R Meller

Summary

Affiliation: Legacy Research
Country: USA

Publications

  1. ncbi request reprint In vitro evidence that 5-hydroxytryptamine increases efflux of glial glutamate via 5-HT(2A) receptor activation
    R Meller
    University Department of Clinical Pharmacology, Radcliffe Infirmary, Oxford, United Kingdom
    J Neurosci Res 67:399-405. 2002
  2. ncbi request reprint Neuroprotection by osteopontin in stroke
    Robert Meller
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon 97232, USA
    J Cereb Blood Flow Metab 25:217-25. 2005
  3. pmc Rapid degradation of Bim by the ubiquitin-proteasome pathway mediates short-term ischemic tolerance in cultured neurons
    Robert Meller
    Robert S Dow Neurobiology Laboratories, Legacy Clinical Research and Technology Center, 1225 NE 2nd Avenue, Portland, OR 97232, USA
    J Biol Chem 281:7429-36. 2006
  4. pmc Activation of the caspase 8 pathway mediates seizure-induced cell death in cultured hippocampal neurons
    R Meller
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, OR 97232, USA
    Epilepsy Res 70:3-14. 2006
  5. ncbi request reprint Evidence of tumor necrosis factor receptor 1 signaling in human temporal lobe epilepsy
    Akitaka Yamamoto
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, OR, USA
    Exp Neurol 202:410-20. 2006
  6. pmc The role of the ubiquitin proteasome system in ischemia and ischemic tolerance
    Robert Meller
    Legacy Clinical Research and Technology Center, Portland, Oregon, USA
    Neuroscientist 15:243-60. 2009
  7. pmc Ubiquitin proteasome-mediated synaptic reorganization: a novel mechanism underlying rapid ischemic tolerance
    Robert Meller
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon 97232, USA
    J Neurosci 28:50-9. 2008
  8. ncbi request reprint Expression, proteolysis and activation of caspases 6 and 7 during rat C6 glioma cell apoptosis
    Robert Meller
    R S Dow Neurobiology Laboratories, Legacy Clinical Research and Technology Center, 1225 NE 2nd Avenue, Portland, OR 97232, USA
    Neurosci Lett 324:33-6. 2002
  9. ncbi request reprint Studies on the role of calcium in the 5-HT-stimulated release of glutamate from C6 glioma cells
    Robert Meller
    University Department of Clinical Pharmacology, Radcliffe Infirmary, Oxford OX2 6HE, UK
    Eur J Pharmacol 445:13-9. 2002
  10. ncbi request reprint CREB-mediated Bcl-2 protein expression after ischemic preconditioning
    Robert Meller
    RS Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon 97232, USA
    J Cereb Blood Flow Metab 25:234-46. 2005

