Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Lack of Effect of the Salmonella Deubiquitinase SseL on the NF-κB Pathway

8 Jan 2013

Abstract excerpt

Intracellular replication of Salmonella enterica requires effector proteins translocated across the Salmonella-containing vacuolar membrane by Salmonella pathogenicity island-2 (SPI-2) encoded type III secretion system (T3SS). The SPI-2 T3SS effector SseL is a deubiquitinase that contributes to virulence in mice. Previous work has produced conflicting evidence as to the involvement of SseL in interference with...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amoebic Infections and Treatments
Share to Cancer Research and Treatments
Share to Salmonella and Campylobacter epidemiology

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 23308136
DOI: 10.1371/journal.pone.0053064

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Lack of Effect of the Salmonella Deubiquitinase SseL on the NF-κB PathwayPMID 23308136Read ↗

The Salmonella Deubiquitinase SseL Inhibits Selective Autophagy of Cytosolic AggregatesSemantic proximity Read ↗

Inhibition of NF-κB signalling by a family of type III secretion system effector proteins during Salmonella infectionSemantic proximity Read ↗

SseK3 Is a Salmonella Effector That Binds TRIM32 and Modulates the Host's NF-κB Signalling Activity.Semantic proximity Read ↗

Ubiquitylome Rewiring by Bacterial E3 Ligases Reveals Multifaceted Host SubversionSemantic proximity Read ↗

The SseL protein inhibits the intracellular NF-κB pathway to enhance the virulence of Salmonella Pullorum in a chicken modelSemantic proximity Read ↗

Interactions between Salmonella and host macrophages – Dissecting NF-κB signaling pathway responsesSemantic proximity Read ↗

USP8 inhibition regulates autophagy flux and controls Salmonella infectionSemantic proximity Read ↗

SseA is required for translocation of Salmonella pathogenicity island-2 effectors into host cells.Semantic proximity Read ↗

Targeting deubiquitinating enzymes (DUBs) and ubiquitin pathway modulators to enhance host defense against bacterial infectionsSemantic proximity Read ↗

Enteropathogenic E. coli non‐LEE encoded effectors NleH1 and NleH2 attenuate NF‐κB activationSemantic proximity Read ↗

N-ethyl-N-nitrosourea-induced mutation in ubiquitin-specific peptidase 18 causes hyperactivation of IFN-αß signaling and suppresses STAT4-induced IFN-γ production, resulting in increased susceptibility to Salmonella typhimurium.Semantic proximity Read ↗

Contribution of increased ISG15, ISGylation and deregulated type I IFN signaling in Usp18 mutant mice during the course of bacterial infections.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.