ArticleCytotechnology2016
Lipopolysaccharides attenuates growth of HS cells through the JNK pathway.
Article in Cytotechnology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 2 citations in OpenAlex.
- The Role of the Dysregulated JNK Signaling Pathway in the Pathogenesis of Human Diseases and Its Potential Therapeutic Strategies: A Comprehensive Review.Biomolecules · 2024Review
- The Roles of c-Jun N-Terminal Kinase (JNK) in Infectious Diseases.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis is characterized by inflammation of the synovial membrane, which can result in joint destruction within the first few years after onset. Lipopolysaccharides (LPS) are glycolipids found in abundance on the outer membranes of all Gram-negative bacteria and incite a vigorous inflammatory response. We studied the potential involvement of mitogen-activated protein kinase serine/threonine kinases in LPS-induced growth of HS synovial cells. Various concentrations of LPS were applied to cultured HS cells and growth rate, as well as changes in the phosphorylation states of extracellular regulated kinase 1/2, Jun N-terminal kinase (JNK), and p38 were determined. As results, growth of LPS-treated HS cells was inhibited primarily by phosphorylated JNK and this phosphorylation was mediated by the LPS receptor. Our results suggest that LPS inhibits growth of HS cells primarily through the JNK pathway.
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What OpenQuestion holds
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.