DAVID ROBINSON LYNCH

Summary

Affiliation: University of Pennsylvania
Country: USA

Publications

  1. ncbi request reprint Performance measures in Friedreich ataxia: potential utility as clinical outcome tools
    David R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 4318, USA
    Mov Disord 20:777-82. 2005
  2. ncbi request reprint Pharmacological characterization of interactions of RO 25-6981 with the NR2B (epsilon2) subunit
    D R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, Children s Seashore House, Philadelphia, PA 19104, USA
    Eur J Pharmacol 416:185-95. 2001
  3. ncbi request reprint Picking up the pieces: the roles of functional remnants of calpain-mediated proteolysis
    David R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Neuron 53:317-9. 2007
  4. ncbi request reprint Ovarian failure in ataxia with oculomotor apraxia type 2
    David R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine
    Am J Med Genet A 143:1775-7. 2007
  5. ncbi request reprint Measuring Friedreich ataxia: complementary features of examination and performance measures
    D R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, and Children s Hospital of Philadelphia, PA 19104 4318, USA
    Neurology 66:1711-6. 2006
  6. ncbi request reprint Lack of effect of polymorphisms in dopamine metabolism related genes on imaging of TRODAT-1 in striatum of asymptomatic volunteers and patients with Parkinson's disease
    David R Lynch
    Department of Neurology, University of Pennsylvania and The Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA
    Mov Disord 18:804-12. 2003
  7. ncbi request reprint Practical approaches to neurogenetic disease
    David R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, USA
    J Neuroophthalmol 22:297-304. 2002
  8. ncbi request reprint Contrast letter acuity as a measure of visual dysfunction in patients with Friedreich ataxia
    David R Lynch
    Department of Neurology, University of Pennsylvania and The Children s Hospital of Philadelphia, 19104, USA
    J Neuroophthalmol 22:270-4. 2002
  9. ncbi request reprint Friedreich ataxia: effects of genetic understanding on clinical evaluation and therapy
    David R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, USA
    Arch Neurol 59:743-7. 2002
  10. ncbi request reprint NMDA receptor pharmacology: perspectives from molecular biology
    D R Lynch
    Department of Neurology, University of Pennsylvania and The Children s Hospital of Philadelphia, 19104 4318, USA
    Curr Drug Targets 2:215-31. 2001

Collaborators

Detail Information

Publications51

  1. ncbi request reprint Performance measures in Friedreich ataxia: potential utility as clinical outcome tools
    David R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 4318, USA
    Mov Disord 20:777-82. 2005
    ..Thus, a composite scale derived from these performance measures may provide the best overall measure for assessing disease progression throughout the illness...
  2. ncbi request reprint Pharmacological characterization of interactions of RO 25-6981 with the NR2B (epsilon2) subunit
    D R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, Children s Seashore House, Philadelphia, PA 19104, USA
    Eur J Pharmacol 416:185-95. 2001
    ..These results suggest that RO 25-6981 shares structural determinants with ifenprodil and other modulators in the NR2B subunit...
  3. ncbi request reprint Picking up the pieces: the roles of functional remnants of calpain-mediated proteolysis
    David R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Neuron 53:317-9. 2007
    ..Together, these papers show the functional importance of fragments of calpain-mediated cleavage...
  4. ncbi request reprint Ovarian failure in ataxia with oculomotor apraxia type 2
    David R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine
    Am J Med Genet A 143:1775-7. 2007
    ..We describe a patient homozygous for a novel mutation of SETX who manifested not only ataxia but also ovarian failure...
  5. ncbi request reprint Measuring Friedreich ataxia: complementary features of examination and performance measures
    D R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, and Children s Hospital of Philadelphia, PA 19104 4318, USA
    Neurology 66:1711-6. 2006
    ..To examine the potential validity of performance measures and examination-based scales in Friedreich ataxia (FA) by examining their correlation with disease characteristics...
