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Rotenone-dependent changes of anterograde motor protein expression and mitochondrial mobility in brain areas related to neurodegenerative diseases.

Authors: Melo, Thaiany Q  D'unhao, Aline M  Martins, Stephanie A  Farizatto, Karen L G  Chaves, Rodrigo S  Ferrari, Merari F R 
Citation: Melo TQ, etal., Cell Mol Neurobiol. 2013 Apr;33(3):327-35. doi: 10.1007/s10571-012-9898-z. Epub 2012 Dec 22.
Pubmed: (View Article at PubMed) PMID:23263842
DOI: Full-text: DOI:10.1007/s10571-012-9898-z

The presence of protein aggregates is common in neurodegenerative disorders; however, the real cause and effect of these aggregates during neurodegeneration is still a matter of investigation. We hypothesize that impairment of intracellular traffic may appear in the absence of protein inclusions and might trigger protein aggregation. In the present study, we aimed to evaluate mitochondria mobility as well as protein and messenger RNA expression of KIF1B and KIF5 that are molecular motors for neuronal anterograde traffic, in hippocampus, substantia nigra, and locus coeruleus of 10-month-old Lewis rats and cultured cells, from these same areas, following exposure to low doses of rotenone that do not lead to protein inclusions. The present study showed alteration in KIF1B and KIF5 expression, as well as in mitochondria mobility prior to protein aggregation involved in neurodegenerative disorders. These findings suggest that change in intracellular trafficking might be critical and one of the primary events for impairment of cell physiology during neurodegeneration associated with protein inclusions.


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RGD Object Information
RGD ID: 12738403
Created: 2017-02-03
Species: All species
Last Modified: 2017-02-03
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.