Research Topics
Genomes and Genes
| Solomon H SnyderSummaryAffiliation: Johns Hopkins University Country: USA Publications
Research Grants
| Collaborators
|
Detail Information
Publications
Molecules of madnessSolomon H Snyder
The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Cell 139:1212-5. 2009..Hopefully, the tale of my quirky impatient curiosity about "too many" different areas will be useful for young scientists embarking on their own careers...
Neuroscience. Adam finds an exciting mateSolomon H Snyder
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Science 313:1744-5. 2006- Turning off neurotransmittersSolomon H Snyder
Department of Neuroscience, Johns Hopkins University, 725 N Wolfe Street, WBSB 813 Baltimore, MD 21205, USA
Cell 125:13-5. 2006.... - Novel neurotransmitters and their neuropsychiatric relevanceS H Snyder
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205 2185, USA
Am J Psychiatry 157:1738-51. 2000..The purpose of this review is to integrate insights regarding novel neurotransmitters or neuromodulators of neuropsychiatric significance... - Neuroscience at Johns HopkinsSolomon H Snyder
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, Maryland 21205, USA
Neuron 48:201-11. 2005 - Opiate receptor revisitedSolomon H Snyder
Department of Neuroscience, Johns Hopkins University, Baltimore, MD, USA
Anesthesiology 107:659-61. 2007 - Huntington's disease is a disorder of the corpus striatum: focus on Rhes (Ras homologue enriched in the striatum)Srinivasa Subramaniam
Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Neuropharmacology 60:1187-92. 2011..The attendant loss of protein translational stimulation may explain the pronounced striatal atrophy of HD. This article is part of a Special Issue entitled 'Trends in neuropharmacology: in memory of Erminio Costa'... 
Inositol pyrophosphates inhibit Akt signaling, thereby regulating insulin sensitivity and weight gainAnutosh Chakraborty
The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Cell 143:897-910. 2010..IP6K1 knockout mice manifest insulin sensitivity and are resistant to obesity elicited by high-fat diet or aging. Inhibition of IP6K1 may afford a therapeutic approach to obesity and diabetes...- Historical review: Opioid receptorsSolomon H Snyder
Johns Hopkins University School of Medicine, Department of Neuroscience, 725 N Wolfe Street, Baltimore, MD 21205, USA
Trends Pharmacol Sci 24:198-205. 2003..Receptor influences in binding paradigms and smooth muscle pharmacology permitted the identification and isolation of endogenous opioid peptides... - Opiate receptors and beyond: 30 years of neural signaling researchSolomon H Snyder
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, WBSB 813, Baltimore, MD 21205, USA
Neuropharmacology 47:274-85. 2004..These techniques also permitted characterization of intracellular signaling systems such as the IP3 receptor and immunophilins. Even more novel than the enkephalins have been the gaseous neurotransmitters NO and CO and D-serine... - Mind moleculesSolomon H Snyder
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
J Biol Chem 286:21023-32. 2011..In the interests of brevity, this Reflections article is highly selective, and, with a few exceptions, literature citations are only of findings of our laboratory that illustrate notable themes... - What dopamine does in the brainSolomon H Snyder
The Solomon H Snyder Department of Neuroscience, Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 108:18869-71. 2011.... - GOSPEL: a neuroprotective protein that binds to GAPDH upon S-nitrosylationNilkantha Sen
Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Neuron 63:81-91. 2009..In intact mice, virally delivered GOSPEL selectively diminishes NMDA neurotoxicity. Thus, GOSPEL may physiologically regulate the viability of neurons and other cells... - NMDA receptor-nitric oxide transmission mediates neuronal iron homeostasis via the GTPase Dexras1Jaime H Cheah
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Neuron 51:431-40. 2006..As selective iron chelation prevents NMDA neurotoxicity in cortical cultures, the NMDA-NO-Dexras1-PAP7-DMT1-iron uptake signaling cascade also appears to mediate NMDA neurotoxicity... - S-nitrosylated GAPDH initiates apoptotic cell death by nuclear translocation following Siah1 bindingMakoto R Hara
