Huntingtin controls neurotrophic support and survival of neurons by enhancing BDNF vesicular transport along microtubules.

By L. Gauthier, Bénédicte C. Charrin, M. Borrell-Pages, J. Dompierre, Hélène Rangone, Fabrice Cordelières, J. D. De Mey, M. MacDonald, Volkmar Lessmann, S. Humbert and 1 more. Cell, 2004

1,200 citations recorded by the source corpus.

Subfields: Cell Biology, Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e12afe4c1989172e562064c15743c0fcc8383ea2

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. E. Holzbaur
2. Alison E. Twelvetrees

In Cellular and Molecular Neuroscience

1. C. Zuccato
2. E. Cattaneo
3. M. Valenza

In Molecular Biology

1. E. Holzbaur
2. K. Verstrepen
3. M. Valenza
4. E. Cattaneo
5. C. Zuccato
6. Alison E. Twelvetrees

Citations in the corpus

• Full-Length Human Mutant Huntingtin with a Stable Polyglutamine Repeat Can Elicit Progressive and Selective Neuropathogenesis in BACHD Mice (2008, background): “…BDNF is a well known molecular player in modulation of synaptic transmission and plasticity (Lu, 2003) and axonal transport (Baquet et al., 2004; Gauthier et al., 2004) and cortical BDNF expression (Zuccato et al., 2001) is affected in existing HD mice and HD patients, we examined whether an…”
• Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, background): “report from Gauthier and colleagues (202), this paper”
• GDNF, NGF and BDNF as therapeutic options for neurodegeneration. (2013, background): “In fact BDNF cortical tissue levels may be reduced by up to 45% in HD (Ferrer et al., 2000; Zuccato et al., 2001); and support for the striatal neurones is worsened by impaired huntingtin-mediated BDNF transport from the cortex (Gauthier et al., 2004).”
• Sustained therapeutic reversal of Huntington’s disease by transient repression of huntingtin synthesis (2012, neutral): “A continued need for huntingtin in the CNS has been proposed from efforts in mouse models with deletion of both huntingtin alleles at embryonic day 15.5 or postnatal day 5 (Dragatsis et al., 2000) and in cultured neuronal cells (Gauthier et al., 2004; Zuccato et al., 2003).”
• Variable tandem repeats accelerate evolution of coding and regulatory sequences. (2010, background): “Decreased axonal transport of BDNF-containing vesicles and altered Ca+2 signaling at the mitochondrial membrane also contribute to pathogenesis (40, 97).”
• AXONAL TRANSPORT: CARGO-SPECIFIC MECHANISMS OF MOTILITY AND REGULATION (2014, background): “Scaffolding proteins are also key: huntingtin is involved in the regulation of BDNF-positive vesicles (Gauthier et al., 2004) and autophagosomes (Wong and Holzbaur, 2014); JIP1 is involved in the regulation of APP-positive vesicles and autophagosomes (Fu and Holzbaur, 2013; Fu et al., 2014); JIP3…”
• Potential therapeutic uses of BDNF in neurological and psychiatric disorders (2011, background): “; in Huntington's disease, BDNF transport from the cortex to the striatum is impaire”