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. 2013 Jun 28;9(8):1256–1257. doi: 10.4161/auto.25483

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Figure 1. Hypothetical model: Putative role of allelic variants of autophagy receptor CALCOCO2/NDP52 in susceptibility to Crohn disease. Under physiological conditions (left), the wild-type allele of CALCOCO2 is capable of inhibiting proinflammatory NFKB signaling by facilitating selective degradation of adaptors of TLRs or other PAMP receptors (‘adaptophagy’). In CD, the risk allele of CALCOCO2 (Ala248, caused by a low-frequency missense mutation) fails to recognize polyubiquitinated adaptors, resulting in adaptor stabilization and excessive NFKB activity (right). A, adaptor; UB, ubiquitin chains.