ArticleCell host & microbe2020
The Salmonella Secreted Effector SarA/SteE Mimics Cytokine Receptor Signaling to Activate STAT3.
Article in Cell host & microbe, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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
35 citing papers in PubMed, 60 citations in OpenAlex.
- Host-microbiota-pathogen interactions drive Salmonella enterica serovar Typhimurium pathogenesis.Nature reviews. Microbiology · 2026Review
- The Manipulation of Host Cells byInternational journal of molecular sciences · 2026Review
- The Brucella effector protein BtpB facilitates STAT3 activation to regulate polarization in macrophages during infection.Veterinary research · 2026Article
- Formononetin alleviates ovarian fibrosis and inflammation via targeting SOCS3 and inhibiting TGF-Chinese herbal medicines · 2026Article
- GWAS and Machine Learning Screening of Genomic Determinants Underlying Host Adaptation in Swine and ChickenMicroorganisms · 2026Article
- Article
- Cellular signaling meets bacterial infection: the integrative role of STAT3.Frontiers in cellular and infection microbiology · 2026Review
- Bacterial effectors mediate kinase reprogramming through mimicry of conserved eukaryotic motifs.EMBO reports · 2025Article
- A single amino acid in the Salmonella effector SarA/SteE triggers supraphysiological activation of STAT3 for anti-inflammatory gene expression.Cell reports · 2025Article
- The interplay betweenCell insight · 2025Review
- Review
- Infection biology ofEcoSal Plus · 2024Review
- Article
- Dynamics of macrophage polarization supporteLife · 2024Article
- Salmonella spvC gene suppresses macrophage/neutrophil antibacterial defense mediated by gasdermin D.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- The Sdp-SH3b2 domain contained inFrontiers in immunology · 2024Article
- Review
- Turning foes into permissive hosts: manipulation of macrophage polarization by intracellular bacteria.Current opinion in immunology · 2023Review
- Paired single-cell host profiling with multiplex-tagged bacterial mutants reveals intracellular virulence-immune networks.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Speaking the host language: howMicrobiology (Reading, England) · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Bacteria masterfully co-opt and subvert host signal transduction. As a paradigmatic example, Salmonella uses two type-3 secretion systems to inject effector proteins that facilitate Salmonella entry, establishment of an intracellular niche, and modulation of immune responses. We previously demonstrated that the Salmonella anti-inflammatory response activator SarA (Stm2585, GogC, PagJ, SteE) activates the host transcription factor STAT3 to drive expression of immunomodulatory STAT3-targets. Here, we demonstrate-by sequence, function, and biochemical measurement-that SarA mimics the cytoplasmic domain of glycoprotein 130 (gp130, IL6ST). SarA is phosphorylated at a YxxQ motif, facilitating binding to STAT3 with greater affinity than gp130. Departing from canonical gp130 signaling, SarA function is JAK-independent but requires GSK-3, a key regulator of metabolism and development. Our results reveal that SarA undergoes host phosphorylation to recruit a STAT3-activating complex, circumventing cytokine receptor activation. Effector mimicry of gp130 suggests GSK-3 can regulate normal cytokine signaling, potentially enabling metabolic and immune crosstalk.
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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.