Disruption of axonal transport by loss of huntingtin or expression of pathogenic polyQ proteins in Drosophila.

By Shermali Gunawardena, L. Her, R. Brusch, R. A. Laymon, Ingrid R. Niesman, B. Gordesky-Gold, L. Sintasath, N. Bonini, L. Goldstein. Neuron, 2003

677 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0e9debf459b32d3fe9a0ac8cf26938f66bf81d03

How researchers see this paper

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

In Cellular and Molecular Neuroscience

1. C. Zuccato
2. E. Cattaneo
3. M. Valenza
4. Volkmar Lessmann
5. U. Pandey
6. R. Schwarzenbacher
7. Marcel van den Heuvel
8. Ruben J. Cauchi

In Molecular Biology

1. Volkmar Lessmann
2. Jennifer L. Wacker
3. M. Valenza
4. E. Cattaneo
5. R. Schwarzenbacher
6. Marcel van den Heuvel
7. C. Zuccato
8. Ruben J. Cauchi

Citations in the corpus

• Selective vulnerability and pruning of phasic motoneuron axons in motoneuron disease alleviated by CNTF (2006, background): “Indeed, investigations of pathogenic mechanisms in Drosophila models have provided evidence that the loss of huntingtin, the overexpression of polyQ proteins or the overexpression of amyloid precursor protein mutants all specifically induce disruptions of axonal transpor”
• Molecular mechanisms and potential therapeutical targets in Huntington's disease. (2010, background): “They found that reduction in Drosophila huntingtin disrupts axonal transport (230).”
• Molecular pathways to neurodegeneration (2004, background): “Similarly, expression of mutant Htt in Drosophila produces an axonal transport phenotyp”
• The Fly as a Model for Neurodegenerative Diseases: Is It Worth the Jump? (2007, positive): “HD is an autosomal dominant disease caused by the expansion of a polyQ repeat in the huntingtin (Htt) protein. Characterised by a combination of chorea, cognitive impairment and affective changes, HD is one of the polyQ diseases that was successfully modelled in the fly. Indeed, both reduced express”
• Modulation of neurodegeneration by molecular chaperones (2005, background): “More recently, it has been shown that, in flies, HSC70 overexpression restores neuronal transport and suppresses the cell death that is caused by polyQ protein”
• Huntingtin controls neurotrophic support and survival of neurons by enhancing BDNF vesicular transport along microtubules. (2004, result): “Finally, we find that the polyQ(Gunawardena et al., 2003; Szebenyi et al., 2003).”
• Human Disease Models in Drosophila melanogaster and the Role of the Fly in Therapeutic Drug Discovery (2011, background): “…2001, 2005; Brignull et al., 2006 D. melanogaster Axonal transport defect, lethality, neurodegeneration, behavioral and electrophysiological defects Gunawardena et al., 2003; Romero et al., 2008 Spinal and bulbar muscular atrophy Zebrafish Massive neuronal apoptosis, small eyes and heads and…”