@article{d830c97f55784e7387d979e67d0ca0d0,
title = "The mouse C9ORF72 ortholog is enriched in neurons known to degenerate in ALS and FTD",
abstract = "Using transgenic mice harboring a targeted LacZ insertion, we studied the expression pattern of the C9ORF72 mouse ortholog (3110043O21Rik). Unlike most genes that are mutated in amyotrophic lateral sclerosis (ALS), which are ubiquitously expressed, the C9ORF72 ortholog was most highly transcribed in the neuronal populations that are sensitive to degeneration in ALS and frontotemporal dementia. Thus, our results provide a potential explanation for the cell type specificity of neuronal degeneration caused by C9ORF72 mutations.",
author = "Naoki Suzuki and Maroof, {Asif M.} and Merkle, {Florian T.} and Kathryn Koszka and Atsushi Intoh and Ian Armstrong and Rob Moccia and Davis-Dusenbery, {Brandi N.} and Kevin Eggan",
note = "Funding Information: The authors wish to thank all members of the Eggan laboratory for their technical support and helpful discussions. We also thank the Harvard Stem Cell and Regenerative Biology Histology Core. This work was supported by the Howard Hughes Medical Institute, Project ALS, p2ALS, Target ALS and National Institute of Neurological Disorders and Stroke grant #164520. N.S. was supported by the 2011 Lilly Scientific Fellowship Program.",
year = "2013",
doi = "10.1038/nn.3566",
language = "English (US)",
volume = "16",
pages = "1725--1727",
journal = "Nature Neuroscience",
issn = "1097-6256",
publisher = "Nature Publishing Group",
number = "12",
}