Collaborators

Detail Information

Publications26

  1. ncbi request reprint In vitro evidence that 5-hydroxytryptamine increases efflux of glial glutamate via 5-HT(2A) receptor activation
    R Meller
    University Department of Clinical Pharmacology, Radcliffe Infirmary, Oxford, United Kingdom
    J Neurosci Res 67:399-405. 2002
    ..In conclusion, 5-HT stimulates the efflux of glutamate from C6 glioma cells following 5-HT(2A) receptor activation and involves a calcium-dependent mechanism...
  2. ncbi request reprint Neuroprotection by osteopontin in stroke
    Robert Meller
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon 97232, USA
    J Cereb Blood Flow Metab 25:217-25. 2005
    ..These data suggest that OPN is a potent neuroprotectant against ischemic injury...
  3. pmc Rapid degradation of Bim by the ubiquitin-proteasome pathway mediates short-term ischemic tolerance in cultured neurons
    Robert Meller
    Robert S Dow Neurobiology Laboratories, Legacy Clinical Research and Technology Center, 1225 NE 2nd Avenue, Portland, OR 97232, USA
    J Biol Chem 281:7429-36. 2006
    ..This suggests that the rapid degradation of cell death-promoting proteins by the ubiquitin-proteasome pathway may represent a novel therapeutic strategy to reduce cell damage following neuropathological insults, e.g. stroke...
  4. pmc Activation of the caspase 8 pathway mediates seizure-induced cell death in cultured hippocampal neurons
    R Meller
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, OR 97232, USA
    Epilepsy Res 70:3-14. 2006
    ..Taken together, our data suggests the extrinsic cell death pathway-associated caspase 8 is activated following seizures in vitro...
  5. ncbi request reprint Evidence of tumor necrosis factor receptor 1 signaling in human temporal lobe epilepsy
    Akitaka Yamamoto
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, OR, USA
    Exp Neurol 202:410-20. 2006
    ..These data suggest that TNFR1 signaling is engaged in the hippocampus of patients with refractory temporal lobe epilepsy...
  6. pmc The role of the ubiquitin proteasome system in ischemia and ischemic tolerance
    Robert Meller
    Legacy Clinical Research and Technology Center, Portland, Oregon, USA
    Neuroscientist 15:243-60. 2009
    ..The aim of this review is to discuss some of the recent advances in the understanding of protein ubiquitination and its implications for novel stroke therapies...
  7. pmc Ubiquitin proteasome-mediated synaptic reorganization: a novel mechanism underlying rapid ischemic tolerance
    Robert Meller
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon 97232, USA
    J Neurosci 28:50-9. 2008
    ..Together these data suggest that rapid tolerance results from changes to the postsynaptic density mediated by the ubiquitin-proteasome system, rendering neurons resistant to excitotoxicity...
  8. ncbi request reprint Expression, proteolysis and activation of caspases 6 and 7 during rat C6 glioma cell apoptosis
    Robert Meller
    R S Dow Neurobiology Laboratories, Legacy Clinical Research and Technology Center, 1225 NE 2nd Avenue, Portland, OR 97232, USA
    Neurosci Lett 324:33-6. 2002
    ..Activation of caspase-6 was paralleled by cleavage of the nuclear envelope protein lamin-A. These results highlight temporal differences in the activation of the triad of executioner caspases 3, 6 and 7 during glial cell apoptosis...
  9. ncbi request reprint Studies on the role of calcium in the 5-HT-stimulated release of glutamate from C6 glioma cells
    Robert Meller
    University Department of Clinical Pharmacology, Radcliffe Infirmary, Oxford OX2 6HE, UK
    Eur J Pharmacol 445:13-9. 2002
    ..We conclude that the 5-HT-induced efflux of glutamate from C6 glioma cells is Ca(2+)-dependent and involves, at least in part, the mobilisation of Ca(2+) from inositol (1,4,5) tris phosphate (IP(3)) sensitive intracellular stores...
  10. ncbi request reprint CREB-mediated Bcl-2 protein expression after ischemic preconditioning
    Robert Meller
    RS Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon 97232, USA
    J Cereb Blood Flow Metab 25:234-46. 2005
    ..H89, KN62, and U0126 reduced CREB activation and Bcl-2 expression. Taken together, these data suggest that after ischemic preconditioning CREB activation regulates the expression of the prosurvival protein Bcl-2...
  11. ncbi request reprint Cleavage of bid may amplify caspase-8-induced neuronal death following focally evoked limbic seizures
    D C Henshall
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon 97232, USA
    Neurobiol Dis 8:568-80. 2001
    ..These data suggest that intervention in caspase-8 and/or death receptor signaling may confer protection on the brain from the injurious effects of seizures...
  12. ncbi request reprint Seizure-like activity leads to the release of BAD from 14-3-3 protein and cell death in hippocampal neurons in vitro
    R Meller
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, OR 97232, USA
    Cell Death Differ 10:539-47. 2003
    ..However, the absence of neuroprotective effects of pathway intervention suggests that BAD may perform a reinforcement rather than instigator role in cell death following seizures in vitro...
  13. ncbi request reprint Formation of the Apaf-1/cytochrome c complex precedes activation of caspase-9 during seizure-induced neuronal death
    D C Henshall
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, OR 97232, USA
    Cell Death Differ 8:1169-81. 2001
    ..These data suggest seizures induce formation of the Apaf-1/cytochrome c complex prior to caspase-9 activation and caspase-9 may be a potential therapeutic target in the treatment of brain injury associated with seizures...
  14. ncbi request reprint Formation of a tumour necrosis factor receptor 1 molecular scaffolding complex and activation of apoptosis signal-regulating kinase 1 during seizure-induced neuronal death
    Sachiko Shinoda
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon, USA
    Eur J Neurosci 17:2065-76. 2003
    ..These data suggest ASK1 may be involved in the mechanism of seizure-induced neuronal death downstream of a TNFR1 death-signalling complex...
