Gillian P. Bates

Optimisation of region-specific reference gene selection and relative gene expression analysis methods for pre-clinical trials of Huntington's disease (2008)

Benn, Caroline L, Fox, Helen, Bates, Gillian P

Abstract Background Transcriptional dysregulation is an early, key pathogenic mechanism in Huntington's disease (HD). Therefore, gene expression analyses have biomarker potential for measuring...

Mutant huntingtin's effects on striatal gene expression in mice recapitulate changes observed in human Huntington's disease brain and do not differ with mutant huntingtin length or wild-type huntingtin dosage (2007)

Kuhn, Alexandre, Goldstein, Darlene R., Hodges, Angela, Strand, Andrew D., Sengstag, Thierry, Kooperberg, Charles, ...

To test the hypotheses that mutant huntingtin protein length and wild-type huntingtin dosage have important effects on disease-related transcriptional dysfunction, we compared the changes in mRNA in...

Hsp27 overexpression in the R6/2 mouse model of Huntington's disease: chronic neurodegeneration does not induce Hsp27 activation (2007)

Zourlidou, Alexandra, Gidalevitz, Tali, Kristiansen, Mark, Landles, Christian, Woodman, Ben, Wells, Dominic J., ...

Huntington's disease (HD) is caused by an expanded polyglutamine tract in the huntingtin protein. Mitochondrial dysfunction and free radical damage occur in both R6/2 mice and HD patient brains and...

recapitulate changes (2007)

Re Kuhn, Darlene R. Goldstein, Angela Hodges, Andrew D. Str, Thierry Sengstag, Charles Kooperberg, ...

Mutant huntingtin's effects on striatal gene expression in mice

Hsp27 overexpression in the R6/2 mouse model of Huntington's Disease: Chronic Neurodegeneration does not Induce Hsp27 Activation (2007)

Zourlidou, Alexandra, Gidalevitz, Tali, Kristiansen, Mark, Landles, Christian, Woodman, Ben, Wells, Dominic J., ...

Huntington's disease (HD) is caused by an expanded polyglutamine tract in the huntingtin protein. Mitochondrial dysfunction and free radical damage occur in both R6/2 mice and HD patient brains and...

Proteasome impairment does not contribute to pathogenesis in R6/2 Huntington's disease mice: exclusion of proteasome activator REG{gamma} as a therapeutic target (2006)

Bett, John S., Goellner, Geoffrey M., Woodman, Ben, Pratt, Gregory, Rechsteiner, Martin, Bates, Gillian P.

Huntington's disease (HD) is one of a group of neurodegenerative disorders caused by the pathological expansion of a glutamine tract. A hallmark of these so-called polyglutamine diseases is the...

Progressive Alterations in the Hypothalamic-Pituitary-Adrenal Axis in the R6/2 Transgenic Mouse Model of Huntington's disease (2006)

Björkqvist, Maria, Petersén, Åsa, Bacos, Karl, Isaacs, Jeremy, Norlén, Per, Gil, Joana, ...

Huntington's disease (HD) is characterised by a triad of motor, psychiatric, and cognitive symptoms. While many of these symptoms are likely to be related to central nervous system pathology, others...

Progressive alterations in the hypothalamic-pituitary-adrenal axis in the R6/2 transgenic mouse model of Huntington's disease (2006)

Björkqvist, Maria, Petersén, Åsa, Bacos, Karl, Isaacs, Jeremy, Norlén, Per, Gil, Joana, ...

Huntington's disease (HD) is characterized by a triad of motor, psychiatric and cognitive symptoms. Although many of these symptoms are likely to be related to central nervous system pathology,...

Contribution of nuclear and extranuclear polyQ to neurological phenotypes in mouse models of Huntington's disease (2005)

Benn, Caroline L., Landles, Christian, Li, He, Strand, Andrew D., Woodman, Ben, Sathasivam, Kirupa, ...

In postmortem Huntington's disease brains, mutant htt is present in both nuclear and cytoplasmic compartments. To dissect the impact of nuclear and extranuclear mutant htt on the initiation and...

Progressive decrease in chaperone protein levels in a mouse model of huntington's disease and induction of stress proteins as a therapeutic approach (2004)

Hay, David G., Sathasivam, Kirupa, Tobaben, Sönke, Stahl, Bernd, Marber, Michael, Mestril, Ruben, ...

The manipulation of chaperone levels has been shown to inhibit aggregation and/or rescue cell death in cell culture, S. cerevisiae, C. elegans and D. melanogaster models of Huntington's disease (HD)...

Progressive decrease in chaperone protein levels in a mouse model of Huntington's disease and induction of stress proteins as a therapeutic approach (2004)

Hay, David G., Sathasivam, Kirupa, Tobaben, Sönke, Stahl, Bernd, Marber, Michael, Mestril, Ruben, ...

The manipulation of chaperone levels has been shown to inhibit aggregation and/or rescue cell death in Saccharomyces cerevisiae, Caenorhabditis elegans, Drosophila melanogaster and cell culture...