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Nat Cell Biol 7:665-74. 2005..The NO-S-nitrosylation-GAPDH-Siah1 cascade may represent an important molecular mechanism of cytotoxicity... - S-nitrosylation/activation of COX-2 mediates NMDA neurotoxicityJing Tian
Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 105:10537-40. 2008..nNOS, via its PDZ domain, binds COX-2 with the generated NO S-nitrosylating and activating the enzyme. Selective disruption of nNOS-COX-2 binding prevents NMDA neurotoxicity... - Serine racemase deletion protects against cerebral ischemia and excitotoxicityAsif K Mustafa
Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
J Neurosci 30:1413-6. 2010..Infarct volume following middle cerebral artery occlusion is dramatically diminished in several regions of the brains of SR mutant mice despite evidence of increased NMDA receptor number and sensitivity... - Nitric oxide-induced nuclear GAPDH activates p300/CBP and mediates apoptosisNilkantha Sen
Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Nat Cell Biol 10:866-73. 2008..Our findings reveal a pathway in which NO-induced nuclear GAPDH mediates cell death through p300/CBP... - RACK1 binds to inositol 1,4,5-trisphosphate receptors and mediates Ca2+ releaseRanden L Patterson
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 101:2328-32. 2004..These findings establish RACK1 as a physiologic mediator of agonist-induced Ca2+ release... - p53 mediates cellular dysfunction and behavioral abnormalities in Huntington's diseaseByoung Il Bae
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Neuron 47:29-41. 2005..Genetic deletion of p53 suppresses neurodegeneration in mHtt-Tg flies and neurobehavioral abnormalities of mHtt-Tg mice. Our findings suggest that p53 links nuclear and mitochondrial pathologies characteristic of HD... - Modulation of D-serine levels in brains of mice lacking PICK1Takatoshi Hikida
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
Biol Psychiatry 63:997-1000. 2008..D-serine is an endogenous coagonist of the N-methyl-D-aspartate subtype glutamate receptor. Genetic association studies have implicated genes coding for enzymes associated with D-serine metabolism in schizophrenia and bipolar disorder... - Mutant huntingtin: nuclear translocation and cytotoxicity mediated by GAPDHByoung Il Bae
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 103:3405-9. 2006..Depletion of GAPDH or Siah1 by RNA interference diminishes nuclear translocation of mHtt... - HSP90 regulates cell survival via inositol hexakisphosphate kinase-2Anutosh Chakraborty
The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 105:1134-9. 2008..Thus, the prosurvival actions of HSP90 reflect the inhibition of IP6K2, suggesting that selectively blocking this interaction could provide effective and safer modes of chemotherapy... - Rhes, a striatal-enriched small G protein, mediates mTOR signaling and L-DOPA-induced dyskinesiaSrinivasa Subramaniam
The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Nat Neurosci 15:191-3. 2012..Moreover, Rhes(-/-) mice showed reduced striatal mTOR signaling and diminished dyskinesia, but maintained motor improvement on L-DOPA treatment, suggesting a therapeutic benefit for Rhes-binding drugs... - Protein pyrophosphorylation by inositol pyrophosphates is a posttranslational eventRashna Bhandari
The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 104:15305-10. 2007..Pyrophosphorylation may represent a novel mode of signaling to proteins... - A peptide inhibitor of cytochrome c/inositol 1,4,5-trisphosphate receptor binding blocks intrinsic and extrinsic cell death pathwaysDarren Boehning
Department of Neuroscience, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 102:1466-71. 2005..Small-molecule inhibitors of cytochrome c/IP3R interactions may prove useful in treating disorders associated with inappropriate intrinsic and extrinsic apoptotic signaling... - Alternatively spliced neuronal nitric oxide synthase mediates penile erectionK Joseph Hurt
Department of Urology, Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 103:3440-3. 2006..Thus, alternatively spliced forms of nNOS are major mediators of penile erection and so may be targets for therapeutic intervention... - Serine racemase: activation by glutamate neurotransmission via glutamate receptor interacting protein and mediation of neuronal migrationPaul M Kim
