ArticleHeliyon2022
Long-term exposure to low levels of okadaic acid accelerates cell cycle progression in colonic epithelial cells via p53 and Jak/Stat3 signaling pathways.
Article in Heliyon, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Regular exposure to low dose of diarrheic shellfish toxins: Implications for the seafood consumer.Current research in food science · 2026Article
- The Benthic DinoflagellateMarine drugs · 2025Article
- Okadaic Acid Is at Least as Toxic as Dinophysistoxin-1 after Repeated Administration to Mice by Gavage.Toxins · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a major component of diarrheic shellfish poisoning (DSP) toxins, okadaic acid (OA) is widely distributed worldwide, and causes a series of serious public health problems. In colon tissue, previous studies have shown that high doses of OA can affect various intracellular processes, including destroy intercellular communication at gap junctions, induce cell apoptosis and trigger cell cycle arrest. However, there is a scarcity of studies on the effect and mechanism of action of low doses of OA in colonic tissues. In this study, we observed that exposure to low levels of OA altered cell cycle progression
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Registered trials
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