ReviewVirus research2014
Coronavirus-induced ER stress response and its involvement in regulation of coronavirus-host interactions.
Review in Virus research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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
81 citing papers in PubMed, 135 citations in OpenAlex.
- HERPUD1 suppresses porcine epidemic diarrhea virus replication by recruiting HRD1 to degrade viral ORF3 protein.Journal of virology · 2026Article
- RepurNet: A network medicine framework for systematic drug repurposing and disease vulnerability discovery.iScience · 2026Article
- A stable subgenomic reporter coronavirus enables transcriptional profiling of bystander cells.The Journal of general virology · 2026Article
- The host protein SSR4 mediates PRRSV-induced endoplasmic reticulum stress via interaction with Nsp2.Journal of virology · 2026Article
- Chemical modulation of the unfolded protein response reveals an antiviral role for the PERK pathway in human coronavirus 229E infection.RSC chemical biology · 2026Article
- RETRACTED: Plant rhabdovirus glycoprotein activates unfolded protein response-mediated antiviral ER-phagy in insect vectors.PLoS pathogens · 2026Article
- Therapeutic Targeting of Viral N-Glycosylation Modification: From Molecular Mechanisms to Clinical Application Prospects.Infectious diseases and therapy · 2025Review
- Article
- Anti-interferon armamentarium of human coronaviruses.Cellular and molecular life sciences : CMLS · 2025Review
- Equivocating and Deliberating on the Probability of COVID-19 Infection Serving as a Risk Factor for Lung Cancer and Common Molecular Pathways Serving as a Link.Pathogens (Basel, Switzerland) · 2024Review
- Porcine epidemic diarrhea virus E protein induces unfolded protein response through activating both PERK and ATF6 rather than IRE1 signaling pathway.Virus genes · 2024Article
- African swine fever virus modulates the endoplasmic reticulum stress-ATF6-calcium axis to facilitate viral replication.Emerging microbes & infections · 2024Article
- AMFR-mediated Flavivirus NS2A ubiquitination subverts ER-phagy to augment viral pathogenicity.Nature communications · 2024Article
- Host response to Aplysia Abyssovirus 1 in nervous system and gill.Developmental and comparative immunology · 2024Article
- SARS-CoV-2 variant-specific differences in inhibiting the effects of the PKR-activated integrated stress response.Virus research · 2024Article
- Nitazoxanide mitigates methotrexate hepatotoxicity in rats: role in inhibiting apoptosis and regulating endoplasmic reticulum stress.Frontiers in pharmacology · 2024Article
- Sigma Receptor Ligands Prevent COVID Mortality In Vivo: Implications for Future Therapeutics.International journal of molecular sciences · 2023Article
- The paradigm of prophylactic viral outbreaks measures by microbial biosurfactants.Journal of infection and public health · 2023Review
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- Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronavirus replication is structurally and functionally associated with the endoplasmic reticulum (ER), a major site of protein synthesis, folding, modification and sorting in the eukaryotic cells. Disturbance of ER homeostasis may occur under various physiological or pathological conditions. In response to the ER stress, signaling pathways of the unfolded protein response (UPR) are activated. UPR is mediated by three ER transmembrane sensors, namely the PKR-like ER protein kinase (PERK), the inositol-requiring protein 1 (IRE1) and the activating transcriptional factor 6 (ATF6). UPR facilitates adaptation to ER stress by reversible translation attenuation, enhancement of ER protein folding capacity and activation of ER-associated degradation (ERAD). In cells under prolonged and irremediable ER stress, UPR can also trigger apoptotic cell death. Accumulating evidence has shown that coronavirus infection causes ER stress and induces UPR in the infected cells. UPR is closely associated with a number of major signaling pathways, including autophagy, apoptosis, the mitogen-activated protein (MAP) kinase pathways, innate immunity and pro-inflammatory response. Therefore, studies on the UPR are pivotal in elucidating the complicated issue of coronavirus-host interaction. In this paper, we present the up-to-date knowledge on coronavirus-induced UPR and discuss its potential involvement in regulation of innate immunity and apoptosis.
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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.