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1. Full Text S-Nitrosylation of Drp1 Mediates β-Amyloid: Related Mitochondrial Fission and Neuronal Injury
by Dong-Hyung Cho and Tomohiro Nakamura and Jianguo Fang and Piotr Cieplak and Adam Godzik and Zezong Gu and Stuart A. Lipton
Science, ISSN 0036-8075, 4/2009, Volume 324, Issue 5923, pp. 102 - 105
Mitochondria continuously undergo two opposing processes, fission and fusion. The disruption of this dynamic equilibrium may herald cell injury or death and... 
Oligomers | Brain | Mitochondria | HEK293 cells | Neurons | Cell death | Cell lines | Reports | Dimers | CHO cells | Dimerization | APOPTOSIS | PROTEIN | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | NITRIC-OXIDE | NEURODEGENERATION | DYNAMIN | Microtubule-Associated Proteins - chemistry | Cysteine - analogs & derivatives | Microtubule-Associated Proteins - metabolism | Amyloid beta-Peptides - pharmacology | Humans | Protein Multimerization | Male | Peptide Fragments - pharmacology | Cerebral Cortex - cytology | Mitochondria - ultrastructure | Alzheimer Disease - pathology | Cysteine - genetics | GTP Phosphohydrolases - chemistry | Neurons - ultrastructure | Mitochondrial Proteins - metabolism | Amyloid beta-Peptides - metabolism | Cysteine - pharmacology | Female | Cysteine - metabolism | Neurons - drug effects | Protein Structure, Tertiary | Cell Line | S-Nitrosothiols - pharmacology | Peptide Fragments - metabolism | Models, Molecular | Mice, Transgenic | Mitochondria - drug effects | Amino Acid Motifs | Animals | GTP Phosphohydrolases - metabolism | Alzheimer Disease - metabolism | Mitochondrial Proteins - chemistry | Cell Line, Tumor | Mice | Mutation | Mitochondria - physiology | Nitric Oxide - metabolism | Index Medicus
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2. Full Text S-Nitrosylation of Peroxiredoxin II E Promotes Peroxynitrite-Mediated Tyrosine Nitration
by Maria C. Romero-Puertas and Miriam Laxa and Alessandro Mattè and Federica Zaninotto and Iris Finkemeier and Alex M. E. Jones and Michele Perazzolli and Elodie Vandelle and Karl-Josef Dietz and Massimo Delledonne
The Plant Cell, ISSN 1040-4651, 12/2007, Volume 19, Issue 12, pp. 4120 - 4130
Nitric oxide (NO) is a free radical product of cell metabolism that plays diverse and important roles in the regulation of cellular function. S-Nitrosylation... 
Nitration | Leaves | Gels | Cell death | Antibodies | Oxides | Lipids | Plants | Nitrogen | Plant cells | APOPTOSIS | ARABIDOPSIS-THALIANA | DEFENSE RESPONSES | BIOCHEMISTRY & MOLECULAR BIOLOGY | DISEASE RESISTANCE RESPONSE | TOBACCO | PLANT SCIENCES | CELL BIOLOGY | REACTIVE NITROGEN | 2-CYS PEROXIREDOXIN | SIGNALING PATHWAY | NITRIC-OXIDE | REDUCTASE | Arabidopsis Proteins - genetics | Peroxiredoxins - metabolism | Arabidopsis - metabolism | Peroxiredoxins - chemistry | Arabidopsis - genetics | Arabidopsis Proteins - metabolism | Nitrates - metabolism | Tandem Mass Spectrometry | Nitrates - chemistry | Tyrosine - metabolism | Peroxiredoxins - genetics | Arabidopsis Proteins - chemistry | Models, Biological | Plants, Genetically Modified | Peroxynitrous Acid - metabolism | Chromatography, Liquid | Peroxynitrous Acid - chemistry | Lipid Peroxidation | Post-translational modification | Arabidopsis thaliana | Tyrosine | Evaluation | Nitric oxide | Physiological aspects | Peroxidase | Index Medicus
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3. Full Text On—off system for PI3-kinase—Akt signaling through S-nitrosylation of phosphatase with sequence homology to tensin (PTEN)
by Naoki Numajiri and Kumi Takasawa and Tadashi Nishiya and Hirotaka Tanaka and Kazuki Ohno and Wataru Hayakawa and Mariko Asada and Hiromi Matsuda and Kaoru Azumi and Hideaki Kamata and Tomohiro Nakamura and Hideaki Hara and Masabumi Minami and Stuart A. Lipton and Takashi Uehara
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2011, Volume 108, Issue 25, pp. 10349 - 10354
Nitric oxide (NO) physiologically regulates numerous cellular responses through S-nitrosylation of protein cysteine residues. We performed antibody-array... 
