Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry

By L. Travassos, L. Carneiro, Mahendrasingh Ramjeet, S. Hussey, Yun-Gi Kim, J. Magalhaes, L. Yuan, F. Soares, Evelyn Chea, L. Bourhis and 6 more. Nature Immunology, 2010

1,352 citations recorded by the source corpus.

Subfields: Endocrinology, Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/097c4df251b9da7e9d2c2990831074d512ba9252

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In Endocrinology

1. F. Powrie
2. K. Maloy
3. N. Mizushima

In Epidemiology

1. D. Tang
2. R. Kang
3. M. Komatsu
4. N. Mizushima
5. I. Slaninová
6. Michael Lotze
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In Immunology

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4. R. Kang
5. K. Papadakis
6. Michael Lotze
7. V. Dixit
8. R. Wiest

Citations in the corpus

• PAMPs and DAMPs: Signal 0s that Spur Autophagy and Immunity (2012, background): “In mammalian cells, NOD1 and NOD2 signal to induce autophagy and functionally interact with Atg16L1 (138, 148).”
• Genetics and pathogenesis of inflammatory bowel disease (2011, background): “For example, MDP stimulation induces autophagy, which controls bacterial replication and antigen presentation, and acts on dendritic cells in conjunction with TLR ligands to promote T H 17-cell differentiatio”
• Innate and adaptive immunity in inflammatory bowel disease. (2014, background): “Interestingly, while immune stimulation via TLRs had been shown to activate autophagy [33], recent studies have linked NOD2 with autophagy induction and have shown that both NOD2 and ATG16L1 variants induce altered autophagy, antigen presentation and intracellular bacterial handling by DCs [34,35].”
• Autophagy: Renovation of Cells and Tissues (2011, background): “When yeast cells are cultured in nitrogen-free medium, autophagy-deficient cells rapidly decrease intracellular amino acid levels (Onodera and Ohsumi, 2005) and lose their viability (Tsukada and Ohsumi, 1993).”
• Autophagy in malignant transformation and cancer progression (2015, neutral): “…hence sustaining colorectal carcinogenesis, and gallbladder carcinoma), as well as Chlamydia pneumoniae (an etiological determinant in some forms of lung cancer) (Nakagawa et al , 2004; Travassos et al , 2010; Yasir et al , 2011; Conway et al , 2013; Griffin et al , 2013; Zhang et al , 2014).”
• Pathological bacterial translocation in liver cirrhosis. (2014, background): “, failure to recruit autophagy protein ATG16L1 and thus impaired wrapping of invading bacteria by autophagosomes [175].”
• Mechanisms of Disease: Inflammatory Bowel Diseases. (2019, background): “Not only through NOD2 but also via CD risk locus ATG16L1, Paneth cells function in autophagy is compromised in patients with CD (25, 75).”