Publications de Valérie Gafner

TLR4- and TRIF-dependent stimulation of B lymphocytes by peptide liposomes enables T cell-independent isotype switch in mice

Andrea Pfeifer, Marija Vukicevic, Valérie Gafner, Andreas Muhs, Anna Lucia Buccarello, Pedro Miguel Nunes Pereira de Almeida Reis

Immunoglobulin class switching from IgM to IgG in response to peptides is generally T cell-dependent and vaccination in T cell-deficient individuals is inefficient. We show that a vaccine consisting of a dense array of peptides on liposomes induced peptide ...

Amer Soc Hematology2013

Dysregulation of gene expression in primary neuron models of Huntington's disease shows that polyglutamine-related effects on the striatal transcriptome may not be dependent on brain circuitry

Diana Zala, Patrick Aebischer, Valérie Gafner, Nicole Déglon, Heike Runne, Ozgün Gökce

Gene expression changes are a hallmark of the neuropathology of Huntington's disease (HD), but the exact molecular mechanisms of this effect remain uncertain. Here, we report that in vitro models of disease comprised of primary striatal neurons expressing ...

2008

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

Patrick Aebischer, Valérie Gafner, 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

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

Valérie Gafner

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

Akt is altered in an animal model of Huntington's disease and in patients

Patrick Aebischer, Valérie Gafner, Nicole Déglon

The insulin-like growth factor I (IGF-1)/Akt pathway plays a crucial role in Huntington's disease by phosphorylating the causative protein, polyQ-huntingtin, and abolishing its toxic properties [Humbert et al. (2002)Dev. Cell, 2, 831-837; Rangone et al. (2 ...

2005

Progressive and selective striatal degeneration in primary neuronal cultures using lentiviral vector coding for a mutant huntingtin fragment

Diana Zala, Patrick Aebischer, Valérie Gafner, Nicole Déglon

A lentiviral vector expressing a mutant huntingtin protein (htt171-82Q) was used to generate a chronic model of Huntington's disease (HD) in rat primary striatal cultures. In this model, the majority of neurons expressed the transgene so that Western blot ...

2005

Early and reversible neuropathology induced by tetracycline-regulated lentiviral overexpression of mutant huntingtin in rat striatum

Patrick Aebischer, Valérie Gafner, Nicole Déglon

The ability to overexpress full-length huntingtin or large fragments represents an important challenge to mimic Huntington's pathology and reproduce all stages of the disease in a time frame compatible with rodent life span. In the present study, tetracycl ...

Oxford University Press2003