ArticleJournal of virology2022
The Immune-Specific E3 Ubiquitin Ligase MARCH1 Is Upregulated during Human Cytomegalovirus Infection to Regulate Iron Levels.
Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- A proximity ligation screen identifies SNAT2 as a novel target of the MARCH1 E3 ubiquitin ligase.Biology open · 2026Article
- Trace Elements and Viral Infectious Diseases: Dual Roles in Pathogenesis and Immunity.Infectious disease reports · 2026Review
- Human cytomegalovirus promotesJournal of virology · 2025Article
- The HCMV tegument protein UL88 degrades MyD88 and reduces innate immune activation.Journal of virology · 2025Article
- HCMV infection downregulates GPX4 and stimulates lipid peroxidation but does not induce ferroptosis.Journal of virology · 2025Article
- Genetic Markers of Postmortem Brain Iron.Journal of neurochemistry · 2025Article
- Article
- CLPTM1L is a GPI-anchoring pathway component targeted by HCMV.The Journal of cell biology · 2023Article
- Regulation of MHC class II and CD86 expression by March-I in immunity and disease.Current opinion in immunology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Human cytomegalovirus (HCMV) modulates numerous cellular pathways to facilitate infection. Iron is essential to many cellular processes and is often incorporated into proteins and enzymes involved in oxidative phosphorylation and DNA synthesis and repair, among others. Despite its prominent role in the cell, little is known about the regulation of iron metabolism during HCMV infection. Herein, we observe modulation of the transferrin receptor (TfR) during infection and a corresponding change in the cellular labile iron pool. TfR and the iron pool are increased early during infection and then return to mock levels at the late stages of infection. We identified the cellular ubiquitin ligase MARCH1 as an important regulator of TfR. MARCH1 plays a proviral role during infection, as its knockdown leads to a decrease in infectious titers. Knockdown of MARCH1 also leads to an increase in ROS, lipid peroxidation, and mitochondrial dysfunction. Inhibiting an early increase in TfR expression during infection also decreases virus production. These findings indicate the importance of tightly regulating iron metabolism during HCMV infection to facilitate efficient virus production.
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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.