G Brent Irvine

Summary

Affiliation: Queen's University Belfast
Country: UK

Publications

  1. ncbi request reprint Alpha-synuclein aggregation
    Angela M Bodles
    University of Arkansas for Medical Sciences, Donald W Reynolds Center on Aging, Little Rock, AR 72205, USA
    Protein Pept Lett 11:271-9. 2004
  2. pmc Protein aggregation in the brain: the molecular basis for Alzheimer's and Parkinson's diseases
    G Brent Irvine
    School of Medicine and Dentistry, The Queen s University of Belfast, Belfast, Northern Ireland
    Mol Med 14:451-64. 2008
  3. pmc Identification of valid reference genes for the normalization of RT qPCR gene expression data in human brain tissue
    David T R Coulson
    Division of Psychiatry and Neuroscience, School of Medicine and Dentistry, Queen s University Belfast, Whitla Medical Building, Belfast, BT9 7BL, Northern Ireland, UK
    BMC Mol Biol 9:46. 2008
  4. ncbi request reprint High-performance size-exclusion chromatography of peptides
    G Brent Irvine
    Centre for Peptide and Protein Engineering, School of Biology and Biochemistry, Queen s University Belfast, Medical Biology Centre, 97 Lisburn Road, Belfast BT9 7BL, UK
    J Biochem Biophys Methods 56:233-42. 2003
  5. doi request reprint α-Synuclein mRNA and soluble α-synuclein protein levels in post-mortem brain from patients with Parkinson's disease, dementia with Lewy bodies, and Alzheimer's disease
    Joseph G Quinn
    Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen s University Belfast, N Ireland, UK
    Brain Res 1459:71-80. 2012
  6. doi request reprint Zinc transporter mRNA levels in Alzheimer's disease postmortem brain
    Nancy Beyer
    Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen s University Belfast, Belfast, N Ireland
    J Alzheimers Dis 29:863-73. 2012
  7. doi request reprint Variation in RTN3 and PPIL2 genes does not influence platelet membrane beta-secretase activity or susceptibility to alzheimer's disease in the northern Irish population
    Robyn Carson
    Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen s University Belfast, Whitla Medical Building, 97 Lisburn Road, Belfast, BT9 7BL, Northern Ireland, UK
    Neuromolecular Med 11:337-44. 2009
  8. doi request reprint BACE1 mRNA expression in Alzheimer's disease postmortem brain tissue
    David T R Coulson
    Queen s University Belfast, School of Medicine, Dentistry and Biomedical Sciences, Northern Ireland
    J Alzheimers Dis 22:1111-22. 2010
  9. pmc ZnT3 mRNA levels are reduced in Alzheimer's disease post-mortem brain
    Nancy Beyer
    Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen s University Belfast, Northern Ireland
    Mol Neurodegener 4:53. 2009
  10. doi request reprint IQ motif selectivity in human IQGAP1: binding of myosin essential light chain and S100B
    Sevvel Pathmanathan
    Medical Biology Centre, School of Biological Sciences, Queen s University Belfast, 97 Lisburn Road, Belfast, BT9 7BL, UK
    Mol Cell Biochem 318:43-51. 2008