  6. ncbi request reprint Lack of effect of polymorphisms in dopamine metabolism related genes on imaging of TRODAT-1 in striatum of asymptomatic volunteers and patients with Parkinson's disease
    David R Lynch
    Department of Neurology, University of Pennsylvania and The Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA
    Mov Disord 18:804-12. 2003
    ..These results demonstrate that these specific genetic variations do not alter the fidelity of (99)Tc-TRODAT-1 as a measure of dopaminergic function in asymptomatic volunteer individuals or patients with PD...
  7. ncbi request reprint Practical approaches to neurogenetic disease
    David R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, USA
    J Neuroophthalmol 22:297-304. 2002
    ....
  8. ncbi request reprint Contrast letter acuity as a measure of visual dysfunction in patients with Friedreich ataxia
    David R Lynch
    Department of Neurology, University of Pennsylvania and The Children s Hospital of Philadelphia, 19104, USA
    J Neuroophthalmol 22:270-4. 2002
    ..We sought to identify a simple, reliable method for assessing clinical and subclinical visual dysfunction in patients with Friedreich ataxia...
  9. ncbi request reprint Friedreich ataxia: effects of genetic understanding on clinical evaluation and therapy
    David R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, USA
    Arch Neurol 59:743-7. 2002
    ..Although no proven therapy is yet available, antioxidants are a potential method for therapeutic intervention...
  10. ncbi request reprint NMDA receptor pharmacology: perspectives from molecular biology
    D R Lynch
    Department of Neurology, University of Pennsylvania and The Children s Hospital of Philadelphia, 19104 4318, USA
    Curr Drug Targets 2:215-31. 2001
    ..This suggests that NMDA receptor subtype selective drugs can be created, and further understanding of subtype specific mechanisms ultimately may allow successful use of NMDA receptor antagonists as therapeutic agents...
  11. ncbi request reprint Near infrared muscle spectroscopy in patients with Friedreich's ataxia
    David R Lynch
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    Muscle Nerve 25:664-73. 2002
    ..These results suggest that NIRS may be an effective tool for monitoring the biochemical and functional features of Friedreich's ataxia in parallel...
  12. ncbi request reprint Excitotoxicity: perspectives based on N-methyl-D-aspartate receptor subtypes
    David R Lynch
    Department of Neurology, University of Pennsylvania and The Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104 4318, USA
    J Pharmacol Exp Ther 300:717-23. 2002
    ..This review discusses these models and the current understanding of the relationship between NMDA receptor subtypes and excitotoxicity...
  13. doi request reprint A phase 3, double-blind, placebo-controlled trial of idebenone in friedreich ataxia
    David R Lynch
    Division of Neurology, Children s Hospital of Philadelphia, 502 Abramson Bldg, Philadelphia, PA 19104 4318, USA
    Arch Neurol 67:941-7. 2010
    ..To assess the efficacy of idebenone on neurological function in patients with Friedreich ataxia...
  14. pmc Measuring the rate of progression in Friedreich ataxia: implications for clinical trial design
    Lisa S Friedman
    Department of Neurology, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    Mov Disord 25:426-32. 2010
    ..These results help to establish norms for progression in FRDA that can be useful in measuring the long-term success of therapeutic agents and defining sample-size calculations for double-blind clinical trials...
  15. pmc Developmental and cell-selective variations in N-methyl-D-aspartate receptor degradation by calpain
    Yi Na Dong
    Department of Neurology and Pediatrics, University of Pennsylvania and The Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104 4318, USA
    J Neurochem 99:206-17. 2006
    ..Our data suggest that the susceptibility of the NMDA receptor to cleavage by calpain varies with neuronal maturity in a manner that may alter its electrophysiological properties...
  16. pmc Paraneoplastic anti-N-methyl-D-aspartate receptor encephalitis associated with ovarian teratoma
    Josep Dalmau
    Department of Neurology, Division of Neuro Oncology, University of Pennsylvania, Philadelphia, PA 19104, USA
    Ann Neurol 61:25-36. 2007
    ..To report the autoantigens of a new category of treatment-responsive paraneoplastic encephalitis...
  17. ncbi request reprint Interactions of postsynaptic density-95 and the NMDA receptor 2 subunit control calpain-mediated cleavage of the NMDA receptor
    Yi Na Dong
    Department of Neurology, University of Pennsylvania and The Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104 4318, USA
    J Neurosci 24:11035-45. 2004
    ..PSD-95 could regulate the susceptibility of NMDA receptors to calpain-mediated cleavage during synaptic transmission and excitotoxicity...