Phosphorylation | Phosphatases | Low concentrations | Neurons | Antibodies | Oxides | Oxidation | Gene expression regulation | Penumbra | Endothelial cells | Ischemia | Apoptosis | SURVIVAL | MULTIDISCIPLINARY SCIENCES | oxidation | apoptosis | NEURONAL CELL-DEATH | AKT | TUMOR-SUPPRESSOR PTEN | AKT/PROTEIN KINASE-B | ischemia | NITRIC-OXIDE PRODUCTION | INHIBITION | PATHWAY | ENDOTHELIAL-CELLS | PARKINSONS-DISEASE | PTEN Phosphohydrolase - genetics | Humans | PTEN Phosphohydrolase - metabolism | Neurons - cytology | Phosphatidylinositol 3-Kinases - metabolism | Proto-Oncogene Proteins c-akt - genetics | Phosphatidylinositol 3-Kinases - genetics | Sequence Homology | Animals | HEK293 Cells | Neurons - physiology | Signal Transduction - physiology | Mice | Protein Processing, Post-Translational | Enzyme Activation | Nitric Oxide - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Nitrogen oxide | Physiological aspects | Cysteine | Cellular signal transduction | Research | Protein kinases | Brain | Signal transduction | Enzyme kinetics | Nitric oxide | Rodents | Cells | Index Medicus | Biological Sciences
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4. Full Text S-nitrosylation of Bcl-2 inhibits its ubiquitin-proteasomal degradation: A novel antiapoptotic mechanism that suppresses apoptosis
by Azad, Neelam and Vallyathan, Val and Wang, Liying and Tantishaiyakul, Vimon and Stehlik, Christian and Leonard, Stephen S and Rojanasakul, Yon
Journal of Biological Chemistry, ISSN 0021-9258, 11/2006, Volume 281, Issue 45, pp. 34124 - 34134
Bcl-2 is a key apoptosis regulatory protein of the mitochondrial death pathway whose function is dependent on its expression levels. Although Bcl-2 expression... 
CYTOCHROME-C | LUNG-CANCER | CELLS | PHOSPHORYLATION | NITRIC-OXIDE SYNTHASE | PROTEIN-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CHROMIUM(VI)-INDUCED APOPTOSIS | FAS | UP-REGULATION | EXPRESSION | Immunoprecipitation | Mutagenesis, Site-Directed | Apoptosis - drug effects | Nitric Oxide - pharmacology | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Blotting, Western | Proto-Oncogene Proteins c-bcl-2 - metabolism | Caspases - metabolism | Flow Cytometry | Nitroso Compounds - metabolism | Transfection | Plasmids | Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors | Chromates - pharmacology | Protein Processing, Post-Translational | Apoptosis - physiology | Mutation | Proteasome Inhibitors | Proto-Oncogene Proteins c-bcl-2 - genetics | Ubiquitins - antagonists & inhibitors | Ubiquitins - metabolism | Index Medicus
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5. Full Text S-Nitrosylation activates Cdk5 and contributes to synaptic spine loss induced by β-amyloid peptide
by Jing Qu and Tomohiro Nakamura and Gang Cao and Emily A. Holland and Scott R. McKercher and Stuart A. Lipton
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 8/2011, Volume 108, Issue 34, pp. 14330 - 14335
The activity of Cdk5 and its regulatory subunit p35 is thought to be important in both normal brain function and neurodegenerative disease pathogenesis.... 
