Solomon H Snyder

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. ncbi request reprint Neuroscience. Adam finds an exciting mate
    Solomon H Snyder
    Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
    Science 313:1744-5. 2006
  2. pmc Sulfhydration mediates neuroprotective actions of parkin
    M Scott Vandiver
    Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Nat Commun 4:1626. 2013
  3. pmc GAPDH mediates nitrosylation of nuclear proteins
    Michael D Kornberg
    Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Nat Cell Biol 12:1094-100. 2010
  4. doi request reprint Molecules of madness
    Solomon H Snyder
    The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cell 139:1212-5. 2009
  5. pmc Mind molecules
    Solomon H Snyder
    Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Biol Chem 286:21023-32. 2011
  6. ncbi request reprint Neuroscience at Johns Hopkins
    Solomon H Snyder
    Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, Maryland 21205, USA
    Neuron 48:201-11. 2005
  7. pmc Inositol pyrophosphates inhibit Akt signaling, thereby regulating insulin sensitivity and weight gain
    Anutosh Chakraborty
    The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cell 143:897-910. 2010
  8. ncbi request reprint Novel neurotransmitters and their neuropsychiatric relevance
    S H Snyder
    Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205 2185, USA
    Am J Psychiatry 157:1738-51. 2000
  9. ncbi request reprint Turning off neurotransmitters
    Solomon H Snyder
    Department of Neuroscience, Johns Hopkins University, 725 N Wolfe Street, WBSB 813 Baltimore, MD 21205, USA
    Cell 125:13-5. 2006
  10. pmc What dopamine does in the brain
    Solomon 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

Research Grants

  1. DRUG ABUSE RESEARCH CENTER
    SOLOMON SNYDER; Fiscal Year: 2007
  2. NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGS
    SOLOMON SNYDER; Fiscal Year: 2007
  3. NEUROTRANSMITTER RECEPTORS
    SOLOMON SNYDER; Fiscal Year: 2007
  4. NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGS
    Solomon H Snyder; Fiscal Year: 2010

