Hasil Pencarian - Gillian P Bates

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  1. 1
    Hdac6 knock-out increases tubulin acetylation but does not modify disease progression in the R6/2 mouse model of Huntington's disease.

    Hdac6 knock-out increases tubulin acetylation but does not modify disease progression in the R6/2 mouse model of Huntington's disease. oleh Anna Bobrowska, Paolo Paganetti, Patrick Matthias, Gillian P Bates

    Diterbitkan 2011-01-01
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  2. 2
    In Vivo Profiling Reveals a Competent Heat Shock Response in Adult Neurons: Implications for Neurodegenerative Disorders.

    In Vivo Profiling Reveals a Competent Heat Shock Response in Adult Neurons: Implications for Neurodegenerative Disorders. oleh Alisia Carnemolla, Hayley Lazell, Saliha Moussaoui, Gillian P Bates

    Diterbitkan 2015-01-01
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  3. 3
    The ubiquitin-proteasome reporter GFPu does not accumulate in neurons of the R6/2 transgenic mouse model of Huntington's disease.

    The ubiquitin-proteasome reporter GFPu does not accumulate in neurons of the R6/2 transgenic mouse model of Huntington's disease. oleh John S Bett, Casey Cook, Leonard Petrucelli, Gillian P Bates

    Diterbitkan 2009-01-01
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  4. 4
    Regulatory mechanisms of incomplete huntingtin mRNA splicing

    Regulatory mechanisms of incomplete huntingtin mRNA splicing oleh Andreas Neueder, Anaelle A. Dumas, Agnesska C. Benjamin, Gillian P. Bates

    Diterbitkan 2018-09-01
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  5. 5
    Genetic knock-down of HDAC3 does not modify disease-related phenotypes in a mouse model of Huntington's disease.

    Genetic knock-down of HDAC3 does not modify disease-related phenotypes in a mouse model of Huntington's disease. oleh Lara Moumné, Ken Campbell, David Howland, Yingbin Ouyang, Gillian P Bates

    Diterbitkan 2012-01-01
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  6. 6
    Ablation of kynurenine 3-monooxygenase rescues plasma inflammatory cytokine levels in the R6/2 mouse model of Huntington’s disease

    Ablation of kynurenine 3-monooxygenase rescues plasma inflammatory cytokine levels in the R6/2 mouse model of Huntington’s disease oleh Marie Katrin Bondulich, Yilan Fan, Yeojin Song, Flaviano Giorgini, Gillian P. Bates

    Diterbitkan 2021-03-01
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  7. 7
    Depletion of rabphilin 3A in a transgenic mouse model (R6/1) of Huntington's disease, a possible culprit in synaptic dysfunction

    Depletion of rabphilin 3A in a transgenic mouse model (R6/1) of Huntington's disease, a possible culprit in synaptic dysfunction oleh Ruben Smith, Åsa Petersén, Gillian P. Bates, Patrik Brundin, Jia-Yi Li

    Diterbitkan 2005-12-01
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  8. 8
    Formation of polyglutamine inclusions in a wide range of non-CNS tissues in the HdhQ150 knock-in mouse model of Huntington's disease.

    Formation of polyglutamine inclusions in a wide range of non-CNS tissues in the HdhQ150 knock-in mouse model of Huntington's disease. oleh Hilary Moffitt, Graham D McPhail, Ben Woodman, Carl Hobbs, Gillian P Bates

    Diterbitkan 2009-11-01
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  9. 9
    Correlations of behavioral deficits with brain pathology assessed through longitudinal MRI and histopathology in the R6/2 mouse model of HD.

    Correlations of behavioral deficits with brain pathology assessed through longitudinal MRI and histopathology in the R6/2 mouse model of HD. oleh Ivan Rattray, Edward Smith, Richard Gale, Kaoru Matsumoto, Gillian P Bates, Michel Modo

    Diterbitkan 2013-01-01
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  10. 10
    The Huntington's disease-related cardiomyopathy prevents a hypertrophic response in the R6/2 mouse model.