  18. pmc A patient with encephalitis associated with NMDA receptor antibodies
    Lauren H Sansing
    Hospital of the University of Pennsylvania, Philadelphia, PA, USA
    Nat Clin Pract Neurol 3:291-6. 2007
    ..There was muscle rigidity, frequent facial grimacing, rhythmic abdominal contractions, kicking motions of the legs, and intermittent dystonic postures of the right arm...
  19. pmc Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies
    Josep Dalmau
    Department of Neurology, University of Pennsylvania, Philadelphia, PA 19104, USA
    Lancet Neurol 7:1091-8. 2008
    ..We aimed to analyse the clinical and immunological features of patients with the disorder and examine the effects of antibodies against NMDA receptors in neuronal cultures...
  20. ncbi request reprint Calpain and synaptic function
    Hai Yan Wu
    Department of Pediatrics, Children s Hospital of Philadelphia and The University of Pennsylvania, Philadelphia, PA, USA
    Mol Neurobiol 33:215-36. 2006
    ..This article focuses on recent findings on the role of calpain-mediated proteolytic processes in potentially regulating synaptic substrates in physiological and pathophysiological events in the nervous system...
  21. pmc Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis in children and adolescents
    Nicole R Florance
    Division of Neurology, Department of Pediatrics, Children s Hospital of Philadelphia, Philadelphia, PA, USA
    Ann Neurol 66:11-8. 2009
    ..To report the clinical features of anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis in patients < or = 18 years old...
  22. ncbi request reprint Cytosolic catechols inhibit alpha-synuclein aggregation and facilitate the formation of intracellular soluble oligomeric intermediates
    Joseph R Mazzulli
    The Joseph Stokes Jr Research Institute, The Children s Hospital of Philadelphia and the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 26:10068-78. 2006
    ..These data indicate that intraneuronal dopamine levels can be a major modulator of alpha-syn aggregation and inclusion formation, with important implications on the selective degeneration of these neurons in Parkinson's disease...
  23. ncbi request reprint Selective activation induced cleavage of the NR2B subunit by calpain
    Kelly L Simpkins
    Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania 19104 4306, USA
    J Neurosci 23:11322-31. 2003
    ..Such forms could contribute to excitotoxicity and synaptic remodeling...
  24. pmc AMPA receptor antibodies in limbic encephalitis alter synaptic receptor location
    Meizan Lai
    Department of Neurology, University of Pennsylvania, Philadelphia, PA 19104, USA
    Ann Neurol 65:424-34. 2009
    ..To report the clinical and immunological features of a novel autoantigen related to limbic encephalitis (LE) and the effect of patients' antibodies on neuronal cultures...
  25. ncbi request reprint Distinct cleavage patterns of normal and pathologic forms of alpha-synuclein by calpain I in vitro
    Amanda J Mishizen-Eberz
    Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA
    J Neurochem 86:836-47. 2003
    ..Elucidating the role of calpain I in the proteolytic processing of alpha-syn in normal and diseased brains may clarify mechanisms of neurodegenerative alpha-synucleinopathies...
  26. ncbi request reprint Cleavage of alpha-synuclein by calpain: potential role in degradation of fibrillized and nitrated species of alpha-synuclein
    Amanda J Mishizen-Eberz
    Department of Neurology, University of Pennsylvania and The Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA
    Biochemistry 44:7818-29. 2005
    ..These results provide insight into possible disease mechanisms underlying synucleinopathies since the formation of alpha-syn fibrils could be causally linked to the onset/progression of these disorders...
  27. ncbi request reprint Effects of a functional COMT polymorphism on prefrontal cognitive function in patients with 22q11.2 deletion syndrome
    Carrie E Bearden
    Children s Hospital of Philadelphia, Department of Child Development, USA
    Am J Psychiatry 161:1700-2. 2004
    ..The goal of the present study was to examine COMT genotype as a predictor of prefrontal cognitive function in patients with 22q11.2 deletion syndrome...
