ArticleJournal of virology2013
Human cytomegalovirus inhibits apoptosis by proteasome-mediated degradation of Bax at endoplasmic reticulum-mitochondrion contacts.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mitochondrial changes associated with viral infectious diseases in the paediatric population.Reviews in medical virology · 2021Pooled it
- Herpes simplex virus type-1 ocular infection in thrombospondin-1 deficient C57BL/6J mice.PloS one · 2026Article
- Does human cytomegalovirus provide a novel therapeutic target for patients with glioblastoma?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Review
- Human cytomegalovirus and neonatal infection.Current research in microbial sciences · 2024Review
- Review
- Restructured membrane contacts rewire organelles for human cytomegalovirus infection.Nature communications · 2022Article
- Dual inhibition of innate immunity and apoptosis by human cytomegalovirus protein UL37x1 enables efficient virus replication.Nature microbiology · 2022Article
- Human Cytomegalovirus vMIA Inhibits MAVS Oligomerization at Peroxisomes in an MFF-Dependent Manner.Frontiers in cell and developmental biology · 2022Article
- Human Cytomegalovirus miR-UL70-3p Downregulates the HInternational journal of molecular sciences · 2021Article
- Cytoplasmic mRNA decay represses RNA polymerase II transcription during early apoptosis.eLife · 2021Article
- Herpesvirus Regulation of Selective Autophagy.Viruses · 2021Review
- Contribution of Yeast Studies to the Understanding of BCL-2 Family Intracellular Trafficking.International journal of molecular sciences · 2021Review
- Apoptosis Disorder, a Key Pathogenesis of HCMV-Related Diseases.International journal of molecular sciences · 2021Review
- Mitochondria and Peroxisome Remodeling across Cytomegalovirus Infection Time Viewed through the Lens of Inter-ViSTA.Cell reports · 2020Article
- Human Cytomegalovirus pUL37x1 Is Important for Remodeling of Host Lipid Metabolism.Journal of virology · 2019Article
- Mitochondria-Associated Membranes (MAMs) are involved in Bax mitochondrial localization and cytochrome c release.Microbial cell (Graz, Austria) · 2019Article
- Location is everything: protein translocations as a viral infection strategy.Current opinion in chemical biology · 2019Review
- Human Cytomegalovirus Protein pUL38 Prevents Premature Cell Death by Binding to Ubiquitin-Specific Protease 24 and Regulating Iron Metabolism.Journal of virology · 2018Article
- Domain Interaction Studies of Herpes Simplex Virus 1 Tegument Protein UL16 Reveal Its Interaction with Mitochondria.Journal of virology · 2017Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Human cytomegalovirus (HCMV) encodes the UL37 exon 1 protein (pUL37x1), which is the potent viral mitochondrion-localized inhibitor of apoptosis (vMIA), to increase survival of infected cells. HCMV vMIA traffics from the endoplasmic reticulum (ER) to ER subdomains, which are physically linked to mitochondria known as mitochondrion-associated membranes (MAM), and to mitochondria. The antiapoptotic function of vMIA is thought to primarily result from its ability to inhibit Bax-mediated permeabilization of the outer mitochondrial membrane (OMM). Here, we establish that vMIA retargets Bax to the MAM as well as to the OMM from immediate early through late times of infection. However, MAM localization of Bax results in its increased ubiquitination and proteasome-mediated degradation. Surprisingly, HCMV infection does not increase OMM-associated degradation (OMMAD) of Bax, even though the ER and mitochondria are physically connected at the MAM. It was recently found that lipid rafts at the plasma membrane can connect extrinsic and intrinsic apoptotic pathways and can serve as sites of apoptosome assembly. In transfected permissive human fibroblasts, vMIA mediates, through its cholesterol affinity, association of Bax and apoptosome components with MAM lipid rafts. While Bax association with MAM lipid rafts was detected in HCMV-infected cells, association of apoptosome components was not. These results establish that Bax recruitment to the MAM and its MAM-associated degradation (MAMAD) are a newly described antiapoptotic mechanism used by HCMV infection to increase cell survival for its growth.
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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.