ArticleThe American journal of pathology1996
Cytoplasmic sequestration of p53 in cytomegalovirus-infected human endothelial cells.
Article in The American journal of pathology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 93 citations in OpenAlex.
- Mitochondrial Dysfunction in the Cardiovascular Disease Continuum: Problems of Studying the Progression During the Follow-Up of the Pathologies.International journal of molecular sciences · 2025Review
- Is the vIL-10 Protein from Cytomegalovirus Associated with the Potential Development of Acute Lymphoblastic Leukemia?Viruses · 2025Review
- Breaking Bad: How Viruses Subvert the Cell Cycle.Frontiers in cellular and infection microbiology · 2018Review
- Article
- Is HCMV a tumor promoter?Virus research · 2011Review
- The presence of p53 influences the expression of multiple human cytomegalovirus genes at early times postinfection.Journal of virology · 2009Article
- The ORF3 protein of porcine circovirus type 2 interacts with porcine ubiquitin E3 ligase Pirh2 and facilitates p53 expression in viral infection.Journal of virology · 2007Article
- Human cytomegalovirus UL38 protein blocks apoptosis.Journal of virology · 2007Article
- Human cytomegalovirus disrupts both ataxia telangiectasia mutated protein (ATM)- and ATM-Rad3-related kinase-mediated DNA damage responses during lytic infection.Journal of virology · 2007Article
- Potential role for p53 in the permissive life cycle of human cytomegalovirus.Journal of virology · 2006Article
- A novel checkpoint in the Bcl-2-regulated apoptotic pathway revealed by murine cytomegalovirus infection of dendritic cells.The Journal of cell biology · 2004Article
- Human cytomegalovirus causes endothelial injury through the ataxia telangiectasia mutant and p53 DNA damage signaling pathways.Circulation research · 2004Article
- Murine cytomegalovirus m41 open reading frame encodes a Golgi-localized antiapoptotic protein.Journal of virology · 2003Article
- A cytomegalovirus-encoded inhibitor of apoptosis that suppresses caspase-8 activation.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Microbes, inflammation and atherosclerosis: will old pathology lessons guide new therapies?Transactions of the American Clinical and Climatological Association · 2001Review
- Metabolic compensation during high energy output in fasting, lactating grey seals (Halichoerus grypus): metabolic ceilings revisited.Proceedings. Biological sciences · 2000Article
- A cytomegalovirus-encoded mitochondria-localized inhibitor of apoptosis structurally unrelated to Bcl-2.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Human umbilical vein endothelial cells were infected with human cytomegalovirus (HCMV) at a multiplicity of infection of 0.1 plaque-forming unit/cell and remained > 95% viable even after 10 days of infection. To induce apoptosis, control human umbilical vein endothelial cells and cells infected with HCMV for 3, 5, and 7 days were serum starved for 48 hours. Almost one-half of the uninfected cells lost viability after 48 hours of serum starvation whereas HCMV-infected cells were virtually unaffected (< 20% death, P < 0.05). Uninfected cells showed typical hallmarks of apoptosis, including unique morphological changes and DNA laddering. HCMV-infected cells, concomitant with their resistance to serum-starvation-induced death, displayed almost none of these characteristics. Active replication of HCMV was necessary for the anti-apoptotic effect, as cells treated with ultraviolet light-inactivated virus were not protected. p53, the G1/S phase cell cycle brake protein, was elevated in HCMV-infected cells. However, rather than accumulating in the nucleus, immunofluorescent and Western blot studies demonstrated remarkable and predominant cytoplasmic sequestration of p53 in HCMV-infected endothelial cells. Although HCMV proteins have already been shown to block apoptosis, we suggest that the aberrant subcellular pattern of p53 is the disturbed cellular mechanism that may be responsible for the anti-apototic properties of HCMV-infected cells. The selective resistance to apoptosis can be important during HCMV replication and may explain the oncogenic potential of HCMV as well as its pathogenic role in intimal-proliferation-mediated vascular diseases.
Indexed as
Identifiers
8909243PMC1865290W203366438What OpenQuestion holds
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.