ArticlePloS one2014
Degradation of AIMP1/p43 induced by hepatitis C virus E2 leads to upregulation of TGF-β signaling and increase in surface expression of gp96.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Glucose-regulated protein 94 (Grp94/gp96) in viral pathogenesis: Insights into its role and therapeutic potentials.European journal of medicinal chemistry · 2025Review
- The mARS complex: a critical mediator of immune regulation and homeostasis.Frontiers in immunology · 2024Review
- Predicted coronavirus Nsp5 protease cleavage sites in the human proteome.BMC genomic data · 2022Article
- Review
- Roles of aminoacyl-tRNA synthetase-interacting multi-functional proteins in physiology and cancer.Cell death & disease · 2020Review
- Phage-Antibiotic Synergy via Delayed Lysis.Applied and environmental microbiology · 2018Article
- Aminoacyl-tRNA synthetases, therapeutic targets for infectious diseases.Biochemical pharmacology · 2018Review
- AIMp1 Potentiates TFrontiers in immunology · 2017Article
- Chaperones in hepatitis C virus infection.World journal of hepatology · 2016Review
- Immunomodulatory effects of transforming growth factor-β in the liver.Hepatobiliary surgery and nutrition · 2014Review
- Transcriptome analysis of porcine thymus following porcine cytomegalovirus infection.PloS one · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) causes chronic hepatitis leading to liver fibrosis and autoimmune diseases. AIMP1/p43 is a multifunctional protein initially known as a cofactor of aminoacyl tRNA synthetase complex. Its function includes negative regulation of TGF-β signaling and suppression of Lupus-like autoimmune disease by inhibition of surface expression of gp96. HCV E2 was shown to directly interact with AIMP1/p43 by GST pulldown assay and coimmunoprecipitation. Their subcellular colocalization was observed in an immunofluorescence confocal microscopy. We showed that HCV E2 led to degradation of AIMP1/p43 in two ways. First, in the presence of HCV E2, endogenous AIMP1/p43 was shown to be degraded in an ubiquitin-dependent proteasome pathway. Second, grp78, an ER chaperone, was shown to interact with and stabilize AIMP1/p43. And HCV E2 inhibited this interaction leading to reduction of cellular AIMP1/p43. The degradation of AIMP1/p43 by HCV E2 resulted in increase of TGF-β signaling and cell surface expression of gp96. Thus we suggest that these are novel mechanisms responsible for liver fibrosis and autoimmune diseases caused by HCV.
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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.