ArticleScientific reports2016
Exogenous avian leukosis virus-induced activation of the ERK/AP1 pathway is required for virus replication and correlates with virus-induced tumorigenesis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Research Progress on Pathogenesis and Prevention of Avian Leukosis Virus J Subgroup (ALV-J).Veterinary sciences · 2026Review
- Lactate-induced activation of tumor-associated fibroblasts and IL-8-mediated macrophage recruitment promote lung cancer progression.Redox biology · 2024Article
- Bone repair and key signalling pathways for cell-based bone regenerative therapy: A review.Journal of Taibah University Medical Sciences · 2023Review
- ALV-miRNA-p19-01 Promotes Viral Replication via Targeting Dual Specificity Phosphatase 6.Viruses · 2022Article
- Avian Leucosis Virus-Host Interaction: The Involvement of Host Factors in Viral Replication.Frontiers in immunology · 2022Review
- JNK signalling regulates antioxidant responses in neurons.Redox biology · 2020Article
- Systematic Identification of Host Immune Key Factors Influencing Viral Infection in PBL of ALV-J Infected SPF Chicken.Viruses · 2020Article
- Cholesterol-25-hydroxylase Is a Chicken ISG That Restricts ALV-J Infection by Producing 25-hydroxycholesterol.Viruses · 2019Article
- A balanced game: chicken macrophage response to ALV-J infection.Veterinary research · 2019Article
- Newcastle Disease Virus V Protein Promotes Viral Replication in HeLa Cells through the Activation of MEK/ERK Signaling.Viruses · 2018Article
- Role of MAPK/MNK1 signaling in virus replication.Virus research · 2018Review
- ALV-J infection induces chicken monocyte death accompanied with the production of IL-1β and IL-18.Oncotarget · 2017Article
- HCMV activation of ERK-MAPK drives a multi-factorial response promoting the survival of infected myeloid progenitors.Journal of molecular biochemistry · 2017Article
- MiR-34b-5p Suppresses Melanoma Differentiation-Associated Gene 5 (Frontiers in cellular and infection microbiology · 2017Article
- Endogenous Retrovirus ev21 Dose Not Recombine with ALV-J and Induces the Expression of ISGs in the Host.Frontiers in cellular and infection microbiology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A proteomics approach was used to reveal the up-regulated proteins involved in the targeted mitogen-activated protein kinase (MAPK) signal transduction pathway in DF-1 cells after ALV subgroup J (ALV-J) infection. Next, we found that ALV-J CHN06 strain infection of DF-1 cells correlated with extracellular signal-regulated kinase 2 (ERK2) activation, which was mainly induced within 15 min, a very early stage of infection, and at a late infection stage, from 108 h to 132 h post-infection. Infection with other ALV subgroup (A/B) strains also triggered ERK/MAPK activation. Moreover, when activating ERK2, ALV subgroups A, B and J simultaneously induced the phosphorylation of c-Jun, an AP1 family member and p38 activation but had no obvious effect on JNK activation at either 15 min or 120 h. Interestingly, only PD98059 inhibited the ALV-induced c-Jun phosphorylation while SP600125 or SB203580 had no influence on c-Jun activation. Furthermore, the viral gp85 and gag proteins were found to contribute to ERK2/AP1 activation. Additionally, the specific ERK inhibitor, PD980509, significantly suppressed ALV replication, as evidenced by extremely low levels of ALV promoter activity and ALV-J protein expression. In vivo analysis of ERK2 activation in tumor cells derived from ALV-J-infected chicken demonstrated a strong correlation between ERK/MAPK activation and virus-associated tumorigenesis.
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