ArticleViruses2022
Gga-miR-30c-5p Enhances Apoptosis in Fowl Adenovirus Serotype 4-Infected Leghorn Male Hepatocellular Cells and Facilitates Viral Replication through Myeloid Cell Leukemia-1.
Article in Viruses, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- Whole-Transcriptome Sequencing Analysis of Fowl Adenovirus Serotype 4 Infection in LMH Cells.International journal of molecular sciences · 2026Article
- MicroRNA expression profiling in fowl adenovirus serotype 4-infected Leghorn male hepatoma cells using small RNA deep sequencing.Poultry science · 2026Article
- Identification of duck type II interferon-stimulated genes and revelation of duIFI35 inhibition of H5N6 AIV replication by promoting apoptosis.Veterinary research · 2026Article
- Host combats porcine reproductive and respiratory syndrome virus infection at non-coding RNAs level.Virulence · 2024Review
- The Knob Domain of the Fiber-1 Protein Affects the Replication of Fowl Adenovirus Serotype 4.Microorganisms · 2024Article
- miRNA profiling of chicken follicles during follicular development.Scientific reports · 2024Article
- Role of microRNAs in host defense against porcine reproductive and respiratory syndrome virus infection: a hidden front line.Frontiers in immunology · 2024Review
- Biological features of fowl adenovirus serotype-4.Frontiers in cellular and infection microbiology · 2024Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fowl adenovirus serotype 4 (FAdV-4) is the primary causative agent responsible for the hepatitis-hydropericardium syndrome (HHS) in chickens, leading to considerable economic losses to stakeholders. Although the pathogenesis of FAdV-4 infection has gained attention, the underlying molecular mechanism is still unknown. Here, we showed that the ectopic expression of gga-miR-30c-5p in leghorn male hepatocellular (LMH) cells enhanced apoptosis in FAdV-4-infected LMH cells by directly targeting the myeloid cell leukemia-1 (Mcl-1), facilitating viral replication. On the contrary, the inhibition of endogenous gga-miR-30c-5p markedly suppressed apoptosis and viral replication in LMH cells. Importantly, the overexpression of Mcl-1 inhibited gga-miR-30c-5p or FAdV-4-induced apoptosis in LMH cells, reducing FAdV-4 replication, while the knockdown of Mcl-1 by RNAi enhanced apoptosis in LMH cells. Furthermore, transfection of LMH cells with gga-miR-30c-5p mimics enhanced FAdV-4-induced apoptosis associated with increased cytochrome
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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.