Department of Pharmacology and Molecular Science, Neuroscience, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 102:2105-10. 2005..Thus, in neuronal migration, glutamate stimulates Bergmann glia to form and release D-serine, which, together with glutamate, activates NMDA receptors on granule neurons, chemokinetically enhancing migration... - S-nitrosylation of N-ethylmaleimide sensitive factor mediates surface expression of AMPA receptorsYunfei Huang
Department of Neuroscience, Johns Hopkins University, School of Medicine, 725 North Wolfe Street, Baltimore, Maryland 21205, USA
Neuron 46:533-40. 2005.... - Inositol 1,4,5-trisphosphate receptor/GAPDH complex augments Ca2+ release via locally derived NADHRanden L Patterson
Department of Neuroscience, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 102:1357-9. 2005..Thus, the IP3R/GAPDH interaction likely enables cellular energy dynamics to impact calcium signaling... - Amino acid signaling to mTOR mediated by inositol polyphosphate multikinaseSeyun Kim
The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Cell Metab 13:215-21. 2011..Substances that block IPMK-mTORC1 binding may afford therapeutic benefit in nutrient amino acid-regulated conditions such as obesity and diabetes... - Glutamatergic regulation of serine racemase via reversal of PIP2 inhibitionAsif K Mustafa
Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 106:2921-6. 2009..Thus mutants of SR that cannot bind PIP2 lose their membrane localizations and display a 4-fold enhancement of catalytic activity. Moreover, mGluR5 activation of SR activity is abolished by inhibiting phospholipase C... - Casein kinase-2 mediates cell survival through phosphorylation and degradation of inositol hexakisphosphate kinase-2Anutosh Chakraborty
The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 108:2205-9. 2011..CK2 phosphorylation at the degradation motif of IP6K2 enhances its ubiquitination and subsequent degradation. IP6K2 mutants at the CK2 sites that are resistant to CK2 phosphorylation are metabolically stable... - Rhes, a striatal specific protein, mediates mutant-huntingtin cytotoxicitySrinivasa Subramaniam
Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Science 324:1327-30. 2009..Using cultured cells, we found Rhes induces sumoylation of mHtt, which leads to cytotoxicity. Thus, Rhes-mHtt interactions can account for the localized neuropathology of HD... - Neuroprotection by pharmacologic blockade of the GAPDH death cascadeMakoto R Hara
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 103:3887-9. 2006..In mice treated with the dopamine neuronal toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), low doses of deprenyl prevent binding of GAPDH and Siah1 in the dopamine-enriched corpus striatum... - Phosphorylation of proteins by inositol pyrophosphatesAdolfo Saiardi
Department of Neuroscience, Johns Hopkins University, School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Science 306:2101-5. 2004..We also observed phosphorylation of endogenous proteins by endogenous IP7 in yeast. Phosphorylation by IP7 is nonenzymatic and may represent a novel intracellular signaling mechanism... - Action of TFII-I outside the nucleus as an inhibitor of agonist-induced calcium entryGabriela Caraveo
Department of Molecular Biology and Genetics, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Science 314:122-5. 2006..Our observations suggest a model in which TFII-I suppresses ACE by competing with TRPC3 for binding to PLC-g... - Heme oxygenase-2 is activated by calcium-calmodulinDarren Boehning
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
J Biol Chem 279:30927-30. 2004..Calcium-calmodulin provides a mechanism for rapid and transient activation of HO2 during neuronal activity... - GAPDH mediates nitrosylation of nuclear proteinsMichael D Kornberg
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Nat Cell Biol 12:1094-100. 2010..Our findings reveal a novel mechanism for targeted nitrosylation of nuclear proteins and suggest that protein-protein transfer of nitric oxide groups may be a general mechanism in cellular signal transduction... - Huntingtin is cleaved by caspases in the cytoplasm and translocated to the nucleus via perinuclear sites in Huntington's disease patient lymphoblastsAkira Sawa
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, MD 21287, USA
Neurobiol Dis 20:267-74. 2005..Our findings suggest that caspase cleavage of Htt is cytoplasmic and precedes sorting to specific perinuclear sites followed by nuclear translocation in HD patient tissue... - Inositol polyphosphate multikinase is a nuclear PI3-kinase with transcriptional regulatory activityAdam C Resnick