Dendritic spines | Brain | Phosphorylation | Neuroscience | HEK293 cells | Neurodegenerative diseases | Neurons | Histones | Physiological regulation | Alzheimers disease | OXIDATIVE STRESS | PROTEIN | P35 | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | NEURONAL NITRIC-OXIDE | CYCLIN-DEPENDENT KINASE-5 | MITOCHONDRIAL FISSION | CELL-DEATH | PARKINSONS-DISEASE | Synapses - drug effects | Dynamins - metabolism | Amyloid beta-Peptides - toxicity | Apoptosis - drug effects | Nitric Oxide - pharmacology | Humans | Brain - enzymology | Rats | Alzheimer Disease - enzymology | Enzyme Activation - drug effects | Mutation - genetics | Alzheimer Disease - pathology | Cyclin-Dependent Kinase 5 - metabolism | N-Methylaspartate - pharmacology | Brain - drug effects | Animals | Synapses - metabolism | Dendritic Spines - drug effects | Dendritic Spines - pathology | Nitrosation - drug effects | HEK293 Cells | Brain - pathology | Cysteine - metabolism | Index Medicus | Biological Sciences
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6. Full Text Simultaneous Measurement of Protein Oxidation and S-Nitrosylation During Preconditioning and Ischemia/Reperfusion Injury With Resin-Assisted Capture
by Kohr, Mark J and Sun, Junhui and Aponte, Angel and Wang, Guanghui and Gucek, Marjan and Murphy, Elizabeth and Steenbergen, Charles
Circulation Research, ISSN 0009-7330, 02/2011, Volume 108, Issue 4, pp. 418 - 426
RATIONALE:Redox modifications play an important role in many cellular processes, including cell death. Ischemic preconditioning (IPC) has been shown to involve... 
ischemic preconditioning | S-nitrosothiol | reactive oxygen species | SIGNAL | CARDIAC & CARDIOVASCULAR SYSTEMS | NITROSATION | REPERFUSION | ISCHEMIA | CARDIOMYOCYTES | MASS-SPECTROMETRY | THIOLS | NITRIC-OXIDE | PERIPHERAL VASCULAR DISEASE | CARDIOPROTECTION | STRESS | HEMATOLOGY | Oxidation-Reduction | Male | Resins, Synthetic - metabolism | S-Nitrosothiols - metabolism | Myocardial Reperfusion Injury - metabolism | Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating) - metabolism | Animals | Proteins - metabolism | Myocardium - metabolism | Ischemic Preconditioning, Myocardial - methods | Models, Animal | Cysteine - metabolism | Mice | Myocardial Reperfusion Injury - prevention & control | Index Medicus
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7. Full Text S-Nitrosylation of Sarcomeric Proteins Depresses Myofilament Ca2+ Sensitivity in Intact Cardiomyocytes
by Figueiredo-Freitas, Cícero and Dulce, Raul A and Foster, Matthew W and Liang, Jingsheng and Yamashita, Aline M.S and Lima-Rosa, Frederico L and Thompson, J. Will and Moseley, M. Arthur and Hare, Joshua M and Nogueira, Leonardo and Sorenson, Martha M and Pinto, José Renato
Antioxidants & Redox Signaling, ISSN 1523-0864, 11/2015, Volume 23, Issue 13, pp. 117 - 1034
Aims: The heart responds to physiological and pathophysiological stress factors by increasing its production of nitric oxide (NO), which reacts with... 