    The Huntington's disease-related cardiomyopathy prevents a hypertrophic response in the R6/2 mouse model. oleh Michal Mielcarek, Marie K Bondulich, Linda Inuabasi, Sophie A Franklin, Thomas Muller, Gillian P Bates

    Diterbitkan 2014-01-01
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  11. 11
    Silencing Srsf6 does not modulate incomplete splicing of the huntingtin gene in Huntington’s disease models

    Silencing Srsf6 does not modulate incomplete splicing of the huntingtin gene in Huntington’s disease models oleh Michael A. Mason, Casandra Gomez-Paredes, Kirupa Sathasivam, Andreas Neueder, Aikaterini-Smaragdi Papadopoulou, Gillian P. Bates

    Diterbitkan 2020-08-01
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  12. 12
    The heat shock response, determined by QuantiGene multiplex, is impaired in HD mouse models and not caused by HSF1 reduction

    The heat shock response, determined by QuantiGene multiplex, is impaired in HD mouse models and not caused by HSF1 reduction oleh Casandra Gomez-Paredes, Michael A. Mason, Bridget A. Taxy, Aikaterini S. Papadopoulou, Paolo Paganetti, Gillian P. Bates

    Diterbitkan 2021-04-01
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  13. 13
    Correlations of Behavioral Deficits with Brain Pathology Assessed through Longitudinal MRI and Histopathology in the HdhQ150/Q150 Mouse Model of Huntington's Disease.

    Correlations of Behavioral Deficits with Brain Pathology Assessed through Longitudinal MRI and Histopathology in the HdhQ150/Q150 Mouse Model of Huntington's Disease. oleh Ivan Rattray, Edward J Smith, William R Crum, Thomas A Walker, Richard Gale, Gillian P Bates, Michel Modo

    Diterbitkan 2017-01-01
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  14. 14
    Correction: SIRT1 Activity Is Linked to Its Brain Region-Specific Phosphorylation and Is Impaired in Huntington's Disease Mice.

    Correction: SIRT1 Activity Is Linked to Its Brain Region-Specific Phosphorylation and Is Impaired in Huntington's Disease Mice. oleh Raffaella Tulino, Agnesska C Benjamin, Nelly Jolinon, Donna L Smith, Eduardo N Chini, Alisia Carnemolla, Gillian P Bates

    Diterbitkan 2016-01-01
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  15. 15
    Correlations of behavioral deficits with brain pathology assessed through longitudinal MRI and histopathology in the R6/1 mouse model of Huntington's disease.

    Correlations of behavioral deficits with brain pathology assessed through longitudinal MRI and histopathology in the R6/1 mouse model of Huntington's disease. oleh Ivan Rattray, Edward J Smith, William R Crum, Thomas A Walker, Richard Gale, Gillian P Bates, Michel Modo

    Diterbitkan 2013-01-01
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  16. 16
    Genetic knock-down of HDAC7 does not ameliorate disease pathogenesis in the R6/2 mouse model of Huntington's disease.

    Genetic knock-down of HDAC7 does not ameliorate disease pathogenesis in the R6/2 mouse model of Huntington's disease. oleh Caroline L Benn, Rachel Butler, Lydia Mariner, Jude Nixon, Hilary Moffitt, Michal Mielcarek, Ben Woodman, Gillian P Bates

    Diterbitkan 2009-06-01
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  17. 17
    SIRT1 Activity Is Linked to Its Brain Region-Specific Phosphorylation and Is Impaired in Huntington's Disease Mice.

    SIRT1 Activity Is Linked to Its Brain Region-Specific Phosphorylation and Is Impaired in Huntington's Disease Mice. oleh Raffaella Tulino, Agnesska C Benjamin, Nelly Jolinon, Donna L Smith, Eduardo N Chini, Alisia Carnemolla, Gillian P Bates

    Diterbitkan 2016-01-01
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  18. 18
    SAHA decreases HDAC 2 and 4 levels in vivo and improves molecular phenotypes in the R6/2 mouse model of Huntington's disease.

    SAHA decreases HDAC 2 and 4 levels in vivo and improves molecular phenotypes in the R6/2 mouse model of Huntington's disease. oleh Michal Mielcarek, Caroline L Benn, Sophie A Franklin, Donna L Smith, Ben Woodman, Paul A Marks, Gillian P Bates

    Diterbitkan 2011-01-01
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  19. 19
    A human single-chain Fv intrabody preferentially targets amino-terminal huntingtin fragments in striatal models of Huntington's disease

    A human single-chain Fv intrabody preferentially targets amino-terminal huntingtin fragments in striatal models of Huntington's disease oleh Todd W. Miller, Chun Zhou, Silvia Gines, Marcy E. MacDonald, Nicholas D. Mazarakis, Gillian P. Bates, James S. Huston, Anne Messer

    Diterbitkan 2005-06-01
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  20. 20
    Mitochondrial clearance and increased HSF-1 activity are coupled to promote longevity in fasted Caenorhabditis elegans

    Mitochondrial clearance and increased HSF-1 activity are coupled to promote longevity in fasted Caenorhabditis elegans oleh Nikolaos Tataridas-Pallas, Yahyah Aman, Rhianna Williams, Hannah Chapman, Kevin J.H. Cheng, Casandra Gomez-Paredes, Gillian P. Bates, John Labbadia

    Diterbitkan 2024-06-01
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