Collaborators

Detail Information

Publications15

  1. ncbi request reprint Alpha-synuclein aggregation
    Angela M Bodles
    University of Arkansas for Medical Sciences, Donald W Reynolds Center on Aging, Little Rock, AR 72205, USA
    Protein Pept Lett 11:271-9. 2004
    ..We have defined a sequence within the NAC region of alpha-synuclein that is necessary for aggregation. Exploitation of chemically modified analogues of this peptide may produce inhibitors of aggregation...
  2. pmc Protein aggregation in the brain: the molecular basis for Alzheimer's and Parkinson's diseases
    G Brent Irvine
    School of Medicine and Dentistry, The Queen s University of Belfast, Belfast, Northern Ireland
    Mol Med 14:451-64. 2008
    ..In this review, we discuss this theme as it relates to the two most common neurodegenerative conditions-Alzheimer's and Parkinson's diseases...
  3. pmc Identification of valid reference genes for the normalization of RT qPCR gene expression data in human brain tissue
    David T R Coulson
    Division of Psychiatry and Neuroscience, School of Medicine and Dentistry, Queen s University Belfast, Whitla Medical Building, Belfast, BT9 7BL, Northern Ireland, UK
    BMC Mol Biol 9:46. 2008
    ..Given that expression of some commonly used reference genes is altered in certain conditions, this study aimed to establish which reference genes were stably expressed in post mortem brain tissue from individuals with AD, PD or DLB...
  4. ncbi request reprint High-performance size-exclusion chromatography of peptides
    G Brent Irvine
    Centre for Peptide and Protein Engineering, School of Biology and Biochemistry, Queen s University Belfast, Medical Biology Centre, 97 Lisburn Road, Belfast BT9 7BL, UK
    J Biochem Biophys Methods 56:233-42. 2003
    ..In this report, HPSEC is described in relation to its application to peptides, especially regarding purification, estimation of molecular weight and study of molecular associations...
  5. doi request reprint α-Synuclein mRNA and soluble α-synuclein protein levels in post-mortem brain from patients with Parkinson's disease, dementia with Lewy bodies, and Alzheimer's disease
    Joseph G Quinn
    Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen s University Belfast, N Ireland, UK
    Brain Res 1459:71-80. 2012
    ..This might result from altered translation, or removal of α-synuclein protein from a soluble detectable state, either by turnover or conversion to an insoluble form...
  6. doi request reprint Zinc transporter mRNA levels in Alzheimer's disease postmortem brain
    Nancy Beyer
    Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen s University Belfast, Belfast, N Ireland
    J Alzheimers Dis 29:863-73. 2012
    ..These expression changes could either reflect or cause the altered cortical Zn2+ distribution in AD, potentially increasing the likelihood of interactions between Zn2+ and Aβ or tau protein...
  7. doi request reprint Variation in RTN3 and PPIL2 genes does not influence platelet membrane beta-secretase activity or susceptibility to alzheimer's disease in the northern Irish population
    Robyn Carson
    Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen s University Belfast, Whitla Medical Building, 97 Lisburn Road, Belfast, BT9 7BL, Northern Ireland, UK
    Neuromolecular Med 11:337-44. 2009
    ..We conclude that common or potentially functional genetic variation in these BACE1 interacting proteins does not affect platelet membrane beta-secretase activity or contribute to risk of AD in this population...
  8. doi request reprint BACE1 mRNA expression in Alzheimer's disease postmortem brain tissue
    David T R Coulson
    Queen s University Belfast, School of Medicine, Dentistry and Biomedical Sciences, Northern Ireland
    J Alzheimers Dis 22:1111-22. 2010
    ..This analysis suggested that increased BACE1 mRNA expression in remaining neuronal cells may contribute to the increased BACE1 protein levels and activity found in brain regions affected by AD...
  9. pmc ZnT3 mRNA levels are reduced in Alzheimer's disease post-mortem brain
    Nancy Beyer
    Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen s University Belfast, Northern Ireland
    Mol Neurodegener 4:53. 2009
    ....
  10. doi request reprint IQ motif selectivity in human IQGAP1: binding of myosin essential light chain and S100B
    Sevvel Pathmanathan
    Medical Biology Centre, School of Biological Sciences, Queen s University Belfast, 97 Lisburn Road, Belfast, BT9 7BL, UK
    Mol Cell Biochem 318:43-51. 2008
    ..This clearly establishes that S100B can interact with its targets through IQ motifs in addition to interacting via previously reported sequences. These results are discussed in terms of the function of IQGAP1 and IQ motif recognition...
  11. doi request reprint A novel reciprocal and biphasic relationship between membrane cholesterol and beta-secretase activity in SH-SY5Y cells and in human platelets
    Wei Wei Liu
    School of Medicine, Dentistry and Biomedical Sciences, Queen s University Belfast, 97 Lisburn Road, Belfast, Northern Ireland, UK
    J Neurochem 108:341-9. 2009
    ....
  12. ncbi request reprint Inhibition of fibril formation and toxicity of a fragment of alpha-synuclein by an N-methylated peptide analogue
    Angela M Bodles
    Centre for Peptide and Protein Engineering, School of Biology and Biochemistry, The Queen s University of Belfast, Medical Biology Centre, Belfast BT9 7BL, UK
    Neurosci Lett 359:89-93. 2004
    ..Moreover, an equimolar mixture of the non-methylated and methylated peptides formed very few fibrils and toxicity was markedly reduced...
  13. pmc Familial genes in sporadic disease: common variants of alpha-synuclein gene associate with Parkinson's disease
    Owen A Ross
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL, USA
    Mech Ageing Dev 128:378-82. 2007
    ..It is now crucial to identify the susceptibility allele and elucidate its functionality which may generate a therapeutic target for PD...
  14. ncbi request reprint Inhibitors of alpha-synuclein oligomerization and toxicity: a future therapeutic strategy for Parkinson's disease and related disorders
    Dena A M Amer
    Department of Biochemistry, Faculty of Medicine and Health Sciences, United Arab Emirates University, P O Box 17666, Al Ain, United Arab Emirates
    Exp Brain Res 173:223-33. 2006
    ..These compounds could serve as lead compounds for the design of new drugs for the treatment of PD and related disorders in the future...
  15. ncbi request reprint Clinical traits of LRRK2-associated Parkinson's disease in Ireland: a link between familial and idiopathic PD
    David Gosal
    Department of Neurology, Mater Misericordiae Hospital, Eccles St, Dublin 7, Ireland
    Parkinsonism Relat Disord 11:349-52. 2005
    ..The influence of the G2019S substitution on protein function and disease phenotype has yet to be fully resolved, but its elucidation will undoubtedly further our understanding of the mechanisms underlying Parkinson's disease...