ArticleOncotarget2017
The inhibiting effect of the transcription factor p53 on dengue virus infection by activating the type I interferon.
Article in Oncotarget, 2017. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
3 citing papers in PubMed, 8 citations in OpenAlex.
- Guanylate binding proteins (GBPs) as novel therapeutic targets against single-stranded RNA viruses.Molecular biology reports · 2025Review
- Identification and validation of ferroptosis-related genes in patients infected with dengue virus: implication in the pathogenesis of DENV.Virus genes · 2023Article
- MicroRNA transcriptome analysis of poly I:C-stimulated and PRRSV-infected porcine alveolar macrophages.Journal of applied genetics · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To investigate the role of the transcription factor p53 in the course of the dengue virus (DV) infection. The human hepatocellular carcinoma cell strain HepG2 with a low expression level of p53 was built by using the retroviral-mediated RNA interference technology, and was detected by Western blot. The wild group and the interference group were respectively infected by the type 2 DV. The viral titration was detected by the Vero plaque assay, the viral multiplication was detected by the immunofluorescence, the cell apoptosis after virus infection was detected by FCM and the level of IFN-β was analyzed by ELISA. Compared to the wild group, the expression level of p53 in the interference group decreased significantly, which indicated that the HepG2 cell strain with the low expression level of p53 was successfully built. 24h after DV infection, the virus titration in the interference group was 100 times higher than that in the wild group. The result of the immunofluorescence showed that, the amount of green fluorescent cells in the interference group was significant higher than that in the wild group. It was indicated that the DV infection was inhibited by p53. However, 24h after DV infection, there was no significant difference in the amount of apoptotic cells in both groups. And the amount of IFN-β in the wild group increased 6 times. The DV infection was inhibited by the transcription factor p53 by activating type I interferon pathway other than promoting the cell apoptosis.
Indexed as
Identifiers
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.