ArticleJournal of clinical immunology2005
Involvement of c-Jun N-terminal kinase in rF1 mediated activation of murine peritoneal macrophages in vitro.
Article in Journal of clinical immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- PCSK9-Mediated Inflammation in Foam Cell Formation and Exploring the Biologically Active Compounds Derived From Natural Resources.Advances in pharmacological and pharmaceutical sciences · 2026Review
- Host response during Yersinia pestis infection of human bronchial epithelial cells involves negative regulation of autophagy and suggests a modulation of survival-related and cellular growth pathways.Frontiers in microbiology · 2015Article
- Characterization of an F1 deletion mutant of Yersinia pestis CO92, pathogenic role of F1 antigen in bubonic and pneumonic plague, and evaluation of sensitivity and specificity of F1 antigen capture-based dipsticks.Journal of clinical microbiology · 2011Article
- The Yersinia pestis caf1M1A1 fimbrial capsule operon promotes transmission by flea bite in a mouse model of bubonic plague.Infection and immunity · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fraction 1 (F1) protein forms a capsule on the surface of Yersinia pestis. Recently, we reported rF1-induced activation of macrophages. In current investigation, we studied the role of JNK MAPK signal transduction pathway in rF1-induced activation of macrophages in vitro. SP600125, a specific inhibitor of JNK, inhibited JNK MAPK phosphorylation, indicating the specificity of the above response. Though, the rF1-induced phosphorylation of JNK MAPK was also inhibited by upstream protein kinase C inhibitor H7, tyrosine kinase inhibitor genestein and PI3-K inhibitor wotmannin. Activation of the transcription factor NF-kB (phosphorylation of IkB) and c-Jun was observed in response to rF1 treatment. The rF1-induced JNK MAPK activity was correlated to the functional activation of macrophages by demonstrating the inhibition of NO, TNF-alpha production and microtubule polymerization caused by SP600125. Taken together, the data suggests the involvement of JNK MAPK/NF-kB pathway in rF1-induced activation of macrophages.
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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.