ArticleVirology2010
Replication of the hepatitis B virus requires a calcium-dependent HBx-induced G1 phase arrest of hepatocytes.
Article in Virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 66 citations in OpenAlex.
- Qingqi Guxue Decoction induces S cell cycle arrest to inhibit replication of severe fever with thrombocytopenia syndrome virus.Virologica Sinica · 2025Article
- Review
- Antioxidants and Calcium Modulators Preclude in Vitro Hepatitis B Virus-Induced Mitochondrial Damage.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023Article
- The Transient Receptor Potential Vanilloid 2 (TRPV2) Channel Facilitates Virus Infection Through the CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Emerging role of mitochondria in response to HBV infection.Journal of clinical laboratory analysis · 2022Article
- Evidence for a Hepatitis B Virus Short RNA Fragment Directly Targeting the Cellular RRM2 Gene.Cells · 2022Article
- Inhibition of Protease Activated Receptor 2 Attenuates HBx-Induced Inflammation and Mitochondria Oxidative Stress.Infection and drug resistance · 2022Article
- Dysregulation of host cell calcium signaling during viral infections: Emerging paradigm with high clinical relevance.Molecular aspects of medicine · 2021Review
- Calcium signaling in hepatitis B virus infection and its potential as a therapeutic target.Cell communication and signaling : CCS · 2021Review
- Screening of the HBx transactivation domain interacting proteins and the function of interactor Pin1 in HBV replication.Scientific reports · 2021Article
- Regulation of Hepatitis B Virus Replication by Cyclin Docking Motifs in Core Protein.Journal of virology · 2021Article
- Mitochondrial dysfunction and liver disease: role, relevance, and potential for therapeutic modulation.Therapeutic advances in gastroenterology · 2021Review
- Pterostilbene inhibits hepatocellular carcinoma proliferation and HBV replication by targeting ribonucleotide reductase M2 protein.American journal of cancer research · 2021Article
- Orchestrated efforts on host network hijacking: Processes governing virus replication.Virulence · 2020Review
- Review
- Effect of HBx on inflammation and mitochondrial oxidative stress in mouse hepatocytes.Oncology letters · 2020Article
- The Severe Fever with Thrombocytopenia Syndrome Virus NSs Protein Interacts with CDK1 To Induce GJournal of virology · 2020Article
- Replenishment of Hepatitis B Virus cccDNA Pool Is Restricted by Baseline Expression of Host Restriction Factors In Vitro.Microorganisms · 2019Article
- The interaction between mitochondria and oncoviruses.Biochimica et biophysica acta. Molecular basis of disease · 2018Review
- Hepatitis B Virus X Protein Upregulates Intracellular Calcium Signaling by Binding C-terminal of Orail Protein.Current medical science · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chronic HBV infections cause hepatocellular carcinoma (HCC). Activities of the HBV HBx protein regulate HBV replication and may contribute to the development of HCC. We previously reported that HBx causes primary rat hepatocytes to exit G0 but stall in G1 phase of the cell cycle; entry into G1 stimulated HBV replication. We now report that the activity of the mitochondria permeability transition pore is required for HBx regulation of cell cycle proteins and HBV replication in primary rat hepatocytes, that progression from G0 to G1 stimulates HBV polymerase activity, and that HBV replication is facilitated by the HBx-induced G1 arrest. HBx stimulation of HBV replication was linked to elevation of the R2 subunit of ribonucleotide reductase. Our studies suggest that HBx uses mitochondrial-dependent calcium signaling to cause hepatocytes to exit G0 but stall in G1 and that this HBx activity alters the cellular environment and stimulates HBV replication.
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.