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 102:12783-8. 2005..In yeast, this inositol lipid kinase activity physiologically regulates transcription... - Phospholipase Cgamma1 controls surface expression of TRPC3 through an intermolecular PH domainDamian B van Rossum
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Nature 434:99-104. 2005..Our findings imply a far greater abundance of PH domains than previously appreciated, and suggest that intermolecular PH-like domains represent a widespread signalling mode... - Inositol pyrophosphates regulate cell death and telomere length through phosphoinositide 3-kinase-related protein kinasesAdolfo Saiardi
Department of Neuroscience, Pharmacology and Molecular Sciences, and Psychiatry and Behavioral Sciences, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 102:1911-4. 2005.... - Inositol pyrophosphates mediate chemotaxis in Dictyostelium via pleckstrin homology domain-PtdIns(3,4,5)P3 interactionsHongbo R Luo
Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA
Cell 114:559-72. 2003..InsP7 competes for PH domain binding with PtdIns(3,4,5)P3 both in vitro and in vivo. InsP7 depletion enhances PH domain membrane translocation and augments downstream chemotactic signaling activity... - Rhes, a physiologic regulator of sumoylation, enhances cross-sumoylation between the basic sumoylation enzymes E1 and Ubc9Srinivasa Subramaniam
Solomon H Snyder Department of Neuroscience, Departments of Pharmacology and Molecular Sciences and Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
J Biol Chem 285:20428-32. 2010..quot; Rhes binds directly to both E1 and Ubc9, enhancing cross-sumoylation as well as thioester transfer from E1 to Ubc9... - Nitric oxide S-nitrosylates serine racemase, mediating feedback inhibition of D-serine formationAsif K Mustafa
Solomon H Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 104:2950-5. 2007..These findings support a model whereby postsynaptic stimulation of nitric-oxide (NO) formation feeds back to presynaptic cells to S-nitrosylate SR and decrease D-serine availability to postsynaptic NMDA receptors... - Bilirubin and glutathione have complementary antioxidant and cytoprotective rolesThomas W Sedlak
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 106:5171-6. 2009..RNA interference depletion of BVR increases oxidation of lipids more than protein. Depletion of BVR or GSH augments cell death in an oxidant-specific fashion... - p53-mediated apoptosis requires inositol hexakisphosphate kinase-2Michael A Koldobskiy
The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 107:20947-51. 2010..IP6K2 acts by binding directly to p53 and decreasing expression of proarrest gene targets such as the cyclin-dependent kinase inhibitor p21... - A nitric oxide signaling pathway controls CREB-mediated gene expression in neuronsAntonella Riccio
Howard Hughes Medical Institute, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, Maryland 21201, USA
Mol Cell 21:283-94. 2006..Thus, in conjunction with CREB phosphorylation, the NO pathway controls CREB-DNA binding and CRE-mediated gene expression... - Agonist-induced Ca2+ entry determined by inositol 1,4,5-trisphosphate recognitionDamian B van Rossum
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 101:2323-7. 2004..We conclude that an IP3-dependent conformational change in the IP3R, not endoplasmic reticulum Ca2+ pool release, triggers ACE... - Death-associated protein kinase-mediated cell death modulated by interaction with DANGERBingnan N Kang
Department of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
J Neurosci 30:93-8. 2010..Accordingly, DANGER may physiologically regulate the viability of neurons and represent a potential therapeutic target for stroke and neurodegenerative diseases... - H2S signals through protein S-sulfhydrationAsif K Mustafa
Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Sci Signal 2:ra72. 2009..Sulfhydration augments GAPDH activity and enhances actin polymerization. Sulfhydration thus appears to be a physiologic posttranslational modification for proteins... - Aspartate racemase, generating neuronal D-aspartate, regulates adult neurogenesisPaul M Kim
