ArticleCell stress & chaperones2021
ER stress-related molecules induced by Hantaan virus infection in differentiated THP-1 cells.
Article in Cell stress & chaperones, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Hantaan virus infection induces human mucosal-associated invariant T cell pyroptosis through IRE1α pathway.Communications biology · 2025Article
- Review
- Development and validation of a novel endoplasmic reticulum stress-related lncRNAs signature in osteosarcoma.Scientific reports · 2024Article
- A novel endoplasmic reticulum stress-related lncRNA signature for prognosis prediction and immune response evaluation in Stomach adenocarcinoma.BMC gastroenterology · 2023Article
- The inhibition of ORMDL3 prevents Alzheimer's disease through ferroptosis by PERK/ATF4/HSPA5 pathway.IET nanobiotechnology · 2023Article
- Increased blood CD226Annals of medicine · 2023Article
- Review
- Construction and validation of a prognostic model for lung adenocarcinoma based on endoplasmic reticulum stress-related genes.Scientific reports · 2022Article
- Development and validation of a novel endoplasmic reticulum stress-related lncRNA prognostic signature and candidate drugs in breast cancer.Frontiers in genetics · 2022Article
- Viruses Run: The Evasion Mechanisms of the Antiviral Innate Immunity by Hantavirus.Frontiers in microbiology · 2021Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endoplasmic reticulum stress (ER stress) can be induced by virus infection. In this part, we explored whether Hantaan virus (HTNV) infection could induce ER stress in differentiated THP-1 (dTHP-1) cells. It showed that the mRNA and protein levels of ER stress-related 78 kDa glucose-regulated protein (GRP78, HSPA5) and mRNA levels of X box-binding protein 1 (XBP-1), activating transcription factor 6(ATF6) and PKR-like ER kinase (PERK) after HTNV infection, were significantly higher than that in uninfected control group. However, the mRNA levels of C/EBP homologous protein (CHOP), glucose-regulated protein 94 (GRP94, HSPC4), and inositol-requiring enzyme1 (IRE1) were not significantly different between the infected group and the untreated group in 2 h after virus infection. It is unusual in activating GRP78 but not GRP94. Meanwhile, dTHP-1 cells infected with HTNV at 12 h did not show obvious apoptosis. These results indicated that the HTNV infection could induce the unfolded protein response (UPR) in dTHP-1 cells, without directly leading to cell apoptosis during 12 h after virus infection.
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