoside conjugates in the presence of 18 mM 

 released a high percentage of *NO (21-48% at 1 h; 37-86% at 16 h).

Calcium regulates S-nitrosylation, denitrosylation, and activity of tissue transglutaminase.

 modifies proteins through nitrosylation of 

, and such modifications are important in mediating NO's biologic activity.

Inducible nitric oxide synthase-derived nitric oxide in gene regulation, cell death and cell survival.

Indeed, due to its S-nitrosating activity in the presence of oxygen,

 can modify the activity of transcription factors containing zinc finger motifs or 

Nitric oxide and macrophage function.

The antimicrobial and cytotoxic actions of

 are enhanced by other macrophage products such as acid, glutathione, 

Cysteine immobilisation on the polyethylene terephthalate surfaces and its effect on the haemocompatibility

Stability studies showed that the immobilised

 release reduced within 6 h. Immobilisation of cysteine derivatives eliminated the possibility of formation of polycysteine and its electrostatic interaction with the carboxylated PET.

Design, Synthesis, and Investigation of Novel Nitric Oxide (NO)-Releasing Prodrugs as Drug Candidates for the Treatment of Ischemic Disorders: Insights into NO-Releasing Prodrug Biotransformation and Hemoglobin-NO Biochemistry.

 (1.8-9.3%) or human serum (2.3-52.5%) and also reduced the affinity of Hb for … blood (ΔP50 of 4.9-21.7 mmHg vs ΔP50 of 25.4-32.1 mmHg for RSR13).

Proteomic Analyses for the Global S-Nitrosylated Proteins in the Brain Tissues of Different Human Prion Diseases

Protein S-nitrosylation, the covalent adduction of a

, plays a role in human brain biology, and brain dysfunction is a prominent feature of prion disease, yet the direct brain targets of S-nitrosylation are largely unknown.

Synthesis, nitric oxide release, and α-glucosidase inhibition of nitric oxide donating apigenin and chrysin derivatives.

All organic nitrate derivatives released low concentrations of

Cysteine 96 of Ntcp is responsible for NO-mediated inhibition of taurocholate uptake.

 (NO) inhibits TC uptake through S-nitrosylation of a 

Sulfide‐ and nitrite‐dependent nitric oxide production in the intestinal tract

We have found that the addition of a reduced sulfur compound, i.e.

Furoxan nitric oxide donor coupled chrysin derivatives: synthesis and vasculoprotection.

Furthermore, the compounds released a low amount of

Estradiol-17beta stimulates specific receptor and endogenous nitric oxide-dependent dynamic endothelial protein S-nitrosylation: analysis of endothelial nitrosyl-proteome.

 [S-nitrosylation (S-NO)] is emerging as a key route for nitric oxide (NO) to directly modulate protein functions.

Inhibition of the transcription factor Yin Yang 1 activity by S-nitrosation.

YY1 is a zinc finger protein and thus, we hypothesized that

 inhibits YY1 activity via S-nitrosation of critical 

Nitric oxide inhibits cornified envelope formation in human keratinocytes by inactivating transglutaminases and activating protein 1.

Titration of thiol groups of transglutaminases indicated that

 regulates their enzymatic activity by chemically modifying a 

An Antiviral Mechanism of Nitric Oxide

 residue in the active site of protease 3C, inhibiting protease activity and interrupting the viral life cycle.

Nitric oxide induces Zn2+ release from metallothionein by destroying zinc-sulphur clusters without concomitant formation of S-nitrosothiol.

 is reinvestigated and it is found that cysteine is quantitatively converted to cystine after 5 min of NO treatment at pH 7.3.

A redox-based mechanism for induction of interleukin-1 production by nitric oxide in a human colonic epithelial cell line (HT29-Cl.16E).

is implicated in the IL-1 alpha production: (i) SIN-1, devoid of any NO+ character, … IL-1 production as compared with SNP; (ii) the reductive action of a thiol such as

, concentration, measured as NO2-/NO3- … decrease in IL-1 production.

