ArticlePloS one2016
Hepatitis B Virus Middle Protein Enhances IL-6 Production via p38 MAPK/NF-κB Pathways in an ER Stress-Dependent Manner.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
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
19 citing papers in PubMed, 20 citations in OpenAlex.
- Effects of dual plasma molecular adsorption system on liver function, electrolytes, inflammation, and immunity in patients with chronic severe hepatitis.Journal of clinical laboratory analysis · 2019Trial
- CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026Review
- New Insights into the Role of NF-κB in Hepatitis B Virus Infection.International journal of biological sciences · 2026Review
- Association between red blood cell distribution width coefficient of variation and post-treatment bilirubin decline velocity in neonatal hyperbilirubinemia.Frontiers in pediatrics · 2025Article
- Regulation of Hepatitis B Virus Replication by Modulating Endoplasmic Reticulum Stress (ER-Stress).International journal of microbiology · 2024Article
- Review
- Phosphoproteomics Unravel HBV Triggered Rewiring of Host Phosphosignaling Events.International journal of molecular sciences · 2022Article
- Increased BST-2 expression by HBV infection promotes HBV-associated HCC tumorigenesis.Journal of gastrointestinal oncology · 2021Article
- Cytokines and Chemokines in HBV Infection.Frontiers in molecular biosciences · 2021Review
- Dexmedetomidine Attenuates Cellular Injury and Apoptosis in H9c2 Cardiomyocytes by Regulating p-38MAPK and Endoplasmic Reticulum Stress.Drug design, development and therapy · 2020Article
- Kainic acid hyperphosphorylates tau via inflammasome activation in MAPT transgenic mice.Aging · 2019Article
- Endoplasmic reticulum stress and liver diseases.Liver research (Beijing, China) · 2019Article
- Cellular Stress Response to Varicella-Zoster Virus Infection of Human Skin Includes Highly Elevated Interleukin-6 Expression.Open forum infectious diseases · 2018Article
- Interleukin-35 Level Is Elevated in Patients with Chronic Hepatitis B Virus Infection.International journal of medical sciences · 2018Article
- Bicyclol Attenuates Liver Inflammation Induced by Infection of Hepatitis C VirusFrontiers in pharmacology · 2018Article
- Pharmacologic targeting ERK1/2 attenuates the development and progression of hyperuricemic nephropathy in rats.Oncotarget · 2017Article
- Mapping out p38MAPK.American journal of reproductive immunology (New York, N.Y. : 1989) · 2017Review
- Crosstalk between Signaling Pathways in Pemphigus: A Role for Endoplasmic Reticulum Stress in p38 Mitogen-Activated Protein Kinase Activation?Frontiers in immunology · 2017Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During hepatitis B virus (HBV) infection, three viral envelope proteins of HBV are overexpressed in the endoplasmic reticulum (ER). The large S protein (LHBs) and truncated middle S protein (MHBst) have been documented to play roles in regulating host gene expression and contribute to hepatic disease development. As a predominant protein at the ultrastructural level in biopsy samples taken from viremic patients, the role of the middle S protein (MHBs) remains to be understood despite its high immunogenicity. When we transfected hepatocytes with an enhanced green fluorescent protein (EGFP)-tagged MHBs expressing plasmid, the results showed that expression of MHBs cause an upregulation of IL-6 at the message RNA and protein levels through activating the p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-kappa B (NF-κB) pathways. The use of specific inhibitors of the signaling pathways can diminish this upregulation. The use of BAPTA-AM attenuated the stimulation caused by MHBs. We further found that MHBs accumulated in the endoplasmic reticulum and increased the amount of glucose regulated protein 78 (GRP78/BiP). Our results provide a possibility that MHBs could be involved in liver disease progression.
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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.