Detail Information

Publications159 found, 100 shown here

  1. ncbi request reprint Neuroscience. Adam finds an exciting mate
    Solomon H Snyder
    Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
    Science 313:1744-5. 2006
  2. pmc Sulfhydration mediates neuroprotective actions of parkin
    M Scott Vandiver
    Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Nat Commun 4:1626. 2013
    ..Parkin sulfhydration is markedly depleted in the brains of patients with Parkinson's disease, suggesting that this loss may be pathologic. This implies that hydrogen sulfide donors may be therapeutic...
  3. pmc GAPDH mediates nitrosylation of nuclear proteins
    Michael 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...
  4. doi request reprint Molecules of madness
    Solomon 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...
  5. pmc Mind molecules
    Solomon 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...
  6. ncbi request reprint Neuroscience at Johns Hopkins
    Solomon H Snyder
    Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, Maryland 21205, USA
    Neuron 48:201-11. 2005
  7. pmc Inositol pyrophosphates inhibit Akt signaling, thereby regulating insulin sensitivity and weight gain
    Anutosh 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...
  8. ncbi request reprint Novel neurotransmitters and their neuropsychiatric relevance
    S 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...
  9. ncbi request reprint Turning off neurotransmitters
    Solomon H Snyder
    Department of Neuroscience, Johns Hopkins University, 725 N Wolfe Street, WBSB 813 Baltimore, MD 21205, USA
    Cell 125:13-5. 2006
    ....
  10. pmc What dopamine does in the brain
    Solomon 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
    ....
  11. doi request reprint 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'...
  12. ncbi request reprint Opiate receptors and beyond: 30 years of neural signaling research
    Solomon 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...
  13. ncbi request reprint Historical review: Opioid receptors
    Solomon 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...
  14. ncbi request reprint Opiate receptor revisited
    Solomon H Snyder
    Department of Neuroscience, Johns Hopkins University, Baltimore, MD, USA
    Anesthesiology 107:659-61. 2007
  15. pmc GOSPEL: a neuroprotective protein that binds to GAPDH upon S-nitrosylation
    Nilkantha 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...
  16. ncbi request reprint S-nitrosylated GAPDH initiates apoptotic cell death by nuclear translocation following Siah1 binding
    Makoto 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...
  17. pmc Inositol pyrophosphates mediate the DNA-PK/ATM-p53 cell death pathway by regulating CK2 phosphorylation of Tti1/Tel2
    Feng Rao
    The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Mol Cell 54:119-32. 2014
    ..This process stimulates p53 phosphorylation at serine 15 to activate the cell death program in human cancer cells and in murine B cells. ..
  18. pmc NMDA receptor-nitric oxide transmission mediates neuronal iron homeostasis via the GTPase Dexras1
    Jaime 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...
  19. pmc Nitric oxide-induced nuclear GAPDH activates p300/CBP and mediates apoptosis
    Nilkantha 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...
  20. pmc Modulation of D-serine levels in brains of mice lacking PICK1
    Takatoshi 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...
  21. pmc Mutant huntingtin: nuclear translocation and cytotoxicity mediated by GAPDH
    Byoung 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...
  22. pmc RACK1 binds to inositol 1,4,5-trisphosphate receptors and mediates Ca2+ release
    Randen 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...
  23. ncbi request reprint S-nitrosylation of N-ethylmaleimide sensitive factor mediates surface expression of AMPA receptors
    Yunfei Huang
    Department of Neuroscience, Johns Hopkins University, School of Medicine, 725 North Wolfe Street, Baltimore, Maryland 21205, USA
    Neuron 46:533-40. 2005
    ....
  24. pmc Serine racemase: activation by glutamate neurotransmission via glutamate receptor interacting protein and mediation of neuronal migration
    Paul 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...
  25. pmc S-nitrosylation/activation of COX-2 mediates NMDA neurotoxicity
    Jing 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...
  26. pmc Serine racemase deletion protects against cerebral ischemia and excitotoxicity
    Asif 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...
  27. ncbi request reprint Cystathionine γ-lyase deficiency mediates neurodegeneration in Huntington's disease
    Bindu D Paul
    The Solomon H Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Nature 509:96-100. 2014
    ....
  28. ncbi request reprint Phospholipase Cgamma1 controls surface expression of TRPC3 through an intermolecular PH domain
    Damian 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...
  29. pmc Neuroprotection by pharmacologic blockade of the GAPDH death cascade
    Makoto 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...
  30. ncbi request reprint Inositol polyphosphate multikinase is a coactivator of p53-mediated transcription and cell death
    Risheng Xu
    Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Sci Signal 6:ra22. 2013
    ..These results suggest that IPMK acts as a transcriptional coactivator for p53 and that it is an integral part of the p53 transcriptional complex facilitating cell death...
  31. ncbi request reprint p53 mediates cellular dysfunction and behavioral abnormalities in Huntington's disease
    Byoung 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...
  32. ncbi request reprint Phosphorylation of proteins by inositol pyrophosphates
    Adolfo 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...
  33. ncbi request reprint Action of TFII-I outside the nucleus as an inhibitor of agonist-induced calcium entry