  28. pmc Axonal α7 nicotinic ACh receptors modulate presynaptic NMDA receptor expression and structural plasticity of glutamatergic presynaptic boutons
    Hong Lin
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Proc Natl Acad Sci U S A 107:16661-6. 2010
    ....
  29. pmc Cellular and synaptic mechanisms of anti-NMDA receptor encephalitis
    Ethan G Hughes
    Department of Neuroscience, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 30:5866-75. 2010
    ..The loss of this subtype of glutamate receptors eliminates NMDAR-mediated synaptic function, resulting in the learning, memory, and other behavioral deficits observed in patients with anti-NMDAR encephalitis...
  30. ncbi request reprint Proteolysis of the N-methyl-d-aspartate receptor by calpain in situ
    Rodney P Guttmann
    Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4318, USA
    J Pharmacol Exp Ther 302:1023-30. 2002
    ..These studies demonstrate that NR2A is a substrate for calpain in situ and that this proteolytic event can modulate NMDA receptor levels...
  31. doi request reprint Pharmacotherapy for Friedreich ataxia
    Amy Y Tsou
    Department of Neurology, University of Pennsylvania School of Medicine, and Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104 4318, USA
    CNS Drugs 23:213-23. 2009
    ..However, continued development of new therapies will require creation of new, more sensitive measures for neurological dysfunction in FA, and clinically relevant measures of cardiac dysfunction...
  32. doi request reprint Health related quality of life measures in Friedreich Ataxia
    Elizabeth Epstein
    Department of Neurology, University of Pennsylvania School of Medicine, USA
    J Neurol Sci 272:123-8. 2008
    ..Findings of this study are consistent with the phenotypic characteristics of FA, and suggest that HRQOL measures are potentially useful as clinical markers of disease status in FA...
  33. pmc Antioxidant use in Friedreich ataxia
    Lauren Myers
    Department of Neurology, University of Pennsylvania School of Medicine, USA
    J Neurol Sci 267:174-6. 2008
    ..This confirms that non-prescription antioxidant use represents a major confounder to formal trials of existing and novel agents for Friedreich ataxia...
  34. ncbi request reprint Apelin, an endogenous neuronal peptide, protects hippocampal neurons against excitotoxic injury
    Lauren A O'Donnell
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Neurochem 102:1905-17. 2007
    ..Thus, apelin/APJ signaling likely represents an endogenous hippocampal neuronal survival response, and therefore apelin should be further investigated as a potential neuroprotectant against hippocampal injury...
  35. pmc Fyn-mediated phosphorylation of NR2B Tyr-1336 controls calpain-mediated NR2B cleavage in neurons and heterologous systems
    Hai Yan Wu
    Departments of Pediatrics and Neurology, University of Pennsylvania, Philadelphia, PA 19104, USA
    J Biol Chem 282:20075-87. 2007
    ..Thus, the Fyn-controlled regulation of NMDA receptor cleavage by calpain may play critical roles in controlling NMDA receptor properties during synaptic plasticity and excitotoxicity...
  36. ncbi request reprint N-methyl-D-aspartate receptor subtype mediated bidirectional control of p38 mitogen-activated protein kinase
    Elisa A Waxman
    Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    J Biol Chem 280:29322-33. 2005
    ..The ability of NMDAR subtype-specific mechanisms to regulate p38 has implications for NMDAR-mediated synaptic plasticity, gene regulation, and excitotoxicity...
  37. ncbi request reprint N-methyl-D-aspartate receptor subtypes: multiple roles in excitotoxicity and neurological disease
    Elisa A Waxman
    Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, USA
    Neuroscientist 11:37-49. 2005
    ..This review examines the roles of NMDA receptor subtypes in excitotoxicity and neurological disorders...
  38. ncbi request reprint The E46K mutation in alpha-synuclein increases amyloid fibril formation
    Eric A Greenbaum
    Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Biol Chem 280:7800-7. 2005
    ..These findings support the notion that aberrant alpha-synuclein polymerization resulting in the formation of pathological inclusions can lead to disease...