Progressive decrease in chaperone protein levels in a mouse model of huntington's disease and induction of stress proteins as a therapeutic approach (2004)

Hay, David G., Sathasivam, Kirupa, Tobaben, Sönke, Stahl, Bernd, Marber, Michael, Mestril, Ruben, ...

The manipulation of chaperone levels has been shown to inhibit aggregation and/or rescue cell death in cell culture, S. cerevisiae, C. elegans and D. melanogaster models of Huntington's disease (HD)...

Mouse models of Huntington's disease (2002)

Bates, Gillian P.

Radically updated to include coverage of developments in the molecular biology and genetics of the condition following isolation of the gene. Includes implications for prediction and genetic...

The huntingtin interacting protein HIP1 is a clathrin and {alpha}-adaptin-binding protein involved in receptor-mediated endocytosis (2001)

Waelter, Stephanie, Scherzinger, Eberhard, Hasenbank, Renate, Nordhoff, Eckhard, Lurz, Rudi, Goehler, Heike, ...

The huntingtin interacting protein (HIP1) is enriched in membrane-containing cell fractions and has been implicated in vesicle trafficking. It is a multidomain protein containing an N-terminal ENTH...

Centrosome disorganization in fibroblast cultures derived from R6/2 Huntington's disease (HD) transgenic mice and HD patients (2001)

Sathasivam, Kirupa, Woodman, Ben, Mahal, Amabirpal, Bertaux, Fabien, Wanker, Erich E., Shima, Dave T., ...

Huntington’s disease (HD) is a progressive neurological disorder caused by a CAG/polyglutamine repeat expansion. We have previously generated the R6/2 mouse model that expresses exon 1 of...

Ultrastructural localization and progressive formation of neuropil aggregates in Huntington's disease transgenic mice (1999)

Li, He, Li, Shi-Hua, Cheng, Anna L., Mangiarini, Laura, Bates, Gillian P., Li, Xiao-Jiang

How aggregates of polyglutamine proteins are involved in the neurological symptoms of glutamine repeat diseases is unknown. We show that huntingtin aggregates are present in the neuronal processes of...

Transcript Map of the Human Chromosome 4p16.3 Consisting of 627 cDNA Clones Derived from 1 Mb of the Huntington's Disease Locus (1996)

Hadano, Shinji, Ishida, Yoshikazu, Tomiyasu, Hitoshi, Yamamoto, Kenji, Bates, Gillian P., Ikeda, Joh-E

Six hundred and twenty-seven cDNA clones from human brain cDNA libraries were characterized and integrated into a transcript map of the 1-Mb region on human chromosome 4p16.3 containing the...

A zinc-finger gene ZNF141 mapping at 4p16.3/D4S90 is a candidate gene for the Wolf-Hirschhorn (4p-) syndrome (1993)

Tommerup, Niels, Aagaard, Lissi, Lund, Connie L., Boel, Esper, Baxendale, Sarah, Bates, Gillian P., ...

Chromosomal aneusomy is a major cause of reproductive wastage and congenital malformations in man. Zinc finger encoding genes would be good candidates for being involved in the multiple developmental...

Self-assembly of polyglutamine-containing huntingtin fragments into amyloid-like fibrils: Implications for Huntington’s disease pathology

Scherzinger, Eberhard, Sittler, Annie, Schweiger, Katja, Heiser, Volker, Lurz, Rudi, Hasenbank, Renate, ...

Huntington’s disease is a progressive neurodegenerative disorder caused by a polyglutamine [poly(Q)] repeat expansion in the first exon of the huntingtin protein. Previously, we showed that...

Nonapoptotic neurodegeneration in a transgenic mouse model of Huntington's disease

Turmaine, Mark, Raza, Aysha, Mahal, Amarbirpal, Mangiarini, Laura, Bates, Gillian P., Davies, Stephen W.

Huntington's disease (HD) is a fatal inherited neurodegenerative disorder characterized by personality changes, motor impairment, and subcortical dementia. HD is one of a number of diseases caused by...

The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription

Steffan, Joan S., Kazantsev, Aleksey, Spasic-Boskovic, Olivera, Greenwald, Marilee, Zhu, Ya-Zhen, Gohler, Heike, ...

Huntington's Disease (HD) is caused by an expansion of a polyglutamine tract within the huntingtin (htt) protein. Pathogenesis in HD appears to include the cytoplasmic cleavage of htt and release of...

Altered brain neurotransmitter receptors in transgenic mice expressing a portion of an abnormal human Huntington disease gene

Cha, Jang-Ho J., Kosinski, Christoph M., Kerner, Julie A., Alsdorf, Stephen A., Mangiarini, Laura, Davies, Stephen W., ...

Loss of neurotransmitter receptors, especially glutamate and dopamine receptors, is one of the pathologic hallmarks of brains of patients with Huntington disease (HD). Transgenic mice that express...

Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, ameliorates motor deficits in a mouse model of Huntington's disease

Hockly, Emma, Richon, Victoria M., Woodman, Benjamin, Smith, Donna L., Zhou, Xianbo, Rosa, Eddie, ...