    Gabriela 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...
  34. pmc HSP90 regulates cell survival via inositol hexakisphosphate kinase-2
    Anutosh 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...
  35. pmc Rhes, a striatal-enriched small G protein, mediates mTOR signaling and L-DOPA-induced dyskinesia
    Srinivasa 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...
  36. pmc Inositol 1,4,5-trisphosphate receptor/GAPDH complex augments Ca2+ release via locally derived NADH
    Randen 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...
  37. pmc Amino acid signaling to mTOR mediated by inositol polyphosphate multikinase
    Seyun 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...
  38. pmc Alternatively spliced neuronal nitric oxide synthase mediates penile erection
    K 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...
  39. pmc A peptide inhibitor of cytochrome c/inositol 1,4,5-trisphosphate receptor binding blocks intrinsic and extrinsic cell death pathways
    Darren 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...
  40. pmc Casein kinase-2 mediates cell survival through phosphorylation and degradation of inositol hexakisphosphate kinase-2
    Anutosh 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...
  41. pmc Glutamatergic regulation of serine racemase via reversal of PIP2 inhibition
    Asif 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...
  42. pmc Protein pyrophosphorylation by inositol pyrophosphates is a posttranslational event
    Rashna 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...
  43. pmc Rhes, a striatal specific protein, mediates mutant-huntingtin cytotoxicity
    Srinivasa 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...
  44. pmc Agonist-induced Ca2+ entry determined by inositol 1,4,5-trisphosphate recognition
    Damian 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...
  45. pmc Bilirubin and glutathione have complementary antioxidant and cytoprotective roles
    Thomas 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...
  46. pmc S-nitrosylation of AMPA receptor GluA1 regulates phosphorylation, single-channel conductance, and endocytosis
    Balakrishnan Selvakumar
    Solomon H Snyder Department of Neuroscience and Departments of Psychiatry and Behavioral Sciences, Pharmacology and Molecular Sciences, and Howard Hughes Medical Institute, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 110:1077-82. 2013
    ....
  47. pmc Inositol polyphosphate multikinase is a nuclear PI3-kinase with transcriptional regulatory activity
    Adam 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...
  48. ncbi request reprint Huntingtin is cleaved by caspases in the cytoplasm and translocated to the nucleus via perinuclear sites in Huntington's disease patient lymphoblasts
    Akira 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...
  49. ncbi request reprint Heme oxygenase-2 is activated by calcium-calmodulin
    Darren 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...
  50. pmc p53-mediated apoptosis requires inositol hexakisphosphate kinase-2
    Michael 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...
  51. pmc H2S signals through protein S-sulfhydration
    Asif 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...
  52. ncbi request reprint A nitric oxide signaling pathway controls CREB-mediated gene expression in neurons
    Antonella 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...
  53. ncbi request reprint Inositol pyrophosphates mediate chemotaxis in Dictyostelium via pleckstrin homology domain-PtdIns(3,4,5)P3 interactions
    Hongbo 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...
  54. pmc Inositol pyrophosphates regulate cell death and telomere length through phosphoinositide 3-kinase-related protein kinases
    Adolfo 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
    ....
  55. pmc Rhes, a physiologic regulator of sumoylation, enhances cross-sumoylation between the basic sumoylation enzymes E1 and Ubc9
    Srinivasa 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
    ..Rhes binds directly to both E1 and Ubc9, enhancing cross-sumoylation as well as thioester transfer from E1 to Ubc9...
  56. pmc Nitric oxide S-nitrosylates serine racemase, mediating feedback inhibition of D-serine formation
    Asif 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...
  57. pmc Hydrogen sulfide-linked sulfhydration of NF-κB mediates its antiapoptotic actions
    Nilkantha 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...
  58. pmc Death-associated protein kinase-mediated cell death modulated by interaction with DANGER
    Bingnan 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...
  59. pmc Aspartate racemase, generating neuronal D-aspartate, regulates adult neurogenesis
    Paul 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...
  60. pmc D-serine in glia and neurons derives from 3-phosphoglycerate dehydrogenase
    Jeffrey T Ehmsen
    Solomon H Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 33:12464-9. 2013
    ..These findings clarify the cellular basis for the regulation of NMDAR neurotransmission by d-serine. ..
  61. pmc Hydrogen sulfide as endothelium-derived hyperpolarizing factor sulfhydrates potassium channels
    Asif 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...
  62. pmc Neurotrophin-mediated degradation of histone methyltransferase by S-nitrosylation cascade regulates neuronal differentiation
    Nilkantha 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...
  63. ncbi request reprint Inositol hexakisphosphate kinase-2, a physiologic mediator of cell death
    Eiichiro 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...
  64. pmc Gene deletion of inositol hexakisphosphate kinase 1 reveals inositol pyrophosphate regulation of insulin secretion, growth, and spermiogenesis
    Rashna 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...
  65. ncbi request reprint Messenger molecules and cell death: therapeutic implications
    Thomas 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...