  39. ncbi request reprint N-methyl-D-aspartate receptor-dependent regulation of the glutamate transporter excitatory amino acid carrier 1
    Elisa A Waxman
    Department of Pharmacology, Children s Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Biol Chem 282:17594-607. 2007
    ..This NMDA receptor-dependent regulation of EAAC1 provides a novel mechanism that may shape excitatory signaling during synaptic plasticity and/or excitotoxicity...
  40. ncbi request reprint Functional consequences of alpha-synuclein tyrosine nitration: diminished binding to lipid vesicles and increased fibril formation
    Roberto Hodara
    Stokes Research Institute and Department of Biochemistry and Biophysics, Children s Hospital of Philadelphia and The University of Pennsylvania, 19104, USA
    J Biol Chem 279:47746-53. 2004
    ..Collectively, these data suggest that post-translational modification of alpha-syn by nitration can promote the formation of intracytoplasmic inclusions that constitute the hallmark of Parkinson disease and other synucleinopathies...
  41. ncbi request reprint Juvenile dentatorubral-pallidoluysian atrophy: new clinical features
    Daniel J Licht
    Division of Child Neurology, The Children s Hospital of Philadelphia, Philadelphia, PA 19104, USA
    Pediatr Neurol 26:51-4. 2002
    ..The present family expands the clinical description of juvenile-onset dentatorubral-pallidoluysian atrophy and emphasizes the importance of considering dentatorubral-pallidoluysian atrophy in children with progressive myoclonus epilepsy...
  42. doi request reprint Novel, complex interruptions of the GAA repeat in small, expanded alleles of two affected siblings with late-onset Friedreich ataxia
    Catherine A Stolle
    The Department of Pathology and Laboratory Medicine, The Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104 4318, USA
    Mov Disord 23:1303-6. 2008
    ..Our observations suggest that interrupted GAA repeats do not clearly impact the age of onset in FA...
  43. ncbi request reprint Human immunodeficiency virus (HIV)-induced neurotoxicity: roles for the NMDA receptor subtypes
    Lauren A O'Donnell
    Department of Neurology, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 26:981-90. 2006
    ..Antagonists of NR2A and NR2B subunits as well as inhibitors of calpain activation offer attractive neuroprotective approaches against HIV in both developing and mature brain...
  44. doi request reprint Pregnancy with Friedreich ataxia: a retrospective review of medical risks and psychosocial implications
    Lisa S Friedman
    Departments of Neurology and Pediatrics, University of Pennsylvania School of Medicine, and Children s Hospital of Philadelphia, Philadelphia, PA, USA
    Am J Obstet Gynecol 203:224.e1-5. 2010
    ..However, little research exists exploring the medical or psychosocial complications that arise from pregnancy with this disease...
  45. doi request reprint Health-related quality of life in children with Friedreich ataxia
    Erin K Paulsen
    Departments of Neurology and Pediatrics, University of Pennsylvania School of Medicine, and The Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104 4318, USA
    Pediatr Neurol 42:335-7. 2010
    ..Additional studies are needed to examine the relationship between health-related quality of life and disease markers and to further establish the validity of the PedsQL 4.0 in this population...
  46. ncbi request reprint Neurogenetics. Introduction
    David R Lynch
    Department of Neurology Pediatrics, Division of Medical Genetics, University of Pennsylvania Medical Center, Philadelphia, PA 19104, USA
    Neurol Clin 20:xi-xii. 2002
  47. doi request reprint Subjective improvement in proprioception in 2 patients with atypical Friedreich ataxia treated with varenicline (Chantix)
    Theresa A Zesiewicz
    Department of Neurology, University of South Florida Ataxia Research Center, Tampa, FL 33612, USA
    J Clin Neuromuscul Dis 10:191-3. 2009
    ....
  48. pmc Calpain and the glutamatergic synapse
    Shachee Doshi
    Division of Neurology, Children s Hospital of Philadelphia, Philadelphia, Pennsylvania
    Front Biosci (Schol Ed) 1:466-76. 2009
    ..As a result, calpain-mediated cleavage in neurons might not only be involved in pathological events like excitotoxicity, but may also have neuroprotective effects and roles in physiological synaptic transmission...
