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TRAF6 and motor neuron loss
Author(s) -
Butler Carrie Lynn,
Dennis John S.,
Kane Michael J.,
Citron Bruce A.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.526.2
Subject(s) - motor neuron , amyotrophic lateral sclerosis , spinal cord , neuroscience , neuron , spinal cord injury , biology , downregulation and upregulation , medicine , disease , gene , pathology , genetics
TNF Receptor Associated Factor Six (TRAF6) activates transcription factor pathways including NF‐kB and c‐Jun. These pathways play roles in cell survival. Amyotrophic lateral sclerosis (ALS) and spinal cord injury are two examples of motor neuron disorders. We sought to identify factors that comprised a common dysregulation theme under motor neuron loss conditions. We analyzed gene expression changes in motor neurons mechanically injured in culture and in vivo traumatic impact injury rat spinal cords with Affymetrix gene arrays and found TRAF6 mRNA to be upregulated. These results were extended to neurodegenerative motor neuron loss, examining TRAF6 mRNA levels in human ALS spinal cords and in the wobbler mouse model of motor neuron disease. The gene expression changes, determined by qRT‐PCR, indicated that TRAF6 was upregulated in human ALS and in the mouse model spinal cords. We have generated cDNA clones of human and mouse TRAF6 to facilitate cause and effect experiments to better understand the relationships between TRAF6 and neuronal survival. Although our protein interactions studies will better define the function of TRAF6 in motor neuron loss, the elevation in TRAF6 in motor neurons programmed for cell death suggests that TRAF6 plays a role in motor neuron loss in spinal cord tissues. This study was supported by the Office of Research and Development, Medical Research Service, Department of Veterans Affairs, the Bay Pines Foundation, and the Alzheimer's Association.