Publication

Gene expression profiling of R6/2 transgenic mice with different CAG repeat lengths reveals genes associated with disease onset and progression in Huntington's disease

Related publications (91)

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

Darlene Goldstein, Mauro Delorenzi, Thierry Sengstag

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 seven genetic mouse models of Huntington's disease (HD) a ...

Oxford University Press2007

Splicy: a web-based tool for the prediction of possible alternative splicing events from Affymetrix probeset data

Philipp Bucher

BACKGROUND: The Affymetrix technology is nowadays a well-established method for the analysis of gene expression profiles in cancer research studies. However, changes in gene expression levels are not the only way to link genes and disease. The existence of ...

2007

A model-based optimization framework for the inference of regulatory interactions using time-course DNA microarray expression data

Vassily Hatzimanikatis, Eleftherios Papoutsakis

Background: Proteins are the primary regulatory agents of transcription even though mRNA expression data alone, from systems like DNA microarrays, are widely used. In addition, the regulation process in genetic systems is inherently non-linear in nature, a ...

2007

Evolutionary morphogenesis for multi-cellular systems

Dario Floreano, Daniel Roggen, Diego Federici

With a gene required for each phenotypic trait, direct genetic encodings may show poor scalability to increasing phenotype length. Developmental systems may alleviate this problem by providing more efficient indirect genotype to phenotype mappings. A novel ...

2007

Neuroprotection by Hsp104 and Hsp27 in lentiviral-based rat models of Huntington's disease

Patrick Aebischer, Nicole Déglon

Huntington's disease (HD) is an inherited neurodegenerative disorder caused by an expansion of glutamine repeats in the huntingtin (htt) protein. Abnormal protein folding and the accumulation of mutated htt are hallmarks of HD neuropathology. Heat-shock pr ...

Elsevier2007

Differential gene expression between adult queens and workers in the ant Lasius niger

Johannes Gräff, Laurent Keller

Ants and other social insects forming large societies are generally characterized by marked reproductive division of labour. Queens largely monopolize reproduction whereas workers have little reproductive potential. In addition, some social insect species ...

Wiley-Blackwell2007

Altering protein folding, intracellular signaling, or the post-transcriptional program as potential therapeutic strategies to counteract Huntington's disease

Huntington's disease (HD) is an autosomal, dominantly inherited neurodegenerative disorder caused by expansion of a glutamine (polyQ) repeat in the huntingtin (htt) protein. The selective striatal neurodegeneration induced by this disease causes choreic in ...

EPFL2006

Exploiting Binary Abstractions in Deciphering Gene Interactions

Giovanni De Micheli, Abhishek Garg

We consider computationally reconstructing gene regulatory networks on top of the binary abstraction of gene expression state information. Unlike previous Boolean network approaches, the proposed method does not handle noisy gene expression values directly ...

2006

Inhibition of calcineurin by FK506 protects against polyglutamine-huntingtin toxicity through an increase of huntingtin phosphorylation at S421

Patrick Aebischer

Huntington's disease (HD) is caused by an abnormal expanded polyglutamine (polyQ) repeat in the huntingtin protein. Insulin-like growth factor-1 acting through the prosurvival kinase Akt mediates the phosphorylation of huntingtin at S421 and inhibits the t ...

2006

CA150 expression delays striatal cell death in overexpression and knock-in conditions for mutant huntingtin neurotoxicity

Patrick Aebischer, Diana Zala

Transcriptional dysregulation caused by expanded polyglutamines (polyGlns) in huntingtin (htt) may be central to cell-autonomous mechanisms for neuronal cell death in Huntington's disease (HD) pathogenesis. We hypothesized that these mechanisms may involve ...

2006

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