Nature Communications (Jun 2017)
E3 Ubiquitin ligase ZNRF4 negatively regulates NOD2 signalling and induces tolerance to MDP
- Pradeep Bist,
- Wan Shoo Cheong,
- Aylwin Ng,
- Neha Dikshit,
- Bae-Hoon Kim,
- Niyas Kudukkil Pulloor,
- Hanif Javanmard Khameneh,
- Matija Hedl,
- Avinash R. Shenoy,
- Vanniarajan Balamuralidhar,
- Najib Bin Abdul Malik,
- Michelle Hong,
- Albert Neutzner,
- Keh-Chuang Chin,
- Koichi S. Kobayashi,
- Antonio Bertoletti,
- Alessandra Mortellaro,
- Clara Abraham,
- John D. MacMicking,
- Ramnik J. Xavier,
- Bindu Sukumaran
Affiliations
- Pradeep Bist
- Program in Emerging Infectious Diseases, Duke-NUS Medical School
- Wan Shoo Cheong
- Program in Emerging Infectious Diseases, Duke-NUS Medical School
- Aylwin Ng
- Gastrointestinal Unit, Center for Computational and Integrative Biology, Massachusetts General Hospital, Harvard Medical School
- Neha Dikshit
- Program in Emerging Infectious Diseases, Duke-NUS Medical School
- Bae-Hoon Kim
- Departments of Microbial Pathogenesis and Immunobiology, HHMI, Yale Systems Biology Institute, Yale University School of Medicine
- Niyas Kudukkil Pulloor
- Program in Emerging Infectious Diseases, Duke-NUS Medical School
- Hanif Javanmard Khameneh
- Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR)
- Matija Hedl
- Department of Internal Medicine, Yale University School of Medicine
- Avinash R. Shenoy
- Departments of Microbial Pathogenesis and Immunobiology, HHMI, Yale Systems Biology Institute, Yale University School of Medicine
- Vanniarajan Balamuralidhar
- Program in Emerging Infectious Diseases, Duke-NUS Medical School
- Najib Bin Abdul Malik
- Program in Emerging Infectious Diseases, Duke-NUS Medical School
- Michelle Hong
- Program in Emerging Infectious Diseases, Duke-NUS Medical School
- Albert Neutzner
- Department of Biomedicine, University Hospital Basel
- Keh-Chuang Chin
- Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR)
- Koichi S. Kobayashi
- Department of Microbial Pathogenesis and Immunology, Texas A&M Health Science Centre
- Antonio Bertoletti
- Program in Emerging Infectious Diseases, Duke-NUS Medical School
- Alessandra Mortellaro
- Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR)
- Clara Abraham
- Department of Internal Medicine, Yale University School of Medicine
- John D. MacMicking
- Departments of Microbial Pathogenesis and Immunobiology, HHMI, Yale Systems Biology Institute, Yale University School of Medicine
- Ramnik J. Xavier
- Gastrointestinal Unit, Center for Computational and Integrative Biology, Massachusetts General Hospital, Harvard Medical School
- Bindu Sukumaran
- Program in Emerging Infectious Diseases, Duke-NUS Medical School
- DOI
- https://doi.org/10.1038/ncomms15865
- Journal volume & issue
-
Vol. 8,
no. 1
pp. 1 – 16
Abstract
Prolonged NOD2 ligand engagement induces tolerance and attenuated NOD2 signalling, but the molecular mechanisms leading to this tolerance induction are unclear. Here the authors show that the degradation of a NOD2 adaptor, RIP2, by the E3 ligase ZNRF4 is essential for the down-regulation of NOD2 signalling.