  15. ncbi request reprint Endogenous mechanisms of neuroprotection
    Roger Simon
    Robert Stone Dow Neurobiology Laboratories, Neurobiology Research, Legacy Clinical Research and Technology, Portland, OR 97208 3950, USA
    Epilepsia 48:72-3. 2007
  16. pmc Ubiquitin-proteasome system as a modulator of cell fate
    Simon J Thompson
    RS Dow Neurobiology Laboratories, Legacy Clinical Research and Technology Center, 1225 NE 2nd Avenue, Portland, OR 97232, USA
    Curr Opin Pharmacol 8:90-5. 2008
    ..With the number of ubiquitin conjugating and de-conjugating enzymes reaching close to the levels of protein kinases and phosphatases, it is clear that ubiquitination is an important biological regulatory step for proteins...
  17. ncbi request reprint In vivo and in vitro characterization of a novel neuroprotective strategy for stroke: ischemic postconditioning
    Giuseppe Pignataro
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon 97232, USA
    J Cereb Blood Flow Metab 28:232-41. 2008
    ..Our data suggest that postconditioning may represent a novel neuroprotective approach for focal ischemia/reperfusion, and one that is mediated, at least in part, by the activation of the protein kinase Akt...
  18. pmc Bcl-w protects hippocampus during experimental status epilepticus
    Brona Murphy
    Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, 123 St Stephen s Green, Dublin 2, Ireland
    Am J Pathol 171:1258-68. 2007
    ..Finally, we detected higher levels of Bcl-w in hippocampus from temporal lobe epilepsy patients compared with autopsy controls. These data identify Bcl-w as an endogenous neuroprotectant that may have seizure-suppressive functions...
  19. ncbi request reprint 5-HT2A receptor activation leads to increased BDNF mRNA expression in C6 glioma cells
    Robert Meller
    SmithKline Beecham Centre for Applied Neuropsychobiology, University Department of Clinical Pharmacology, Radcliffe Infirmary, Oxford
    Neuromolecular Med 1:197-205. 2002
    ..Our data show that 5-HT increases de novo BDNF mRNA synthesis following direct activation of the 5-HT2A receptor, via a calcium-dependent and protein kinase-dependent pathway...
  20. ncbi request reprint Expression and differential processing of caspases 6 and 7 in relation to specific epileptiform EEG patterns following limbic seizures
    David C Henshall
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon, USA
    Neurobiol Dis 10:71-87. 2002
    ..These data highlight differences in expression and activation of caspases 6 and 7 in response to identifiable seizure patterns, focusing potential therapeutic targets for neuroprotection in epilepsy...
  21. pmc Bim regulation may determine hippocampal vulnerability after injurious seizures and in temporal lobe epilepsy
    Sachiko Shinoda
    Robert S Dow Neurobiology Laboratories, Legacy Research, Portland, Oregon 97232, USA
    J Clin Invest 113:1059-68. 2004
    ..We conclude that Bim expression may be a critical determinant of whether seizures damage the brain, and that its control may be neuroprotective in status epilepticus and epilepsy...
  22. ncbi request reprint Death-associated protein kinase expression in human temporal lobe epilepsy
    David C Henshall
    Robert S Dow Neurobiology Laboratories, Legacy Research, Neurological Sciences Center, Portland, OR, USA
    Ann Neurol 55:485-94. 2004
    ..This study provides the first description of DAP kinase and DIP-1 in human brain and suggests DAP kinase is a novel molecular regulator of neuronal death in epilepsy...
  23. ncbi request reprint Effect of ischaemic preconditioning on genomic response to cerebral ischaemia: similarity to neuroprotective strategies in hibernation and hypoxia-tolerant states
    Mary P Stenzel-Poore
    Department of Molecular Microbiology and Immunology, Oregon Health and Science University, Portland, OR 97239, USA
    Lancet 362:1028-37. 2003
    ..We developed a mouse model of neuroprotection in stroke and did gene expression profiling to identify potential neuroprotective genes and their associated pathways...
  24. ncbi request reprint Expression, interaction, and proteolysis of death-associated protein kinase and p53 within vulnerable and resistant hippocampal subfields following seizures
    Tomohiro Araki
    Robert S Dow Neurobiology Laboratories, Legacy Research, 1225 NE 2nd Avenue, Portland, OR 97232, USA
    Hippocampus 14:326-36. 2004
    ..These data suggest that DAP kinase may be involved in the p53 pathway during seizure-induced neuronal death...
  25. ncbi request reprint Endotoxin preconditioning protects against the cytotoxic effects of TNFalpha after stroke: a novel role for TNFalpha in LPS-ischemic tolerance
    Holly L Rosenzweig
    Department of Molecular Microbiology and Immunology, Oregon Health and Science University, Portland, Oregon, USA
    J Cereb Blood Flow Metab 27:1663-74. 2007
    ....
  26. ncbi request reprint Upregulation of mitochondrial base-excision repair capability within rat brain after brief ischemia
    Dexi Chen
    Robert S Dow Neurobiology Laboratories, Legacy Research, Oregon Health Sciences University, Portland 97232, USA
    J Cereb Blood Flow Metab 23:88-98. 2003
    ..These data reveal the differences in BER capacity after brief or prolonged ischemia, which may contribute to the neuron's ability to resist subsequent ischemic insults...

Research Grants5

  1. Protein ubiquitination based neuroprotection for stroke
    Robert Meller; Fiscal Year: 2006
    ....
  2. Rapid ischemic tolerance: Ubiquitin-mediated structural reorganization
    Robert Meller; Fiscal Year: 2007
    ..Indeed, the long-term aim of these studies is to discover endogenous protective mechanisms that can be translated into effective rapid acting neuroprotective agents for stroke. ..
  3. Rapid ischemic tolerance: Synaptic re-organization and reduced excitotoxicity
    Robert Meller; Fiscal Year: 2010
    ..It is our aim to investigate these mechanisms to help develop new therapeutics for stroke, or for circumstances where ischemia can be predicted, such as heart bypass surgery. ..