2022 - Research.com Best Female Scientist Award
The scientist’s investigation covers issues in Huntington's disease, Huntingtin, Huntingtin Protein, Genetics and Neurodegeneration. Her studies deal with areas such as Genetically modified mouse, Cell biology, Neuroscience and Trinucleotide repeat expansion as well as Huntington's disease. The Huntingtin study combines topics in areas such as Molecular biology, Gene expression, Protein aggregation and Immunology.
Gillian P. Bates combines subjects such as Atrophin-1, Polyglutamine tract and Dentatorubral-pallidoluysian atrophy with her study of Huntingtin Protein. Her work on Locus, Allele and Methylation as part of general Genetics study is frequently connected to Lysosomal transport and Cystinosis, therefore bridging the gap between diverse disciplines of science and establishing a new relationship between them. Her work deals with themes such as SETD2, Histone and Biochemistry, which intersect with Neurodegeneration.
Gillian P. Bates mainly investigates Huntington's disease, Huntingtin, Genetics, Cell biology and Huntingtin Protein. Her Huntington's disease study combines topics in areas such as Genetically modified mouse, Neuroscience, Neurodegeneration and Trinucleotide repeat expansion. Her Genetically modified mouse research focuses on Endocrinology and how it relates to Receptor.
Her study in Huntingtin is interdisciplinary in nature, drawing from both Molecular biology and Exon. In her work, Heat shock factor is strongly intertwined with Heat shock, which is a subfield of Cell biology. Her Huntingtin Protein research is multidisciplinary, incorporating elements of Immunology and Dentatorubral-pallidoluysian atrophy.
Gillian P. Bates mainly focuses on Cell biology, Huntingtin, Huntington's disease, Exon and Mutant. Her work carried out in the field of Cell biology brings together such families of science as Neurodegeneration, HSF1, Pathogenesis and Heat shock. Her Huntingtin study incorporates themes from Phenotype, Genetically modified mouse, Neural stem cell and Trinucleotide repeat expansion.
Her biological study focuses on Huntingtin Protein. Her Exon research incorporates themes from Molecular biology, Messenger RNA, RNA splicing and Intron. Her studies in Mutant integrate themes in fields like Inclusion bodies, Gene knockin, Neuroprotection and Phosphorylation.
Gillian P. Bates spends much of her time researching Huntington's disease, Huntingtin, Cell biology, Internal medicine and Neurodegeneration. Gillian P. Bates is interested in Huntingtin Protein, which is a branch of Huntington's disease. Her research integrates issues of Exon, Genetically modified mouse and Trinucleotide repeat expansion in her study of Huntingtin.
Her research in Cell biology intersects with topics in Inclusion bodies, Biochemistry, Neuroprotection and Downregulation and upregulation. Her work investigates the relationship between Internal medicine and topics such as Endocrinology that intersect with problems in Atrophy, Heart failure and Cardiomyopathy. Her biological study spans a wide range of topics, including Protein aggregation, Immunology, Innate immune system, Immune system and Proinflammatory cytokine.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes
Marcy E. MacDonald;Christine M. Ambrose;Mabel P. Duyao;Richard H. Myers.
Exon 1 of the HD Gene with an Expanded CAG Repeat Is Sufficient to Cause a Progressive Neurological Phenotype in Transgenic Mice
Laura Mangiarini;Kirupa Sathasivam;Mary Seller;Barbara Cozens.
A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes. The Huntington's Disease Collaborative Research Group.
M Shah;N Datson;L Srinidhi;VP Stanton.
Aggregation of Huntingtin in Neuronal Intranuclear Inclusions and Dystrophic Neurites in Brain
Marian DiFiglia;Ellen Sapp;Kathryn O. Chase;Stephen W. Davies.
FORMATION OF NEURONAL INTRANUCLEAR INCLUSIONS UNDERLIES THE NEUROLOGICAL DYSFUNCTION IN MICE TRANSGENIC FOR THE HD MUTATION
Stephen W Davies;Mark Turmaine;Barbara A Cozens;Marian DiFiglia.
Huntingtin-Encoded Polyglutamine Expansions Form Amyloid-like Protein Aggregates In Vitro and In Vivo
Eberhard Scherzinger;Rudi Lurz;Mark Turmaine;Laura Mangiarini.
Gillian Bates;K P S J Murphy;P Harper;L Jones.
Oxford University Press (2002)
Characterization of progressive motor deficits in mice transgenic for the human Huntington's disease mutation.
R. J. Carter;L. A. Lione;Trevor Humby;L. Mangiarini.
The Journal of Neuroscience (1999)
The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription.
Joan S. Steffan;Aleksey Kazantsev;Olivera Spasic-Boskovic;Marilee Greenwald.
Proceedings of the National Academy of Sciences of the United States of America (2000)
Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, ameliorates motor deficits in a mouse model of Huntington's disease
E. Hockly;V.M. Richon;B. Woodman;D.L. Smith.
Proceedings of the National Academy of Sciences of the United States of America (2003)
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