The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 107:3175-9. 2010..Because D-aspartate is a potential endogenous ligand for NMDA receptors, the loss of which elicits a phenotype resembling DR depletion, D-aspartate may function as a modulator of adult neurogenesis... - Neurotrophin-mediated degradation of histone methyltransferase by S-nitrosylation cascade regulates neuronal differentiationNilkantha Sen
The Solomon H Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 108:20178-83. 2011..Degradation of SUV39H1 by Siah facilitates histone H3 on lysine 9 acetylation, CREB binding to DNA, enhanced expression of CREB-regulated genes and neurite outgrowth... - Hydrogen sulfide-linked sulfhydration of NF-κB mediates its antiapoptotic actionsNilkantha Sen
The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Mol Cell 45:13-24. 2012..In CSE mutant mice, antiapoptotic influences of NF-κB are markedly diminished. Thus, sulfhydration of NF-κB appears to be a physiologic determinant of its antiapoptotic transcriptional activity... - Inositol hexakisphosphate kinase-2, a physiologic mediator of cell deathEiichiro Nagata
Department of Neuroscience, Pharmacology and Molecular Sciences, School of Medicine, The Johns Hopkins University, Baltimore, Maryland 21205, USA
J Biol Chem 280:1634-40. 2005..The present study provides compelling evidence that endogenous InsP6K2, by generating InsP7, provides physiologic regulation of the apoptotic process... - Cell signaling and neuronal deathMakoto R Hara
The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Annu Rev Pharmacol Toxicol 47:117-41. 2007..Within cells, calcium, the most prominent of all intracellular messengers, mediates diverse forms of cell death with actions modulated by many proteins, including IP3 receptors, calcineurin, calpain, and cytochrome c... - Nitric oxide-GAPDH-Siah: a novel cell death cascadeMakoto R Hara
The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Cell Mol Neurobiol 26:527-38. 2006..The neuroprotective actions of the monoamine oxidase inhibitor R-(-)-deprenyl (deprenyl) reflect blockade of GAPDH-Siah binding. Thus, novel cytoprotective therapies may emerge from agents that prevent GAPDH-Siah binding... - Hydrogen sulfide as endothelium-derived hyperpolarizing factor sulfhydrates potassium channelsAsif K Mustafa
Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Circ Res 109:1259-68. 2011..Hydrogen sulfide (H(2)S) is a prominent EDRF, since mice lacking its biosynthetic enzyme, cystathionine γ-lyase (CSE), display pronounced hypertension with deficient vasorelaxant responses to acetylcholine... - Glutathione is a physiologic reservoir of neuronal glutamateMinori Koga
Department of Psychiatry and Behavioral Sciences, The Johns Hopkins University School of Medicine, Meyer 4 137, 600 North Wolfe Street, Baltimore, MD 21287, USA
Biochem Biophys Res Commun 409:596-602. 2011..Increased glutamate levels following inhibition of glutathione synthesis temporally precede later effects upon oxidative stress... - S-nitrosylation of stargazin regulates surface expression of AMPA-glutamate neurotransmitter receptorsBalakrishnan Selvakumar
Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 106:16440-5. 2009..NMDAR stimulation, well known to activate neuronal nitric oxide synthase, increases both nitrosylation of stargazin and its binding to AMPAR. Thus, S-nitrosylation of stargazin is a physiologic regulator of AMPAR surface expression... - Messenger molecules and cell death: therapeutic implicationsThomas W Sedlak
Department of Neuroscience, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA
JAMA 295:81-9. 2006..These pathways may regulate cell survival in a variety of pathologic states and represent fertile targets for novel therapies... - Gene deletion of inositol hexakisphosphate kinase 1 reveals inositol pyrophosphate regulation of insulin secretion, growth, and spermiogenesisRashna Bhandari
The Solomon H Snyder Department of Neuroscience and Departments of Pharmacology and Molecular Sciences and Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 105:2349-53. 2008..Male mutant mice are sterile with defects in spermiogenesis. Mutant mice are smaller than wild-type despite normal food intake. The mutants display markedly lower circulating insulin... - Genetics. Two genes link two distinct psychosesAkira Sawa
Department of Psychiatry, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Science 310:1128-9. 2005 - Carbon monoxide neurotransmission activated by CK2 phosphorylation of heme oxygenase-2Darren Boehning
