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Autophagy. 2013 Aug;9(8):1256-7. doi: 10.4161/auto.25483. Epub 2013 Jun 28.

Autophagy receptor CALCOCO2/NDP52 takes center stage in Crohn disease.

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  • 1Institute of Clinical Molecular Biology; Christian-Albrechts-University of Kiel; Kiel, Germany; Subramani Lab and San Diego Center for Systems Biology; University of California San Diego; La Jolla, CA USA.


To advance understanding of the complex genetics of Crohn disease (CD) we sequenced 42 whole exomes of patients with CD and five healthy control individuals, resulting in identification of a missense mutation in the autophagy receptor calcium binding and coiled-coil domain 2 (CALCOCO2/NDP52) gene. Protein domain modeling and functional studies highlight the potential role of this mutation in controlling NFKB signaling downstream of toll-like receptor (TLR) pathways. We summarize our recent findings and discuss the role of autophagy as a major modulator of proinflammatory signaling in the context of chronic inflammation.


CALCOCO2; Crohn disease; NDP52; NF-kappaB; adaptophagy; autophagy; inflammation; toll-like receptor

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