Project description:Long noncoding RNAs (lncRNAs) participate in regulating many biological processes. However, their roles in influenza A virus (IAV) pathogenicity are largely unknown. Here, we analyzed the expression profile of lncRNAs and mRNAs in the H3N2-infected cells and H7N9-infected cells by high-throughput sequencing
Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in mouse lung infected with WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus). Groups of 22-week-old C57BL/6 mice were infected with the H7N9 Influenza WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus). Infections were done at 10^4 PFU or time-matched mock infected. Time points were 1, 2, 4 and 7 d.p.i. There were 5 animals/dose/time point. Lung samples were collected for virus load, transcriptional and proteomics analysis. Weight loss and animal survival were also monitored.
Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in mouse lung infected with WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus). Groups of 22-week-old C57BL/6 mice were infected with the H7N9 Influenza WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus). Infections were done at 10^4 PFU or time-matched mock infected. Time points were 1, 2, 4 and 7 d.p.i. There were 5 animals/dose/time point. Lung samples were collected for virus load, transcriptional and proteomics analysis. Weight loss and animal survival were also monitored.
Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in mouse lung infected with WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus).
Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in human Calu-3 cells infected with WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus).
Project description:To clarify the underlying mechanism that regulates the response of iron metabolism to influenza A virus infection, we analyzed gene expression profiles in mouse, bone marrow-derived macrophages (BMDMs) infected with H7N9 virus. In addition, We also analysed the chemokine, inflammation, innate-immunity, lipid-metabolism, transcription mRNA level by micrroarray. So, we gain the global transcriptional response in the BMDMs of mice infected with H7N9 virus.
Project description:The purpose is to obtain samples for mRNA, miRNA, proteomics, lipidomics, metabolomics, and histopathology analysis in mouse lung infected with WT A/Anhui/1/2013 (H7N9; 'AH1'), AH - NS1-103F/106M, and AH1 - 691 (ferret adapted virus).
Project description:To further identified miRNAs of BALB/c mouse lungs infected with A/Anhui/1/2013 (H7N9) (hereafter referred to as H7N9/AH1-PB2-627K(WT)) and mutant variants with PB2 amino acid substitutions (avian-like H7N9/AH1-PB2-627E and mammalian-adapted H7N9/AH1-PB2-627E/701N) , miRNA microarray was carried out.
Project description:With the purpose to elucidate the expression changes of host genes of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus at 24 hours post-infection(hpi) and fowl adenovirus-4 at 48 dpi. The spleens of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus and fowl adenovirus-4 were collected and high throughout sequenced. Compared with the control group, there were 2426 differentially expressed genes were obtained in the duck-origin H7N9 subtype avian influenza virus group, including 913 up-regulated genes and 1513 down-regulated genes, and there were 1534 differentially expressed genes were obtained in the fowl adenovirus-4 group, including 632 up-regulated genes and 902 down-regulated genes.
Project description:Different brain cell types play distinct roles in brain development and disease via cellular mechanisms. Molecular characterization of these cellular mechanisms using cell type-specific approaches, particularly at the protein (proteomic) level, can provide biological and therapeutic insights. Conventional approaches to investigate cell type-specific proteomes from brain pose several technical barriers. To overcome these, in vivo proteomic labeling with proximity dependent biotinylation of cytosolic proteins using TurboID with a Nuclear Export Sequence (TurboID-NES), coupled with mass spectrometry (MS) of labeled proteins, has emerged as a powerful strategy to sample cell type-specific proteomes in the native state of cells without need for cellular isolation. To complement in vivo proximity labeling approaches, in vitro studies are needed to ensure that cellular proteomes using the TurboID-NES approach are representative of the whole cell proteome, and capture cellular responses to stimuli without disruption of cellular processes. We generated murine neuroblastoma (N2A) and microglial (BV2) lines stably expressing TurboID-NES to biotinylate the cellular proteome for downstream purification and analysis using MS. TurboID-NES expression and biotinylation did not significantly impact homeostatic cellular proteomes of BV2 and N2A cells, and did not affect cytokine production or mitochondrial respiration of BV2 cells under resting or lipopolysaccharide (LPS)-stimulated conditions. TurboID-NES mediated biotinylation captured 59% of BV2 and 65% of N2A proteomes under resting conditions. Acute LPS treatment significantly altered microglial proteomes, but not N2A proteomes, and the LPS effect was partly captured by analysis of the TurboID-NES-labeled proteome of BV2 cells.