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Neuron 40:129-37. 2003..Our findings provide a molecular mechanism for the rapid neuronal activation of CO biosynthesis, as required for a gaseous neurotransmitter... - Inositol polyphosphate multikinase is a physiologic PI3-kinase that activates Akt/PKBDavid Maag
The Solomon H Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 108:1391-6. 2011..Drugs regulating IPMK may have therapeutic relevance in influencing cell proliferation... - Biliverdin reductase: a major physiologic cytoprotectantDavid E Baranano
Departments of Neuroscience, Pharmacology and Molecular Sciences, and Psychiatry and Behavioral Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 99:16093-8. 2002..This redox cycle may constitute the principal physiologic function of bilirubin... - Circadian rhythms. Carbon monoxide and clocksDarren Boehning
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Science 298:2339-40. 2002 - Obituary: Julius Axelrod (1912-2004)Solomon H Snyder
Solomon H. Snyder is in the Department of Neuroscience, Johns Hopkins Medical School, 725 North Wolfe Street, Baltimore, Maryland 21205, USA.e-mail
Nature 433:593. 2005 - Forty years of neurotransmitters: a personal accountSolomon H Snyder
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 N Wolfe St, Baltimore, MD 21205, USA
Arch Gen Psychiatry 59:983-94. 2002..It is likely that totally new classes of therapeutic agents will emerge based on these transmitter molecules... - Inositol 1,4,5-trisphosphate receptors as signal integratorsRanden L Patterson
Department of Neuroscience, Johns Hopkins University, Johns Hopkins Medical School, Baltimore, Maryland 21205, USA
Annu Rev Biochem 73:437-65. 2004..We review the unique properties of the IP3R that facilitate cell-type and stimulus-dependent control of function, with special emphasis on protein-binding partners... - Bilirubin benefits: cellular protection by a biliverdin reductase antioxidant cycleThomas W Sedlak
Department of Neuroscience, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA
Pediatrics 113:1776-82. 2004 - Neurotransmitters, receptors, and second messengers galore in 40 yearsSolomon H Snyder
Department of Neuroscience, Johns Hopkins University, Baltimore, Maryland 21205, USA
J Neurosci 29:12717-21. 2009..This essay highlights a selected group of particular notable discoveries, emphasizing seminal findings that have transformed thinking in the field... - Novel neural modulatorsDarren Boehning
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 N Wolfe Street, Baltimore, Maryland 21205, USA
Annu Rev Neurosci 26:105-31. 2003..We review the properties of these "atypical" neural modulators... - Protein S-nitrosylation: a physiological signal for neuronal nitric oxideS R Jaffrey
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Nat Cell Biol 3:193-7. 2001..Targets of NO include metabolic, structural and signalling proteins that may be effectors for neuronally generated NO. These findings establish protein S-nitrosylation as a physiological signalling mechanism for nNOS... - Atypical neural messengersD E Barañano
Johns Hopkins University School of Medicine, Dept of Neuroscience, 725 N Wolfe Street, Baltimore, MD 21205, USA
Trends Neurosci 24:99-106. 2001.... - Haem oxygenase-1 prevents cell death by regulating cellular ironC D Ferris
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Nat Cell Biol 1:152-7. 1999..Thus, cytoprotection by HO1 is attributable to its augmentation of iron efflux, reflecting a role for HO1 in modulating intracellular iron levels and regulating cell viability... - The biotin switch method for the detection of S-nitrosylated proteinsS R Jaffrey
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA E mail
Sci STKE 2001:pl1. 2001..We include examples of the detection of S-nitrosylated proteins in brain lysates after in vitro S-nitrosylation, as well as the detection of endogenous S-nitrosothiols in selected neuronal proteins... - Cytochrome c binds to inositol (1,4,5) trisphosphate receptors, amplifying calcium-dependent apoptosisDarren Boehning
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 N. Wolfe Street, Baltimore, Maryland 21205, USA
Nat Cell Biol 5:1051-61. 2003..Our findings identify a feed-forward mechanism whereby early cytochrome c release increases InsP(3)R function, resulting in augmented cytochrome c release that amplifies the apoptotic signal... - Julius AxelrodSolomon H Snyder
