ArticleBiochemistry2017
Crohn's Disease Variants of Nod2 Are Stabilized by the Critical Contact Region of Hsp70.
Article in Biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Application of bioanalytical and computational methods in decoding the roles of glycans in host-pathogen interactions.Current opinion in chemical biology · 2023Review
- IL-1 and CD40/CD40L platelet complex: elements of induction of Crohn's disease and new therapeutic targets.Archives of pharmacal research · 2021Review
- Revisiting peptidoglycan sensing: interactions with host immunity and beyond.Chemical communications (Cambridge, England) · 2020Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Nod2 is a cytosolic, innate immune receptor responsible for binding to bacterial cell wall fragments such as muramyl dipeptide (MDP). Upon binding, subsequent downstream activation of the NF-κB pathway leads to an immune response. Nod2 mutations are correlated with an increased susceptibility to Crohn's disease (CD) and ultimately result in a misregulated immune response. Previous work had demonstrated that Nod2 interacts with and is stabilized by the molecular chaperone Hsp70. In this work, it is shown using purified protein and in vitro biochemical assays that the critical Nod2 CD mutations (G908R, R702W, and 1007fs) preserve the ability to bind bacterial ligands. A limited proteolysis assay and luciferase reporter assay reveal regions of Hsp70 that are capable of stabilizing Nod2 and rescuing CD mutant activity. A minimal 71-amino acid subset of Hsp70 that stabilizes the CD-associated variants of Nod2 and restores a proper immune response upon activation with MDP was identified. This work suggests that CD-associated Nod2 variants could be stabilized in vivo with a molecular chaperone.
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Registered trials
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