Autophagy receptor CALCOCO2/NDP52 takes center stage in Crohn disease
Copyright policy )Autophagy receptor CALCOCO2/NDP52 takes center stage in Crohn disease
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.
- University of California, San Diego United States
- University of California United States
- Institute of Molecular Biology Germany
- Kiel University Germany
Male, 570, autophagy, Biochemistry & Molecular Biology, 610, Crohn's Disease, Ulcerative, Autoimmune Disease, Oral and gastrointestinal, adaptophagy, Crohn Disease, Genetics, NDP52, 2.1 Biological and endogenous factors, Humans, NF-kappaB, Inflammatory Bowel Disease, Crohn disease, Nuclear Proteins, Biological Sciences, Colitis, CALCOCO2, Repressor Proteins, inflammation, Biochemistry and cell biology, toll-like receptor, Colitis, Ulcerative, Female, Biochemistry and Cell Biology, Digestive Diseases
Male, 570, autophagy, Biochemistry & Molecular Biology, 610, Crohn's Disease, Ulcerative, Autoimmune Disease, Oral and gastrointestinal, adaptophagy, Crohn Disease, Genetics, NDP52, 2.1 Biological and endogenous factors, Humans, NF-kappaB, Inflammatory Bowel Disease, Crohn disease, Nuclear Proteins, Biological Sciences, Colitis, CALCOCO2, Repressor Proteins, inflammation, Biochemistry and cell biology, toll-like receptor, Colitis, Ulcerative, Female, Biochemistry and Cell Biology, Digestive Diseases
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