Epstein-Barr virus (EBV) is present in a state of latency in infected memory B-cells and EBV-associated lymphoid and epithelial cancers. Cell stimulation or differentiation of infected B-cells and epithelial cells induces reactivation to the lytic replication cycle. In each cell type, the EBV transcription and replication factor Zta (BZLF1, EB1) plays a role in mediating the lytic cycle of EBV. Zta is a transcription factor that interacts directly with Zta response elements (ZREs) within viral and cellular genomes. Here we undertake chromatin-precipitation coupled to DNA-sequencing (ChIP-Seq) of Zta-associated DNA from cancer-derived epithelial cells. The analysis identified over 14 000 Zta-binding sites in the cellular genome. We assessed the impact of lytic cycle reactivation on changes in gene expression for a panel of Zta-associated cellular genes. Finally, we compared the Zta-binding sites identified in this study with those previously identified in B-cells and reveal substantial conservation in genes associated with Zta-binding sites.
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http://dx.doi.org/10.1099/acmi.0.000282 | DOI Listing |
Front Pharmacol
January 2025
Cell Biology Laboratory, Federal University of Alagoas, Maceió, Brazil.
The epithelial-mesenchymal transition (EMT) is a biological process in which epithelial cells change into mesenchymal cells with fibroblast-like characteristics. EMT plays a crucial role in the progression of fibrosis. Classical inducers associated with the maintenance of EMT, such as TGF-β1, have become targets of several anti-EMT therapeutic strategies.
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January 2025
Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, An-Najah National University, Nablus, Palestine.
Background And Aim: NK cells and NK-cell-derived cytokines were shown to regulate neutrophil activation in acute lung injury (ALI). However, the extent to which ALI regulates lung tissue-resident NK (trNK) activity and their molecular phenotypic alterations are not well defined. We aimed to assess the impact of 1,25-hydroxy-vitamin-D3 [1,125(OH)D] on ALI clinical outcome in a mouse model and effects on lung trNK cell activations.
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January 2025
The Third Affiliated Hospital of Beijing University of Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Background: Cervical cancer is the fourth most common cancer in women globally, and the main cause of the disease has been found to be ongoing HPV infection. Cervical cancer remains the primary cause of cancer-related death despite major improvements in screening and treatment approaches, especially in low- and middle-income nations. Therefore, it is crucial to investigate the tumor microenvironment in advanced cervical cancer in order to identify possible treatment targets.
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January 2025
Institute of Medical Genetics and Reproductive Immunity, School of Medical Science and Laboratory Medicine, Jiangsu College of Nursing, Huai'an, China.
The intestinal epithelium, beyond its role in absorption and digestion, serves as a critical protective mechanical barrier that delineates the luminal contents and the gut microbiota from the lamina propria within resident mucosal immune cells to maintain intestinal homeostasis. The barrier is manifested as a contiguous monolayer of specialized intestinal epithelial cells (IEC), interconnected through tight junctions (TJs). The integrity of this epithelial barrier is of paramount.
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January 2025
Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, United States.
Cluster of Differentiation 6 (CD6), an established marker of T cells, has multiple and complex functions in regulation of T cell activation and proliferation, and in adhesion of T cells to antigen-presenting cells and epithelial cells in various organs and tissues. Early studies on CD6 demonstrated its role in mediating cell-cell interactions through its first ligand to be identified, CD166/ALCAM. The observation of CD6-dependent functions of T cells that could not be explained by interactions with CD166/ALCAM led to discovery of a second ligand, CD318/CDCP1.
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