Nitric oxide inhibits aromatase activity: Mechanisms of action

 has been reported to alter protein function by reacting with the sulfhydryl group of 

Detection of human IgG antibodies against free N-acetyl-L-cysteine.

 and homocysteine is frequently reduced after 

Plasma cysteine concentrations in infants with respiratory distress.

 and as a precursor of glutathione may be relevant to the pathogenesis and evolution of PPHN and respiratory distress syndrome.

Sodium nitroprusside induces H‐Ras depalmitoylation and alters the cellular response to hypoxia in differentiated and undifferentiated PC12 cells

, which induce H‐Ras activity dysregulation and alter the cellular response to hypoxia.

Identification of novel S-nitrosation sites in soluble guanylyl cyclase, the nitric oxide receptor.

 via a post-translational modification termed S-nitrosation or S-nitrosylation.

Synthesis of organic nitrates of luteolin as a novel class of potent aldose reductase inhibitors.

Allosteric modulation by S-nitrosation in the low-O₂ affinity myoglobin from rainbow trout.

 may generate S-nitroso Mb (Mb-SNO) and contribute further to 

Nitric oxide activates Nrf2 through S-nitrosylation of Keap1 in PC12 cells.

 can modify the function or activity of target proteins through S-nitrosylation of 

, we attempted to investigate whether the cytoprotective effect of NO is mediated through Nrf2 activation by directly modifying cysteine residues of Keap1.

Regulatory Effect of Cinnamaldehyde on Monocyte/Macrophage-Mediated Inflammatory Responses

In particular, thiol compounds with sulphydryl group,

 and dithiothreitol (DTT), strongly abrogated CA-mediated 

Glucocorticoids suppress cystathionine gamma-lyase expression and H2S production in lipopolysaccharide-treated macrophages

Modulation of Cx46 hemichannels by nitric oxide.

We conclude that Cx46 hemichannels are sensitive to NO and that the

 effects are mediated by modification of one or more intracellular 

Persistent susceptibility of cathepsin B to irreversible inhibition by nitroxyl (HNO) in the presence of endogenous nitric oxide.

Additionally, endogenous cellular production of

 could rescue enzyme function by protective nitrosation of 

Effect of staurosporine-induced apoptosis on endothelial nitric oxide synthase in transfected COS-7 cells and primary endothelial cells

) may block apoptosis by inhibiting caspases via S-nitrosylation of 

Nitric oxide-induced resistance to hydrogen peroxide stress is a glutamate cysteine ligase activity-dependent process.

Altered thiol metabolism was observed immediately after 

 exposure as demonstrated by up to 75% decrease in intracellular thiol pools (glutathione, gamma-glutamylcysteine, and 

), which then reaccumulated during the *NO-mediated development of resistance.

Synthesis and biological evaluation of 3,4-diphenyl-1,2,5-oxadiazole-2-oxides and 3,4-diphenyl-1,2,5-oxadiazoles as potential hybrid COX-2 inhibitor/nitric oxide donor agents.

Release of nitric oxide (NO) from the 3,4-diphenylfuroxan compounds (…, 13a,b, 16, 17) was thiol-dependent since the %

 released was higher upon … in the presence of 

 (0.57-3.18%) compared to that in phosphate buffer solution at pH7.4 (0.06-0.15%).

New Insights into Protein S-Nitrosylation

 (NO) are in significant part mediated through S-nitrosylation of 

Nitric Oxide Exposure of CC531 Rat Colon Carcinoma Cells Induces γ-glutamyltransferase which May Counteract Glutathione Depletion and Cell Death

Cells with induced GGT activity obtained after

 incubation showed a higher uptake rate of 

 (2-fold), measured by incubating the cells with 35 S-radiolabeled GSH.

A putative role for S-nitrosoglutathione as the source of nitric oxide in photorelaxation of the mouse gastric fundus.

 inhibited responses to UV irradiation and exogenous 

, but not in the presence of exogenous Cu(2+)/Zn(2+) superoxide dismutase.

Mechanisms of Hepatoprotection by Nitric Oxide

 inhibits cell death or apoptosis by modulation of heat shock proteins, S‐nitrosylation of caspases at their catalytic site 

 residue, triggering of the cGMP pathway, and prevention of mitochondrial dysfunction.