Department of Neuroscience, Johns Hopkins University School of Medicine, USA
Proc Am Philos Soc 151:81-90. 2007 - Poly(ADP-ribosyl)ation basally activated by DNA strand breaks reflects glutamate-nitric oxide neurotransmissionA A Pieper
Departments of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 97:1845-50. 2000..An increase in NAD(+) levels after treatment with NMDA antagonists or NOS inhibitors, as well as in nNOS(-/-) mice, indicates that basal glutamate-PARP activity regulates neuronal energy dynamics... - Neuronal nitric-oxide synthase localization mediated by a ternary complex with synapsin and CAPONSamie R Jaffrey
Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 99:3199-204. 2002..These results suggest a mechanism for specific actions of NO at presynaptic sites... - Akt-dependent phosphorylation of endothelial nitric-oxide synthase mediates penile erectionK Joseph Hurt
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 99:4061-6. 2002..Our findings support a model in which rapid, brief activation of neuronal NOS initiates the erectile process, whereas PI3-kinase/Akt-dependent phosphorylation and activation of eNOS leads to sustained NO production and maximal erection... - Schizophrenia: diverse approaches to a complex diseaseAkira Sawa
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Science 296:692-5. 2002..Here, we provide a brief overview of the parallel approaches being used to identify the molecular causes of schizophrenia and discuss possible directions for future research... - Hydrogen sulfide as a gasotransmitterMoataz M Gadalla
Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2105, USA
J Neurochem 113:14-26. 2010..S-nitrosylation basally affects 1-2% of its target proteins, while 10-25% of H(2)S target proteins are S-sulfhydrated. In summary, H(2)S appears to be a physiologic gasotransmitter of comparable importance to NO and carbon monoxide... - Signaling by gasotransmittersAsif K Mustafa
Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Sci Signal 2:re2. 2009..This Review focuses on mechanisms whereby they signal by binding to metal centers in metalloproteins, such as in guanylyl cyclase, or modifying sulfhydryl groups in protein targets... - Nitric oxide and carbon monoxide: parallel roles as neural messengersS H Snyder
Department of Neuroscience, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA
Brain Res Brain Res Rev 26:167-75. 1998..The role for CO as neurotransmitter is suggested by the altered intestinal motility in mice harboring a genomic deletion of HO2... - Cloned and expressed macrophage nitric oxide synthase contrasts with the brain enzymeC J Lowenstein
Department of Neuroscience, Johns Hopkins Medical Institutions, Baltimore, MD 21205
Proc Natl Acad Sci U S A 89:6711-5. 1992..Macrophage NOS mRNA is strikingly inducible; it is absent in quiescent macrophages or spleen but is prominent 2-6 hr after endotoxin treatment... - Molecularly cloned mammalian glucosamine-6-phosphate deaminase localizes to transporting epithelium and lacks oscillin activityH Wolosker
Department of Neuroscience, The Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205, USA
FASEB J 12:91-9. 1998..Evidence that GNPDA can regulate hexosamine stores comes from our observation that transfection of GNPDA into HEK-293 cells reduces cellular levels of sialic acid... - Dexras1: a G protein specifically coupled to neuronal nitric oxide synthase via CAPONM Fang
Department of Neuroscience, School of Medicine, The Johns Hopkins University, Baltimore, Maryland 21205, USA
Neuron 28:183-93. 2000..These findings identify Dexras1 as a novel physiologic NO effector and suggest that anchoring of nNOS to specific targets is a mechanism by which NO signaling is enhanced... - Targeted gene deletion of heme oxygenase 2 reveals neural role for carbon monoxideR Zakhary
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 94:14848-53. 1997..In nNOSDelta/Delta animals, NOS inhibitors selectively lost their efficacy, and HO inhibitors were inactive in HO-2(Delta)/Delta animals... - GRAB: a physiologic guanine nucleotide exchange factor for Rab3A, which interacts with inositol hexakisphosphate kinaseH R Luo
Department of Neuroscience, School of Medicine, Johns Hopkins University, 725 N Wolfe Street, Baltimore, MD 21205, USA
Neuron 31:439-51. 2001..The association of InsP6K1 with GRAB fits with a role for InsP7 in vesicle exocytosis... - From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinaseSangwon F Kim
