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Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation

ABSTRACT: Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation

PROVIDER: PRJNA598213 | ENA |

REPOSITORIES: ENA

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Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation

Project description:Interactions between human cytomegalovirus (HCMV) infection and environmental factors can increase susceptibility to essential hypertension (EH). Although endothelial dysfunction is the initial factor of EH, the epigenetic mechanisms through which HCMV infection induces endothelial cell dysfunction are poorly understood. Here, we evaluated whether HCMV regulated endothelial cell function and assessed the underlying mechanisms. Microarray analysis in human umbilical vein endothelial cells (HUVECs) treated with HCMV AD169 strain in the presence of hyperglycemia and hyperlipidemia revealed differential expression of genes involved in hypertension.

2020-02-14 | GSE142762 | GEO

Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation.

Project description: Not available

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Downregulation of Neurodevelopmental Gene Expression in iPSC-Derived Cerebral Organoids Upon Infection by Human Cytomegalovirus

Project description:Downregulation of Neurodevelopmental Gene Expression in iPSC-Derived Cerebral Organoids Upon Infection by Human Cytomegalovirus

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Murine cytomegalovirus evolved a cell cycle regulator (m54.5) within the highly conserved viral DNA polymerase gene

Project description:Systems biology approaches have revealed a surprising complexity of herpesvirus gene products. Using advanced sequencing approaches, we discovered a novel gene, m54.5, encoded within a highly conserved region of the murine cytomegalovirus (MCMV) genome. This gene produces a nuclear protein, m54.5p, abundantly expressed early during infection. We show that m54.5p interacts with host cell cycle regulators—the anaphase-promoting complex/cyclosome (APC/C) and phosphatase-6 (PP6)—to arrest cells in G1 phase and block progression into S phase. This function and underlying mechanism is reminiscent of the unrelated UL21a protein in human cytomegalovirus, illustrating how distinct viruses can evolve similar strategies to control host cell division. Despite its role in cell cycle disruption, m54.5p is not required for MCMV replication in cultured cells, suggesting redundant viral mechanisms. Our findings reveal the unexpected plasticity of herpesvirus genomes to evolve new, functional transcripts and proteins even within the most highly conserved genomic regions. Our findings thereby reshape our understanding of herpesvirus evolution and virus-host interaction.

2026-05-16 | PXD066167 | Pride

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Murine Cytomegalovirus research reagents

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SOX11 Downregulation and IL-7/IL22RA2 Upregulation Might be a Potential Mechanism of Exosome in Promoting Schwann Cell Proliferation

Project description:SOX11 Downregulation and IL-7/IL22RA2 Upregulation Might be a Potential Mechanism of Exosome in Promoting Schwann Cell Proliferation

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Cytomegalovirus infection

Project description:Comparison of gene expression profiles of human foreskin fibroblasts (HFF) infected with 3 clinical isolates of cytomegalovirus strains representing three glycoprotein B genotypes. Keywords: other

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