  66. pmc Glutathione is a physiologic reservoir of neuronal glutamate
    Minori 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...
  67. ncbi request reprint Nitric oxide-GAPDH-Siah: a novel cell death cascade
    Makoto 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...
  68. ncbi request reprint Cell signaling and neuronal death
    Makoto 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...
  69. pmc S-nitrosylation of stargazin regulates surface expression of AMPA-glutamate neurotransmitter receptors
    Balakrishnan 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...
  70. ncbi request reprint Genetics. Two genes link two distinct psychoses
    Akira Sawa
    Department of Psychiatry, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
    Science 310:1128-9. 2005
  71. ncbi request reprint Carbon monoxide neurotransmission activated by CK2 phosphorylation of heme oxygenase-2
    Darren 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...
  72. pmc Inositol polyphosphate multikinase is a physiologic PI3-kinase that activates Akt/PKB
    David 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...
  73. pmc Biliverdin reductase: a major physiologic cytoprotectant
    David 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...
  74. ncbi request reprint Circadian rhythms. Carbon monoxide and clocks
    Darren Boehning
    Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Science 298:2339-40. 2002
  75. ncbi request reprint 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
  76. ncbi request reprint Neurotransmitters, receptors, and second messengers galore in 40 years
    Solomon 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...
  77. ncbi request reprint Novel neural modulators
    Darren 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...
  78. ncbi request reprint Inositol 1,4,5-trisphosphate receptors as signal integrators
    Randen 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...
  79. ncbi request reprint Bilirubin benefits: cellular protection by a biliverdin reductase antioxidant cycle
    Thomas W Sedlak
    Department of Neuroscience, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA
    Pediatrics 113:1776-82. 2004
  80. ncbi request reprint Forty years of neurotransmitters: a personal account
    Solomon 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...
  81. ncbi request reprint Haem oxygenase-1 prevents cell death by regulating cellular iron
    C 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...
  82. ncbi request reprint The biotin switch method for the detection of S-nitrosylated proteins
    S 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...
  83. ncbi request reprint Atypical neural messengers
    D 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
    ....
  84. ncbi request reprint Protein S-nitrosylation: a physiological signal for neuronal nitric oxide
    S 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...
  85. ncbi request reprint Julius Axelrod
    Solomon H Snyder
    Department of Neuroscience, Johns Hopkins University School of Medicine, USA
    Proc Am Philos Soc 151:81-90. 2007
  86. ncbi request reprint Cytochrome c binds to inositol (1,4,5) trisphosphate receptors, amplifying calcium-dependent apoptosis
    Darren 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...
  87. pmc Poly(ADP-ribosyl)ation basally activated by DNA strand breaks reflects glutamate-nitric oxide neurotransmission
    A 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...
  88. pmc Hydrogen sulfide as a gasotransmitter
    Moataz 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...
  89. pmc Akt-dependent phosphorylation of endothelial nitric-oxide synthase mediates penile erection
    K 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...
  90. pmc Signaling by gasotransmitters
    Asif 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...
  91. ncbi request reprint Schizophrenia: diverse approaches to a complex disease
    Akira 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...
  92. pmc Neuronal nitric-oxide synthase localization mediated by a ternary complex with synapsin and CAPON
    Samie 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...
  93. pmc Targeted gene deletion of heme oxygenase 2 reveals neural role for carbon monoxide
    R 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...
  94. ncbi request reprint Dexras1: a G protein specifically coupled to neuronal nitric oxide synthase via CAPON
    M 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...
  95. ncbi request reprint Molecularly cloned mammalian glucosamine-6-phosphate deaminase localizes to transporting epithelium and lacks oscillin activity
    H 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...
  96. ncbi request reprint GRAB: a physiologic guanine nucleotide exchange factor for Rab3A, which interacts with inositol hexakisphosphate kinase
    H 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...
  97. ncbi request reprint Nitric oxide and carbon monoxide: parallel roles as neural messengers
    S 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...
  98. pmc Cloned and expressed macrophage nitric oxide synthase contrasts with the brain enzyme
    C 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...
  99. pmc From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinase
    Sangwon 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...
  100. pmc Disrupted-in-Schizophrenia-1 (DISC-1): mutant truncation prevents binding to NudE-like (NUDEL) and inhibits neurite outgrowth
    Yuji 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...

Research Grants8

  1. DRUG ABUSE RESEARCH CENTER
    SOLOMON SNYDER; Fiscal Year: 2007
    ....
  2. NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGS
    SOLOMON 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. ..
  3. NEUROTRANSMITTER RECEPTORS
    SOLOMON SNYDER; Fiscal Year: 2007
    ....
  4. NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGS
    Solomon 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. ..