Role of the arginine-nitric oxide pathway in the regulation of vascular smooth muscle cell proliferation

Experiments with purified, recombinant mammalian ODC revealed that

 inhibits ODC possibly by S-nitrosylation of the active site 

Vascular smooth muscle relaxation mediated by nitric oxide donors: a comparison with acetylcholine, nitric oxide andnitroxyl ion

 (3 mM), inhibited responses to Angeli's salt, acetylcholine and the three 

Differential actions of L‐cysteine on responses to nitric oxide, nitroxyl anions and EDRF in the rat aorta

 and sodium nitroprusside may be attributed to the formation of S‐nitrosocysteine.

Intrathecal S-nitroso-N-acetylpenicillamine and l-cysteine attenuate nerve injury-induced allodynia through noradrenergic activation in rats

, carboxy-PTIO, or depletion of norepinephrine with a specific neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine, prevented the antiallodynic action of intrathecal S-nitroso-N-acetylpenicillamine and 

 is capable of stimulating neuronal norepinephrine release in the presence of thiol-containing compounds such as 

Methionine Adenosyltransferase S-Nitrosylation Is Regulated by the Basic and Acidic Amino Acids Surrounding the Target Thiol*

 inactivates methionine adenosyltransferase viaS-nitrosylation of 

Synergism of Nitric Oxide and Iron in Killing the Transformed Murine Oligodendrocyte Cell Line N20.1

However, dithiothreitol protected against both SNAP and SNP, indicating that S‐nitrosylation of

 plays a major role in the cytotoxicity of both 

Role of glutathione in nitric oxide‐dependent regulation of energy metabolism in rat hepatoma cells

 on the respiration of digitonin‐treated cells was suppressed by either GSH, l 

, or N‐acetylcysteine, but not by oxidized glutathione.

Blockade of nitric oxide-induced relaxation of rabbit aorta by cysteine and homocysteine.

 reduced the SH concentrations of both the supernatant of aortic homogenate and 

 or HoCys on relaxation responses to subsequent additions of 

Water soluble furoxan derivatives as NO prodrugs.

 under physiological conditions (pH 7.4; 37 degrees C).

Salivary thiol oxidase activity of Rhodnius prolixus.

 and other thiol compounds can accelerate the unloading of 

 (NO) from salivary nitrosyl-nitrophorins of the blood sucking bug Rhodnius prolixus.

 concentration is biphasic, showing a maximum between 0.5 and 1 mM cysteine.

Inhibition by nitric oxide of the repair protein, O6-methylguanine-DNA-methyltransferase.

 under aerobic conditions resulted in the formation of an S-nitrosothiol adduct, suggesting that a similar adduct could be responsible for the inactivation.

Pharmacological similarity between nitric oxide and the nitrergic neurotransmitter in the canine ileocolonic junction.

 (1 microM) inhibited the biological activity of both the transferable nitrergic … the canine ileocolonic junction in response to NANC nerve stimulation and 

, but not that of S-nitroso-L-cysteine, … or S-nitroso-N-acetyl-D,L-penicillamine.

In organ bath experiments, pyrogallol (30-100 microM), and to a lesser extent

 (NO)-induced relaxation, but not the NO-mediated non-adrenergic non-cholinergic (NANC) relaxation elicited by field stimulation of the canine ileocolonic junction.

Structure activity relationships of peroxynitrite scavengers an approach to nitric oxide neurotoxicity.

Understanding the controversy over the identity of EDRF

 revealed major differences between the remaining candidates because it reduced the effect of authentic 

 and EDRF on the bioassay tissues but enhanced the survival of S-nitrosocysteine and S-nitroso-cysteamine.

Inhibition by sulfhydryl compounds of vascular relaxation induced by nitric oxide and endothelium-derived relaxing factor.