Original Research Communications | PHOSPHORYLATION | DESENSITIZATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | CARDIOMYOPATHY | ENDOCRINOLOGY & METABOLISM | NITRIC-OXIDE | MUSCLE | PROTEOMIC ANALYSIS | DENITROSYLATION | NITROSOCYSTEINE | STATISTICAL-MODEL | PROTECTS | Myocardial Contraction | Cysteine - analogs & derivatives | Oxidative Stress | Ca(2+) Mg(2+)-ATPase - metabolism | Mice, Inbred C57BL | Cells, Cultured | Mice, 129 Strain | S-Nitrosothiols - metabolism | Animals | Muscle Proteins - metabolism | Myocytes, Cardiac - metabolism | Cysteine - metabolism | Myofibrils - metabolism | Nitric Oxide - metabolism | Calcium Signaling | Sarcomeres | Proteins | Physiology, Pathological | Research | Analysis | Heart cells | Index Medicus
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8. Full Text Protein S-Nitrosylation Controls Glycogen Synthase Kinase 3β Function Independent of its Phosphorylation State
by Wang, Sheng-Bing and Venkatraman, Vidya and Crowgey, Erin L and Liu, Ting and Fu, Zongming and Holewinski, Ronald and Ranek, Mark and Kass, David A and O’Rourke, Brian and Van Eyk, Jennifer E
Circulation Research, ISSN 0009-7330, 03/2018, Volume 122, Issue 11, pp. 1517 - 1531
RATIONALE:Glycogen synthase kinase 3β (GSK3β) is a multifunctional and constitutively active kinase known to regulate a myriad of cellular processes. The... 
glycogen synthase kinase 3 beta | redox regulation | nuclear translocation | kinase-substrates interactome | S-nitrosylation | CARDIAC & CARDIOVASCULAR SYSTEMS | HEART-FAILURE | GSK-3-BETA | SUBCELLULAR-LOCALIZATION | KINASE-3-BETA | INACTIVATION | INSULIN | HYPERTROPHY | GSK3 | NITRIC-OXIDE | PERIPHERAL VASCULAR DISEASE | INHIBITORS | HEMATOLOGY | Heart failure | Neonates | Phosphorylation | Splicing | Cardiac muscle | Glycogen | Serine | DNA damage | Glycogen synthase kinase 3 | Amino acid sequence | Myocytes | Kinases | Ribonucleic acid--RNA | Nuclear transport | Myoblasts | Conserved sequence | Cell cycle | Protein S | Ventricle | Localization | Heart diseases | Cytoplasm | animal model cardiovascular disease | Glycogen synthase kinase 3 beta | proteomics | cell signaling
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9. Full Text Measurement of S-Nitrosylation Occupancy in the Myocardium With Cysteine-Reactive Tandem Mass Tags: Short Communication
by Kohr, Mark J and Aponte, Angel and Sun, Junhui and Gucek, Marjan and Steenbergen, Charles and Murphy, Elizabeth
Circulation Research, ISSN 0009-7330, 10/2012, Volume 111, Issue 10, pp. 1308 - 1312
RATIONALE:S-nitrosylation (SNO) is a reversible, thiol-based protein modification that plays an important role in the myocardium by protecting critical... 
ischemic preconditioning | oxidation | occupancy | S-nitrosylation | CARDIAC & CARDIOVASCULAR SYSTEMS | PERIPHERAL VASCULAR DISEASE | PROTEINS | HEMATOLOGY | S-Nitrosoglutathione - analysis | Myocardium - chemistry | Oxidation-Reduction | Cysteine - analysis | Mice, Inbred C57BL | Male | S-Nitrosoglutathione - metabolism | Ischemic Preconditioning - methods | Myocardial Reperfusion Injury - metabolism | Sulfhydryl Compounds - analysis | Sulfhydryl Compounds - metabolism | Animals | Perfusion | Myocardium - metabolism | Cysteine - metabolism | Mice | Tandem Mass Spectrometry - methods | Index Medicus
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10. Full Text Inhibition of NF-κB by S-nitrosylation
by Marshall, H.E and Stamler, J.S
Biochemistry, ISSN 0006-2960, 02/2001, Volume 40, Issue 6, pp. 1688 - 1693
It is not clear if redox regulation of transcription is the consequence of direct redox-related modifications of transcription factors, or if it occurs at some... 
