ArticleFrontiers in microbiology2022
Latency-associated upregulation of SERBP1 is important for the recruitment of transcriptional repressors to the viral major immediate early promoter of human cytomegalovirus during latent carriage.
Article in Frontiers in microbiology, 2022. 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, 11 citations in OpenAlex.
- Viral entry shapes HCMV latency establishment.Nature communications · 2025Article
- Lytic or Latent Phase in Human Cytomegalovirus Infection: An Epigenetic Trigger.International journal of molecular sciences · 2025Review
- N6-methyladenosine modification of HCMV IE1 transcript promotes the repressive state of viral genome to achieve latent infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Third intracellular loop of HCMV US28 is necessary for signaling and viral reactivation.Journal of virology · 2025Article
- KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025Review
- KAP1/TRIM28 - antiviral and proviral protagonist of herpesvirus biology.Trends in microbiology · 2024Article
- Virus-Specific Nanobody-Chimeras Degrade the Human Cytomegalovirus US28 Protein in CD34+ Cells.Pathogens (Basel, Switzerland) · 2024Article
- Aberrant RNA polymerase initiation and processivity on the genome of a herpes simplex virus 1 mutant lacking ICP27.Journal of virology · 2024Article
- The Human Cytomegalovirus Latency-Associated Gene Product Latency Unique Natural Antigen Regulates Latent Gene Expression.Viruses · 2023Article
- Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Suppression of human cytomegalovirus (HCMV) major immediate early gene (IE) expression from the viral major immediate early promoter (MIEP) is known to be crucial for the establishment and maintenance of HCMV latency in myeloid progenitor cells and their undifferentiated derivatives. This suppression of the MIEP during latent infection is known to result from epigenetic histone modification imparting a repressive chromatin structure around the MIEP in undifferentiated myeloid cells. In contrast, reactivation, resulting from, e.g., myeloid cell differentiation, is associated with activatory chromatin marks around the MIEP. Recently, recruitment of the transcriptional repressor SETDB1,
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