A common variant of the autophagy protein ATG16L1 is a risk factor for Crohn's disease. But the genetic alteration is revealed only when the protein is cleaved by the enzyme caspase 3 during cellular stress. See Article p.456
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 51 print issues and online access
$199.00 per year
only $3.90 per issue
Rent or buy this article
Prices vary by article type
from$1.95
to$39.95
Prices may be subject to local taxes which are calculated during checkout
References
Hampe, J. et al. Nature Genet. 39, 207–211 (2007).
Maloy, K. J. & Powrie, F. Nature 474, 298–306 (2011).
Murthy, A. et al. Nature 506, 456–462 (2014).
Jostins, L. et al. Nature 491, 119–124 (2012).
Saitoh, T. et al. Nature 456, 264–268 (2008).
Levine, B., Mizushima, N. & Virgin, H. W. Nature 469, 323–335 (2011).
McIlwain, D. R., Berger, T. & Mak, T. W. Cold Spring Harb. Perspect. Biol. 5, a008656 (2013).
Khalil, H. et al. Mol. Cell. Biol. 32, 4523–4533 (2012).
Deuring, J. J. et al. Gut http://dx.doi.org/10.1136/gutjnl-2012-303527 (2013).
Adolph, T. E. et al. Nature 503, 272–276 (2013).
Uhlig, H. H. Gut 62, 1795–1805 (2013).
Author information
Authors and Affiliations
Corresponding authors
Rights and permissions
About this article
Cite this article
Kaser, A., Blumberg, R. Stressful genetics in Crohn's disease. Nature 506, 441–442 (2014). https://doi.org/10.1038/nature13060
Published:
Issue Date:
DOI: https://doi.org/10.1038/nature13060
This article is cited by
-
Role of epithelial cells in the pathogenesis and treatment of inflammatory bowel disease
Journal of Gastroenterology (2016)