ArticleThe Journal of biological chemistry2011
Proteasome-independent degradation of canonical NFkappaB complex components by the NleC protein of pathogenic Escherichia coli.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 78 citations in OpenAlex.
- Evolution of N-terminal mechanical lability as a determinant for Type III secretion.Protein science : a publication of the Protein Society · 2026Article
- A Type III secretion system effector evolved to be mechanically labile and initiate unfolding from the N-terminus.bioRxiv : the preprint server for biology · 2026Article
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
- NleB2 from enteropathogenic Escherichia coli is a novel arginine-glucose transferase effector.PLoS pathogens · 2021Article
- The T3SS Effector Protease NleC Is Active withinPathogens (Basel, Switzerland) · 2021Article
- Measuring Effector-Mediated Modulation of Inflammatory Responses to Infection with Enteropathogenic and Shiga Toxin-Producing E. coli.Methods in molecular biology (Clifton, N.J.) · 2021Article
- A Salmonella type III effector, PipA, works in a different manner than the PipA family effectors GogA and GtgA.PloS one · 2021Article
- From Gene to Protein-How Bacterial Virulence Factors Manipulate Host Gene Expression During Infection.International journal of molecular sciences · 2020Review
- Article
- Programmed Cell Death in the Evolutionary Race against Bacterial Virulence Factors.Cold Spring Harbor perspectives in biology · 2020Review
- Bacteria-Catalyzed Arginine Glycosylation in Pathogens and Host.Frontiers in cellular and infection microbiology · 2020Review
- NF-κB Signaling in Macrophages: Dynamics, Crosstalk, and Signal Integration.Frontiers in immunology · 2019Review
- Structure-function analyses of the bacterial zinc metalloprotease effector protein GtgA uncover key residues required for deactivating NF-κB.The Journal of biological chemistry · 2018Article
- Cooperative Immune Suppression by Escherichia coli and Shigella Effector Proteins.Infection and immunity · 2018Review
- A Metalloprotease Homolog Venom Protein From a Parasitoid Wasp Suppresses the Toll Pathway in Host Hemocytes.Frontiers in immunology · 2018Article
- Ubiquitination regulation of inflammatory responses through NF-κB pathway.American journal of translational research · 2018Article
- Epithelial cells detect functional type III secretion system of enteropathogenic Escherichia coli through a novel NF-κB signaling pathway.PLoS pathogens · 2017Article
- Distinct Roles of the Antiapoptotic Effectors NleB and NleF from Enteropathogenic Escherichia coli.Infection and immunity · 2017Article
- Modulation of host signaling in the inflammatory response by enteropathogenic Escherichia coli virulence proteins.Cellular & molecular immunology · 2017Review
- The Type III Effector NleD from Enteropathogenic Escherichia coli Differentiates between Host Substrates p38 and JNK.Infection and immunity · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The NFκB transcription factor is a key component of immune and inflammatory signaling as its activation induces the expression of antimicrobial reagents, chemokines, cytokines, and anti-apoptotic factors. Many pathogens encode effector proteins that target factors regulating NFκB activity and can provide novel insights on regulatory mechanisms. Given the link of NFκB dysfunction with inflammatory diseases and some cancers, these effectors have therapeutic potential. Here, screening enteropathogenic Escherichia coli proteins for those implicated in suppressing NFκB function revealed that eGFP-NleC, unlike eGFP, strongly inhibited basal and TNFα-induced NFκB reporter activity to prevent secretion of the chemokine, IL-8. Work involving NleC variants, chemical inhibitors, and immunoprecipitation studies support NleC being a zinc metalloprotease that degrades NFκB-IκBα complexes. The findings are consistent with features between residues 33-65 recruiting NFκB for proteasomal-independent degradation by a mechanism inhibited by metalloprotease inhibitors or disruption of a consensus zinc metalloprotease motif spanning NleC residues 183-187. This raises the prospect that mammalian cells, or other pathogens, employ a similar mechanism to modulate NFκB activity. Moreover, NleC represents a novel tool for validating NFκB as a therapeutic target and, indeed, as a possible therapeutic reagent.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.