Primary neonatal mouse cardiomyocytes: empty adenovirus infection vs. Mettl14-overexpression adenovirus infection
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ABSTRACT:
PROVIDER: PRJNA773497 | ENA |
REPOSITORIES: ENA
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Project description:The adenovirus carrying Mettl14 gene infects primary neonatal mouse cardiomyocytes, which is in contrast with the primary neonatal mouse cardiomyocytes infected with empty virus. The purpose is to explore the effect of Mettl14 on the global mRNA m6A modification level in primary neonatal rat cardiomyocytes.
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Project description:To find the proteins encoded by HSV-1 genome that interact with METTL14, we performed TAP/MS to identify the interacting partners of METTL14 in U87 cells before and after HSV-1 virus infection.
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Project description:As intracellular parasites, viruses exploit cellular proteins at every stage of infection. Adenovirus related outbreaks cause severe acute respiratory illnesses and conjunctivitis, with no specific antiviral therapy yet available. Herein, we investigate human adenovirus (HAdV-D37) pIIIa-host protein interactions by affinity purification and mass spectrometry (AP-MS) screens. We demonstrate that viral pIIIa interacts with ubiquitin-specific protease 9x (USP9x) and Ran-binding protein 2 (RANBP2). As intracellular parasites, viruses exploit cellular proteins at every stage of infection. Adenovirus related outbreaks cause severe acute respiratory illnesses and conjunctivitis, with no specific antiviral therapy yet available. Herein, we investigate human adenovirus (HAdV-D37) pIIIa-host protein interactions by affinity purification and mass spectrometry (AP-MS) screens. We demonstrate that viral pIIIa interacts with ubiquitin-specific protease 9x (USP9x) and Ran-binding protein 2 (RANBP2).
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Project description:A timecourse of adenovirus infection of human HeLa cells, using RNA-seq
2012-10-27 | E-MTAB-1277 | biostudies-arrayexpress
Project description:The human adenovirus type 5 (HAdV-C5) early region 1B 55-kDa protein (E1B-55K) is a multifunctional protein that promotes viral replication and adenovirus-mediated cell transformation through various mechanisms that primarily counteract host intrinsic and innate immunity. These include post-translational activities that exploit the host cell ubiquitin- and SUMO-conjugation machineries to regulate antiviral cellular restriction factors. However, despite significant advancements in this field, several underlying mechanisms governing these processes remain unidentified to date. Here, we performed SILAC-based quantitative SUMO proteomics to better understand cellular consequences of E1B-55K-mediated host cell modulation and adenovirus infection in general. We assessed cellular proteins for abundance changes and SUMO2 conjugate proteome changes during infection with wild type HAdV-C5 or E1B-55K deletion mutants. We provide evidence that changes in the SUMOylated proteome have the potential to regulate the DNA damage response, cell cycle control, chromatin assembly, and gene transcription. Strikingly, we identified a SUMO-dependent ubiquitin-mediated degradation mechanism for some SUMO substrates, suggesting that E1B-55K may use multiple mechanisms to alter the activity of restrictive cellular pathways.
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Project description:Adenovirus infection leads to increased glycolytic metabolism in host cells. Expression of a single gene product encoded within the E4 early transcription region, E4ORF1, is sufficient to promote increased glycolytic flux in cultured epithelial cells. E4ORF1 reprograms cellular glucose metabolism by augmenting MYC-dependent transcription of metabolic genes. To gain insight into the mechanism by which E4ORF1 promotes increased glycolytic flux, we conducted a global microarray analysis of changes in RNA expression in MCF10A cells induced to accutely express ORF1 versus an empty vector.
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Project description:METTL3 and METTL14 are considered to faithfully form the m6A writing complex in a 1:1 ratio, regulating the fate of mRNA by adding m6A modifications. However, recent studies have shown inconsistent expression and prognostic value of METTL3 and METTL14 in some tumors, suggesting that they may not be faithful in tumors. Pan-cancer analysis based on TCGA data reveals significant differences in expression, function, tumor burden correlation, and immune correlation between METTL3 and METTL14, especially in esophageal squamous cell carcinoma (ESCC). Knockdown of METTL3 significantly inhibits the cell proliferation in vitro and in vivo in ESCC EC109 cells, while the impact of METTL14 knockdown on proliferation is limited, and it cannot abolish the expression of METTL3 protein. mRNA-seq results indicate that METTL3 independently regulates the expression of 1615 genes, while only 776 genes are co-regulated by METTL3 and METTL14. Furthermore, through immunofluorescence co-localization, it is observed that METTL3 and METTL14 have certain inconsistencies in cellular localization. HPLC-MS results show that METTL3 independently binds to the Nop56p-associated pre-rRNA complex and mRNA splicing complex, separate from METTL14. Through bioinformatics and various omics studies, we have preliminarily discovered that METTL3 independently regulating tumor cell proliferation, and the participation in mRNA splicing may be a critical molecular mechanism. Our study provides an experimental basis and theoretical foundation for further understanding of the m6A writing complex and tumor therapy targeting METTL3.
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