ACTIVATION | MECHANISM | NITROSATIVE STRESS | REDOX REGULATION | NITRIC-OXIDE SYNTHASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | ALPHA | INDUCTION | EXPRESSION | P50 SUBUNIT | DNA-BINDING ACTIVITY | Cysteine - analogs & derivatives | Transcription, Genetic - drug effects | Humans | Nitric Oxide Synthase - antagonists & inhibitors | NF-kappa B - metabolism | DNA-Binding Proteins - metabolism | Nitroso Compounds - pharmacology | Nitroso Compounds - metabolism | Transfection | Protein Binding - drug effects | Cysteine - pharmacology | Mercaptoethanol | Cysteine - metabolism | Cell Line | NF-KappaB Inhibitor alpha | NF-kappa B - antagonists & inhibitors | DNA-Binding Proteins - antagonists & inhibitors | NF-kappa B p50 Subunit | Enzyme Inhibitors - pharmacology | I-kappa B Proteins | DNA - metabolism | Down-Regulation - drug effects | DNA - antagonists & inhibitors | Animals | NF-kappa B - genetics | NF-kappa B - isolation & purification | Active Transport, Cell Nucleus - drug effects | Nitrosation - drug effects | NF-kappa B - physiology | Mice | Nitric Oxide Synthase - metabolism | S-Nitrosothiols | Cytokines - pharmacology | S-nitrosocysteine | dithiothreitol | Index Medicus
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11. Full Text S-Nitrosylation of Cofilin-1 Mediates Estradiol-17β-Stimulated Endothelial Cytoskeleton Remodeling
by Zhang, Hong-hai and Lechuga, Thomas J and Tith, Tevy and Wang, Wen and Wing, Deborah A and Chen, Dong-bao
Molecular Endocrinology, ISSN 0888-8809, 03/2015, Volume 29, Issue 3, pp. 434 - 444
Rapid nitric oxide (NO) production via endothelial NO synthase (eNOS) activation represents a major signaling pathway for the cardiovascular protective effects... 
PATHWAY | NITRIC-OXIDE SYNTHASE | CELL-MIGRATION | ACTIN POLYMERIZATION | PROTRUSION | ESTROGEN-RECEPTOR-ALPHA | ESTRADIOL | ENDOCRINOLOGY & METABOLISM | PROTEINS | IDENTIFICATION | ARTERY | Human Umbilical Vein Endothelial Cells - drug effects | Human Umbilical Vein Endothelial Cells - metabolism | Humans | Actins - metabolism | Phosphoserine - metabolism | Pseudopodia - drug effects | Cofilin 1 - metabolism | Human Umbilical Vein Endothelial Cells - enzymology | Pseudopodia - metabolism | Models, Biological | Nitrosation - drug effects | Protein Binding - drug effects | Cytoskeleton - metabolism | Cysteine - metabolism | Nitric Oxide Synthase Type III - metabolism | Phosphorylation - drug effects | Nitric Oxide - metabolism | Cytoskeleton - drug effects | Estradiol - pharmacology | Index Medicus | Original Research
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12. Full Text RhoA S-nitrosylation as a regulatory mechanism influencing endothelial barrier function in response to G+-bacterial toxins
by Chen, F and Wang, Y and Rafikov, R and Haigh, S and Zhi, W.B and Kumar, S and Doulias, P.T and Rafikova, O and Pillich, H and Chakraborty, T and Lucas, R and Verin, A.D and Catravas, J.D and She, J.X and Black, S.M and Fulton, D.J.R
Biochemical Pharmacology, ISSN 0006-2952, 03/2017, Volume 127, pp. 34 - 45
Disruption of the endothelial barrier in response to Gram positive (G ) bacterial toxins is a major complication of acute lung injury (ALI) and can be further... 