  49. ncbi request reprint Increased prevalence of unprovoked seizures in patients with a 22q11.2 deletion
    Amy Kao
    Division of Neurology, Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA
    Am J Med Genet A 129:29-34. 2004
    ..2 deletion syndrome should be considered in patients with epilepsy and other signs suggestive of this interstitial deletion syndrome, and have implications for the identification of potential genetic loci for idiopathic epilepsy...
  50. doi request reprint Urinary isoprostanes in Friedreich ataxia: lack of correlation with disease features
    Lauren M Myers
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
    Mov Disord 23:1920-2. 2008
    ..Thus, urinary F(2)-isoprostanes are not a useful biomarker in FA...
  51. doi request reprint Clinical measures of dysarthria in Friedreich Ataxia
    Arunjot Singh
    Department of Neurology, University of Pennsylvania School of Medicine and The Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104 4318, USA
    Mov Disord 25:108-11. 2010
    ..Thus, four of five measures capture speech dysfunction in FA and may provide feasible, inexpensive, quantitative testing for therapeutic monitoring in FA...

Research Grants12

  1. Regulation of NMDA Receptors in Excitotoxicity by Calpain and FYN
    DAVID ROBINSON LYNCH; Fiscal Year: 2010
    ..Through understanding of this process, the proposal may facilitate therapies for preventing damage in neurologic disorders such as stroke. ..
  2. NMDA RECEPTORS, PROTEIN KINASE C, AND EXCITOTOXICITY
    David Lynch; Fiscal Year: 1999
    ..This systematic approach should provide critical information on the complete mechanisms of control of NMDA receptors by PKC and their significance in physiologic and pathophysiologic processes. ..
  3. Regulation of NMDA Receptors in Excitotoxicity by Calpain and FYN
    David Lynch; Fiscal Year: 2009
    ..Through understanding of this process, the proposal may facilitate therapies for preventing damage in neurologic disorders such as stroke. ..
  4. Regulation of NMDA Receptors in Excitotoxicity by Calpain and FYN
    David Lynch; Fiscal Year: 2007
    ..abstract_text> ..
  5. Calpain Mediated Cleavage of NR2 in Excitotoxicity
    David Lynch; Fiscal Year: 2006
    ..Overall, the present I proposal will define how calpain proteolysis of the NMDA receptor modulates receptor properties, allowing us to determine the role of this process in neuronal function and disease processes. ..
  6. Calpain Mediated Cleavage of NR2 in Excitotoxicity
    David Lynch; Fiscal Year: 2005
    ..Overall, the present I proposal will define how calpain proteolysis of the NMDA receptor modulates receptor properties, allowing us to determine the role of this process in neuronal function and disease processes. ..
  7. Calpain Mediated Cleavage of NR2 in Excitotoxicity
    David Lynch; Fiscal Year: 2004
    ..Overall, the present I proposal will define how calpain proteolysis of the NMDA receptor modulates receptor properties, allowing us to determine the role of this process in neuronal function and disease processes. ..
  8. Calpain Mediated Cleavage of NR2 in Excitotoxicity
    David Lynch; Fiscal Year: 2003
    ..Overall, the present I proposal will define how calpain proteolysis of the NMDA receptor modulates receptor properties, allowing us to determine the role of this process in neuronal function and disease processes. ..
  9. NMDA RECEPTORS, PROTEIN KINASE C, AND EXCITOTOXICITY
    David Lynch; Fiscal Year: 2002
    ..This systematic approach should provide critical information on the complete mechanisms of control of NMDA receptors by PKC and their significance in physiologic and pathophysiologic processes. ..
  10. NMDA RECEPTORS, PROTEIN KINASE C, AND EXCITOTOXICITY
    David Lynch; Fiscal Year: 2001
    ..This systematic approach should provide critical information on the complete mechanisms of control of NMDA receptors by PKC and their significance in physiologic and pathophysiologic processes. ..
  11. NMDA RECEPTORS, PROTEIN KINASE C, AND EXCITOTOXICITY
    David Lynch; Fiscal Year: 2000
    ..This systematic approach should provide critical information on the complete mechanisms of control of NMDA receptors by PKC and their significance in physiologic and pathophysiologic processes. ..