|  Help  |  About  |  Contact Us

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

First Author  Gauthier LR Year  2004
Journal  Cell Volume  118
Issue  1 Pages  127-38
PubMed ID  15242649 Mgi Jnum  J:91294
Mgi Id  MGI:3046393 Doi  10.1016/j.cell.2004.06.018
Citation  Gauthier LR, et al. (2004) Huntingtin controls neurotrophic support and survival of neurons by enhancing BDNF vesicular transport along microtubules. Cell 118(1):127-38
abstractText  Polyglutamine expansion (polyQ) in the protein huntingtin is pathogenic and responsible for the neuronal toxicity associated with Huntington's disease (HD). Although wild-type huntingtin possesses antiapoptotic properties, the relationship between the neuroprotective functions of huntingtin and pathogenesis of HD remains unclear. Here, we show that huntingtin specifically enhances vesicular transport of brain-derived neurotrophic factor (BDNF) along microtubules. Huntingtin-mediated transport involves huntingtin-associated protein-1 (HAP1) and the p150(Glued) subunit of dynactin, an essential component of molecular motors. BDNF transport is attenuated both in the disease context and by reducing the levels of wild-type huntingtin. The alteration of the huntingtin/HAP1/p150(Glued) complex correlates with reduced association of motor proteins with microtubules. Finally, we find that the polyQ-huntingtin-induced transport deficit results in the loss of neurotrophic support and neuronal toxicity. Our findings indicate that a key role of huntingtin is to promote BDNF transport and suggest that loss of this function might contribute to pathogenesis.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

5 Bio Entities

Trail: Publication

0 Expression