The Solomon H Snyder Department of Neuroscience, Departments of Pharmacology and Molecular Sciences and Psychiatry and Behavioral Sciences, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 104:3456-9. 2007..These findings may afford a means of developing more effective therapeutic agents and provide insight into the hypothalamic regulation of food intake... - Disrupted-in-Schizophrenia-1 (DISC-1): mutant truncation prevents binding to NudE-like (NUDEL) and inhibits neurite outgrowthYuji Ozeki
Division of Neurobiology and Department of Psychiatry, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 100:289-94. 2003..As schizophrenia is thought to reflect defects in cortical development that are determined by cytoskeletal protein activities, the cellular disturbances we observe with mutant DISC-1 may be relevant to psychopathologic mechanisms... - UDP-glucuronate decarboxylase, a key enzyme in proteoglycan synthesis: cloning, characterization, and localizationJohn L Moriarity
Department of Neurological Surgery, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA
J Biol Chem 277:16968-75. 2002..Subcellular studies and histochemistry localized UGD protein to the perinuclear Golgi where xylosylation of proteoglycan core proteins is known to occur... - Inducible nitric oxide synthase binds, S-nitrosylates, and activates cyclooxygenase-2Sangwon F Kim
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Science 310:1966-70. 2005..Selectively disrupting iNOS-COX-2 binding prevented NO-mediated activation of COX-2. This synergistic molecular interaction between two inflammatory systems may inform the development of anti-inflammatory drugs... - Carbon monoxide mediates vasoactive intestinal polypeptide-associated nonadrenergic/noncholinergic neurotransmissionCrystal C Watkins
Department of Neuroscience, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 101:2631-5. 2004..By using a combination of pharmacology and genetic knockout of the biosynthetic enzymes for CO and NO, we show that the physiologic effects of exogenous and endogenous VIP in the IAS are mediated by HO2-synthesized CO... - Phospholipase C gamma 1 is a physiological guanine nucleotide exchange factor for the nuclear GTPase PIKEKeqiang Ye
Johns Hopkins University School of Medicine, Department of Neuroscience, 725 N Wolfe Street, Baltimore, Maryland 21205, USA
Nature 415:541-4. 2002..This enzymatic activity accounts for the mitogenic properties of PLC-gamma 1... - Schizophrenia: neural mechanisms for novel therapiesAkira Sawa
Department of Neuroscience, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA
Mol Med 9:3-9. 2003..The search for genes linked to schizophrenia has revealed several leads that may permit development of novel therapeutic agents. Promising genes include disrupted-in-schizophrenia-1, dysbindin, and neuregulin... - Purification of serine racemase: biosynthesis of the neuromodulator D-serineH Wolosker
The Johns Hopkins University, School of Medicine, Departments of Neuroscience, Pharmacology and Molecular Sciences, and Psychiatry, 725 North Wolfe Street, Baltimore, MD 21205, USA
Proc Natl Acad Sci U S A 96:721-5. 1999..Properties such as pH optimum, Km values, and the requirement for pyridoxal phosphate resemble those of bacterial racemases, suggesting that the biosynthetic pathway for D-amino acids is conserved from bacteria to mammalian brain... - Two novel odorant receptor families expressed in spermatids undergo 5'-splicingL D Walensky
Department of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
J Biol Chem 273:9378-87. 1998..5'-Splicing of OdRs may regulate the expression of functional chemoreceptors...
Research Grants
- DRUG ABUSE RESEARCH CENTERSOLOMON SNYDER; Fiscal Year: 2007....
- NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGSSOLOMON SNYDER; Fiscal Year: 2007..We will characterize putative protein phosphorylation by PP-IP 5. We will also complete purif aboutcation and cloning of PP-IPs kinase which forms bis PP-IP4, which contains two pyrophosphate groups. ..
- NEUROTRANSMITTER RECEPTORSSOLOMON SNYDER; Fiscal Year: 2007....
- NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGSSolomon H Snyder; Fiscal Year: 2010..Akt/mTOR signaling is critical for brain function so that our elucidation of its regulation by inositol pyrophosphates may have therapeutic relevance. ..