Endothelial | Permeability | Nitric oxide | G+-toxins | RhoA | S-nitrosylation | toxins | ACTIVATION | NITROSATION | OXIDE-INDUCED INHIBITION | KINASE-C-ALPHA | LUNG INJURY | G(+)-toxins | DENITROSYLATION | RESPIRATORY-DISTRESS-SYNDROME | RYANODINE RECEPTOR | NITRIC-OXIDE | PHARMACOLOGY & PHARMACY | Hemolysin Proteins - pharmacology | Calcium - metabolism | Endothelial Cells - metabolism | Humans | Microvessels - metabolism | Cercopithecus aethiops | rhoA GTP-Binding Protein - metabolism | rhoA GTP-Binding Protein - genetics | Heat-Shock Proteins - pharmacology | Animals | Nitroso Compounds - metabolism | Bacterial Toxins - pharmacology | Endothelium, Vascular - metabolism | HEK293 Cells | Mutation | Nitric Oxide Donors - pharmacology | Lung - blood supply | Nitric Oxide - metabolism | COS Cells | Index Medicus
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13. Full Text S -nitrosylation regulates apoptosis
by Bernassola, Francesca and Knight, Richard A and Nistic, Giuseppe and Finazzi-Agr, Alessandro and Melino, Gerry and Corasaniti, Maria Tiziana
Nature, ISSN 0028-0836, 07/1997, Volume 388, Issue 6641, pp. 432 - 433
Nitric oxide (NO) modulates the biological activity of proteins by direct interactions with their iron centres. It can also S-nitrosylate cysteines to form... 
PROGRAMMED CELL-DEATH | NITRIC-OXIDE | K RO MULTIDISCIPLINARY SCIENCES | MULTIDISCIPLINARY SCIENCES | S-Nitroso-N-Acetylpenicillamine | Jurkat Cells | Humans | Penicillamine - analogs & derivatives | Penicillamine - metabolism | fas Receptor - metabolism | Necrosis | Poly(ADP-ribose) Polymerases - metabolism | Cysteine Endopeptidases - metabolism | GTP Phosphohydrolases - metabolism | Transglutaminases - metabolism | Caspase 3 | Cysteine - metabolism | Caspases | GTP-Binding Proteins | Tumor Cells, Cultured | Nitric Oxide - metabolism | Apoptosis | Research | Cell death | Nitric oxide | Index Medicus
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14. Full Text Activation of the Cardiac Calcium Release Channel (Ryanodine Receptor) by Poly-S-Nitrosylation
by Le Xu and Jerry P. Eu and Gerhard Meissner and Jonathan S. Stamler
Science, ISSN 0036-8075, 1/1998, Volume 279, Issue 5348, pp. 234 - 237
Several ion channels are reportedly redox responsive, but the molecular basis for the changes in activity is not known. The mechanism of nitric oxide action on... 
Receptors | Thiols | Calcium | Canines | Disulfides | Oxides | Reports | Oxidation | Ion channels | Physiological regulation | Sulfur | OXIDATION | PROTEIN-KINASE-C | MECHANISM | SULFHYDRYLS | CA2+ RELEASE | MULTIDISCIPLINARY SCIENCES | NITRIC-OXIDE | SARCOPLASMIC-RETICULUM | FROG SKELETAL-MUSCLE | CA-2+ RELEASE | FUNCTIONAL CONSEQUENCES | Cysteine - analogs & derivatives | Calcium - metabolism | Proteolipids - metabolism | Ryanodine Receptor Calcium Release Channel - metabolism | Electric Conductivity | Molsidomine - analogs & derivatives | Glutathione - pharmacology | Nitroso Compounds - pharmacology | Sulfhydryl Compounds - metabolism | Nitroso Compounds - metabolism | Myocardium - metabolism | Cysteine - pharmacology | Mercaptoethanol | Ethylmaleimide - pharmacology | S-Nitrosoglutathione | Dithiothreitol - pharmacology | Glutathione - analogs & derivatives | Oxidation-Reduction | Ryanodine Receptor Calcium Release Channel - drug effects | Nitrosation | Animals | Cyclic GMP - metabolism | Dogs | Molsidomine - pharmacology | Liposomes - metabolism | S-Nitrosothiols | Nitric Oxide - metabolism | Physiological aspects | Calcium channels | Nitric oxide | Cellular control mechanisms | Heart | Ions | Biochemistry | Molecular biology | Index Medicus
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