In a perfusion-bioassay system in which EDRF was released … from endothelium of a perfused segment of rabbit aorta,

 and DTT (20 microM), but not GSH, infused into the perfusate between … and an endothelium-denuded bioassay ring, partially inhibited relaxation by the 

In organ chamber experiments, the large transient relaxation of endothelium-denuded rings produced by 75 nM nitric oxide 

) was partially inhibited in a concentration-dependent manner by 

Nitric oxide-independent, thiol-associated ADP-ribosylation inactivates aldehyde dehydrogenase.

 inhibits the activity of glyceraldehyde-3-phosphate dehydrogenase and stimulates NAD-dependent automodification of a 

 (Dimmeler, S., Lottspeich, F., and Brüne, B. (1992) J. Biol.

L-cysteine augments the vasorelaxation induced by sodium nitrite and SIN-1 but not that due to acetylcholine.

Role of intracellular thiols in release of EDRF from cultured endothelial cells.

The availability of intracellular reduced thiols, such as

 or glutathione (GSH), may be critically important for the biosynthesis of 

On the Mechanism of NO Release from Sydnonimines

 induced a marked shift from NO3− to NO2− with a small reduction in 

 release, which is paralleled by a weak rightward shift of the EC50 at the guanylate cyclase.

S‐nitrosothiols as vasodilators: implications regarding tolerance to nitric oxide‐containing vasodilators

 were attenuated in the presence of N‐acetylcysteine, 

Nitric Oxide Regulates Macrophage Fungicidal Activity via S-nitrosylation of Dectin-1

 in pattern recognition molecules to disassemble and alter protein function.

S-nitrosothiols function during abiotic stress in plants.

S-nitrosation is a reversible redox NO-PTM consisting of the addition of

 (Cys) residue leading to S-nitrosothiols (SNOs) formation.

Contribution of nitric oxide and protein S-nitrosylation to variation in fresh meat quality.

 exerts these pleiotropic effects mainly through the covalent attachment to the sulfhydryl group of 

 to form S-nitrosothiol (protein S-nitrosylation).

NO-sGC Pathway Modulates Ca2+ Release and Muscle Contraction in Zebrafish Skeletal Muscle

 post-translationally modifies proteins via S-nitrosylation of the thiol group of 

Nitric Oxide Alleviates Salt Stress Inhibited Photosynthetic Performance by Interacting with Sulfur Assimilation in Mustard

The enhanced S-assimilation of these plants receiving

 plus S resulted in increased production of cysteine (

Now we NO.

 residue to form an S-nitrosothiol adduct, which has also been observed in some haem proteins9,10.

Linking omentum and ovarian cancer: NO

The post-translational modification of metabolic enzymes caused by binding of

 residue (s-nitrosylation) may play a crucial role.

Potential role of glutathione in evolution of thiol-based redox signaling sites in proteins

 is susceptible to a variety of modifications by reactive oxygen and 

 species, including glutathionylation; and when two cysteines are involved, disulfide formation.

S-nitrosothiols regulate nitric oxide production and storage in plants through the nitrogen assimilation pathway

An important mechanism by which NO regulates plant development and stress responses is through S-nitrosylation, i.e. covalent attachment of

Mechanisms of Nitrosylation and Denitrosylation of Cytoplasmic Glyceraldehyde-3-phosphate Dehydrogenase from Arabidopsis thaliana*

 is a reversible post-translational modification of 

 playing a major role in cellular regulation and signaling in many organisms, including plants where it has been implicated in the regulation of immunity and cell death.

Nitric oxide suppresses growth and development in the unicellular green alga Micrasterias denticulata.

 inhibits activity of enzymes involved in the secretory pathway, such as GAPDH, via S-nitrosylation of the 

 residue and, consequently, modulates cell growth in M. denticulata.

S‐nitrosylated proteins of a medicinal CAM plant Kalanchoe pinnata– ribulose‐1,5‐bisphosphate carboxylase/oxygenase activity targeted for inhibition

 post‐translationally modifies proteins by S‐nitrosylation of 

NO-mediated cytoprotection: instant adaptation to oxidative stress in bacteria.

 transiently suppresses the enzymatic reduction of 

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Possible Interaction: Cysteine and Nitric Oxide

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