ArticleJournal of virology2006
Negative regulation of the alpha interferon-induced antiviral response by the Ras/Raf/MEK pathway.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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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.
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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
52 citing papers in PubMed, 84 citations in OpenAlex.
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- IL-1 receptor antagonism reveals a yin-yang relationship between NFκB and interferon signaling in chronic lymphocytic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Porcine deltacoronavirus nucleocapsid protein interacts with the Grb2 through its proline-rich motifs to induce activation of the Raf-MEK-ERK signal pathway and promote virus replication.The Journal of general virology · 2024Article
- Intertumoral heterogeneity impacts oncolytic vesicular stomatitis virus efficacy in mouse pancreatic cancer cells.Journal of virology · 2023Article
- Targeting Human Proteins for Antiviral Drug Discovery and Repurposing Efforts: A Focus on Protein Kinases.Viruses · 2023Review
- Serum proteomics reveals a tolerant immune phenotype across multiple pathogen taxa in wild vampire bats.Frontiers in immunology · 2023Article
- Interferon regulatory factor 3 mediates effective antiviral responses to human coronavirus 229E and OC43 infection.Frontiers in immunology · 2023Article
- Gastrointestinal organoids in the study of viral infections.American journal of physiology. Gastrointestinal and liver physiology · 2023Review
- MEK reduces cancer-specific PpIX accumulation through the RSK-ABCB1 and HIF-1α-FECH axes.Scientific reports · 2020Article
- Antagonism of interferon signaling by fibroblast growth factors promotes viral replication.EMBO molecular medicine · 2020Article
- AfterNeuro-oncology advances · 2020Review
- Human Papillomavirus 16 E5 Inhibits Interferon Signaling and Supports Episomal Viral Maintenance.Journal of virology · 2020Article
- Genetic Programs Driving Oncogenic Transformation: Lessons from in Vitro Models.International journal of molecular sciences · 2019Article
- Novel Function of Bluetongue Virus NS3 Protein in Regulation of the MAPK/ERK Signaling Pathway.Journal of virology · 2019Article
- Starvation and Pseudo-Starvation as Drivers of Cancer Metastasis through Translation Reprogramming.Cell metabolism · 2019Review
- Unscheduled HDAC4 repressive activity in human fibroblasts triggers TP53-dependent senescence and favors cell transformation.Molecular oncology · 2018Article
- Defects in interferon pathways as potential biomarkers of sensitivity to oncolytic viruses.Reviews in medical virology · 2018Review
- Current understanding of reovirus oncolysis mechanisms.Oncolytic virotherapy · 2018Review
- The Continued Promise and Many Disappointments of Oncolytic Virotherapy in Gastrointestinal Malignancies.Biomedicines · 2017Review
- H-Ras Exerts Opposing Effects on Type I Interferon Responses Depending on Its Activation Status.Frontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon (IFN) is one of the molecules released by virus-infected cells, resulting in the establishment of an antiviral state within infected and neighboring cells. IFN-induced antiviral response may be subject to modulation by the cellular signaling environment of host cells which impact the effectiveness of viral replication. Here, we show that cells with an activated Ras/Raf/MEK signaling cascade allow propagation of viruses in the presence of IFN. Ras-transformed (RasV12) and vector control NIH 3T3 cells were infected with vesicular stomatitis virus (VSV) or an IFN-sensitive vaccinia virus (delE3L) in the presence of alpha interferon. While IFN protected vector control cells from infection by both viruses, RasV12 cells were susceptible to viral infection regardless of the presence of IFN. IFN sensitivity was restored in RasV12 cells upon RNA interference (RNAi) knockdown of Ras. We further investigated which elements downstream of Ras are responsible for counteracting IFN-induced antiviral responses. A Ras effector domain mutant that can only stimulate the Raf kinase family of effectors was able to suppress the IFN response and allow VSV replication. IFN-induced antiviral mechanisms were also restored in RasV12 cells by treatment with a MEK inhibitor (U0126 or PD98059). Moreover, by using RNAi to MEK1 and MEK2, we determined that MEK2, rather than MEK1, is responsible for suppression of the IFN response. In conclusion, our results suggest that activation of the Ras/Raf/MEK pathway downregulates IFN-induced antiviral response.
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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.