Huntington's disease (HD) is an inherited, progressive neurological disorder that is caused by a CAG/polyglutamine repeat expansion and for which there is no effective therapy. Recent evidence...

A potent small molecule inhibits polyglutamine aggregation in Huntington's disease neurons and suppresses neurodegeneration in vivo

Zhang, Xiaoqian, Smith, Donna L., Meriin, Anatoli B., Engemann, Sabine, Russel, Deborah E., Roark, Margo, ...

Polyglutamine (polyQ) disorders, including Huntington's disease (HD), are caused by expansion of polyQ-encoding repeats within otherwise unrelated gene products. In polyQ diseases, the pathology and...

Self-assembly of polyglutamine-containing huntingtin fragments into amyloid-like fibrils: Implications for Huntington’s disease pathology

Scherzinger, Eberhard, Sittler, Annie, Schweiger, Katja, Heiser, Volker, Lurz, Rudi, Hasenbank, Renate, ...

Huntington’s disease is a progressive neurodegenerative disorder caused by a polyglutamine [poly(Q)] repeat expansion in the first exon of the huntingtin protein. Previously, we showed that...

Nonapoptotic neurodegeneration in a transgenic mouse model of Huntington's disease

Turmaine, Mark, Raza, Aysha, Mahal, Amarbirpal, Mangiarini, Laura, Bates, Gillian P., Davies, Stephen W.

Huntington's disease (HD) is a fatal inherited neurodegenerative disorder characterized by personality changes, motor impairment, and subcortical dementia. HD is one of a number of diseases caused by...

The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription

Steffan, Joan S., Kazantsev, Aleksey, Spasic-Boskovic, Olivera, Greenwald, Marilee, Zhu, Ya-Zhen, Gohler, Heike, ...

Huntington's Disease (HD) is caused by an expansion of a polyglutamine tract within the huntingtin (htt) protein. Pathogenesis in HD appears to include the cytoplasmic cleavage of htt and release of...

Altered brain neurotransmitter receptors in transgenic mice expressing a portion of an abnormal human Huntington disease gene

Cha, Jang-Ho J., Kosinski, Christoph M., Kerner, Julie A., Alsdorf, Stephen A., Mangiarini, Laura, Davies, Stephen W., ...

Loss of neurotransmitter receptors, especially glutamate and dopamine receptors, is one of the pathologic hallmarks of brains of patients with Huntington disease (HD). Transgenic mice that express...

Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, ameliorates motor deficits in a mouse model of Huntington's disease

Hockly, Emma, Richon, Victoria M., Woodman, Benjamin, Smith, Donna L., Zhou, Xianbo, Rosa, Eddie, ...

Huntington's disease (HD) is an inherited, progressive neurological disorder that is caused by a CAG/polyglutamine repeat expansion and for which there is no effective therapy. Recent evidence...

A potent small molecule inhibits polyglutamine aggregation in Huntington's disease neurons and suppresses neurodegeneration in vivo

Zhang, Xiaoqian, Smith, Donna L., Meriin, Anatoli B., Engemann, Sabine, Russel, Deborah E., Roark, Margo, ...

Polyglutamine (polyQ) disorders, including Huntington's disease (HD), are caused by expansion of polyQ-encoding repeats within otherwise unrelated gene products. In polyQ diseases, the pathology and...

DNA instability in postmitotic neurons

Gonitel, Roman, Moffitt, Hilary, Sathasivam, Kirupa, Woodman, Ben, Detloff, Peter J., Faull, Richard L. M., ...

Huntington's disease (HD) is caused by a CAG repeat expansion that is unstable upon germ-line transmission and exhibits mosaicism in somatic tissues. We show that region-specific CAG repeat mosaicism...

A novel pathogenic pathway of immune activation detectable before clinical onset in Huntington's disease

Björkqvist, Maria, Wild, Edward J., Thiele, Jenny, Silvestroni, Aurelio, Andre, Ralph, Lahiri, Nayana, ...

Huntington's disease (HD) is an inherited neurodegenerative disorder characterized by both neurological and systemic abnormalities. We examined the peripheral immune system and found widespread...

The Ubiquitin-Proteasome Reporter GFPu Does Not Accumulate in Neurons of the R6/2 Transgenic Mouse Model of Huntington's Disease

Bett, John S., Cook, Casey, Petrucelli, Leonard, Bates, Gillian P.

Impairment of the ubiquitin-proteasome system (UPS) has long been considered an attractive hypothesis to explain the selective dysfunction and death of neurons in polyglutamine disorders such as...

Genetic Knock-Down of HDAC7 Does Not Ameliorate Disease Pathogenesis in the R6/2 Mouse Model of Huntington's Disease

Benn, Caroline L., Butler, Rachel, Mariner, Lydia, Nixon, Jude, Moffitt, Hilary, Mielcarek, Michal, ...

Huntington's disease (HD) is an inherited, progressive neurological disorder caused by a CAG/polyglutamine repeat expansion, for which there is no effective disease modifying therapy. In recent...