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).
Project description:Comparisong of gene expression of human IMR-90 at 27 and 55 population doublings. RNA-seq data comprises 2 groups: 27 and 55 population doublings of IMR-90. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
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.
Project description:Purpose: RNA sequencing has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare Cre-treated versus YFP-treated mouse mesenchymal stem cells regarding gene expression. Mesenchymal miRNA profiles of 10-day-old Eed floxed calvaria infected with YFP and Adenovirus-CRE cells were generated by deep sequencing, in triplicate, using BGISEQ-500. The sequence reads that passed quality filters were mapped using HISAT and Bowtie2. Isoform expression levels were analyzed using RSEM.
