ArticleProceedings of the National Academy of Sciences of the United States of America2009
Suppression of a pro-apoptotic K+ channel as a mechanism for hepatitis C virus persistence.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 70 citations in OpenAlex.
- Targeting virus-interacting host ion channels as a novel antiviral strategy.Acta pharmacologica Sinica · 2026Review
- Cannabidiol Enhances Stress-Induced Cellular Damage: Potential Contribution of Kv2.1 Inhibition.Journal of molecular neuroscience : MN · 2025Article
- Lentiviral Expression of Rabies Virus Glycoprotein in the Rat Hippocampus Strengthens Synaptic Plasticity.Cellular and molecular neurobiology · 2022Article
- Antagonistic roles of Ras-MAPK and Akt signaling in integrin-KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Signaling Induced by Chronic Viral Hepatitis: Dependence and Consequences.International journal of molecular sciences · 2022Review
- Genomics of Viral Hepatitis-Associated Liver Tumors.Journal of clinical medicine · 2021Review
- The regulatory function of mixed lineage kinase 3 in tumor and host immunity.Pharmacology & therapeutics · 2021Review
- Identification of potassium and calcium channel inhibitors as modulators of polyomavirus endosomal trafficking.Antiviral research · 2020Article
- Evasion of a Human Cytomegalovirus Entry Inhibitor with Potent Cysteine Reactivity Is Concomitant with the Utilization of a Heparan Sulfate Proteoglycan-Independent Route of Entry.Journal of virology · 2020Article
- Voltage-Gated Potassium Channels as Regulators of Cell Death.Frontiers in cell and developmental biology · 2020Review
- West Nile Virus Capsid Protein Interacts With Biologically Relevant Host Lipid Systems.Frontiers in cellular and infection microbiology · 2019Article
- Molecular Neuroprotection Induced by Zinc-Dependent Expression of Hepatitis C-Derived Protein NS5A Targeting Kv2.1 Potassium Channels.The Journal of pharmacology and experimental therapeutics · 2018Article
- Methods for Lipid Droplet Biophysical Characterization inFrontiers in microbiology · 2018Review
- Oxidation of KCNB1 potassium channels triggers apoptotic integrin signaling in the brain.Cell death & disease · 2017Article
- Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis.Oncotarget · 2017Review
- Modulation of Potassium Channels Inhibits Bunyavirus Infection.The Journal of biological chemistry · 2016Article
- Intrahepatic mRNA Expression of FAS, FASL, and FOXP3 Genes Is Associated with the Pathophysiology of Chronic HCV Infection.PloS one · 2016Article
- Ion Channels and Oxidative Stress as a Potential Link for the Diagnosis or Treatment of Liver Diseases.Oxidative medicine and cellular longevity · 2016Review
- Hepatitis B and C virus-induced hepatitis: Apoptosis, autophagy, and unfolded protein response.World journal of gastroenterology · 2015Article
- Critical role of Casein kinase 2 in hepatitis C NS5A-mediated inhibition of Kv2.1 K(+) channel function.Neuroscience letters · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
An estimated 3% of the global population are infected with hepatitis C virus (HCV), and the majority of these individuals will develop chronic liver disease. As with other chronic viruses, establishment of persistent infection requires that HCV-infected cells must be refractory to a range of pro-apoptotic stimuli. In response to oxidative stress, amplification of an outward K(+) current mediated by the Kv2.1 channel, precedes the onset of apoptosis. We show here that in human hepatoma cells either infected with HCV or harboring an HCV subgenomic replicon, oxidative stress failed to initiate apoptosis via Kv2.1. The HCV NS5A protein mediated this effect by inhibiting oxidative stress-induced p38 MAPK phosphorylation of Kv2.1. The inhibition of a host cell K(+) channel by a viral protein is a hitherto undescribed viral anti-apoptotic mechanism and represents a potential target for antiviral therapy.
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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.