Transcriptional response to IFN-κ and IFN-κDual in A549 cell line
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ABSTRACT:
PROVIDER: PRJNA598133 | ENA |
REPOSITORIES: ENA
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Project description:Type I interferon (IFN) is the first line of defense against virus infection. By using both in vivo and in vitro influenza infection models, we found that type I IFN-κ, limited the replication of influenza viruses by stimulating a IFNAR-MAPK-cFos-CHD6 axis. Similarly, Zika virus (ZIKV) was also highly sensitive to IFN-κ-mediated suppression. With an IAV infected mouse model, we found that IFN-κ was the earliest responding type I interferon among all known members in mice after H9N2 infection, a low-pathogenic Avian Influenza, whereas this early induction did not occur upon highly pathogenic H7N9 infection. IFN-κ can efficiently contain both low- and high-pathogenic influenza replication in cultured human lung cells, and CHD6 was the major effector responsive molecule for IFN-κ, but not for IFN-α/β. Furthermore, we discovered that both IFNAR1 and IFNAR2 subunits of type I interferon receptor and their downstream axis of p38-cFos are engaged in IFN-κ signaling cascade to acti vate CHD6, which didn`t require STAT1 activity. In addition, we showed that the pre-treatment with IFN-κ before IAV challenge protected mice from high mortality. Altogether, our study identified an IFN-κ-specific pathway that suppressed influenza A virus in vitro and in vivo. Thus, IFN-κ may have potential as a new prevention and treatment agents against emerging viruses
2020-04-09 | GSE142708 | GEO
Project description:Using doxycycline-inducible IFN-kappa expression in CIN612-9E cells, which maintain extrachromosomally replicating HPV31 genomes, we demonstrate that IFN-kappa inhibits the growth of these cells and reduces viral transcription and replication. Interestingly, the initiation of viral early transcription was already inhibited 4-6h after IFN-kappa expression. This was also observed with recombinant IFN-beta suggesting a common mechanism of IFNs. RNA-seq analysis identified 1367 IFN-kappa regulated genes of which 221 were modulated >2-fold. The majority of those (71%) matched known ISGs confirming that IFN-kappa acts as a bona fide type I IFN in hr-HPV-positive keratinocytes. RNAi and co-transfection experiments indicate that the inhibition of viral transcription is mainly due to the induction of Sp100 proteins by IFN-kappa. CIN612-9E/pInd-IFN-kappa were induced for 4h with 1µg/ml doxycyclin or not. Three biological replicates were analyzed.
2015-11-04 | E-GEOD-74658 | biostudies-arrayexpress
Project description:Using doxycycline-inducible IFN-kappa expression in CIN612-9E cells, which maintain extrachromosomally replicating HPV31 genomes, we demonstrate that IFN-kappa inhibits the growth of these cells and reduces viral transcription and replication. Interestingly, the initiation of viral early transcription was already inhibited 4-6h after IFN-kappa expression. This was also observed with recombinant IFN-beta suggesting a common mechanism of IFNs. RNA-seq analysis identified 1367 IFN-kappa regulated genes of which 221 were modulated >2-fold. The majority of those (71%) matched known ISGs confirming that IFN-kappa acts as a bona fide type I IFN in hr-HPV-positive keratinocytes. RNAi and co-transfection experiments indicate that the inhibition of viral transcription is mainly due to the induction of Sp100 proteins by IFN-kappa.
2015-11-04 | GSE74658 | GEO
Project description:Type I interferon (IFN) is the first line of defense against virus infection. By using both in vivo and in vitro influenza infection models, we found that type I IFN-κ, limited the replication of influenza viruses by stimulating a IFNAR-MAPK-cFos-CHD6 axis. Similarly, Zika virus (ZIKV) was also highly sensitive to IFN-κ-mediated suppression. With an IAV infected mouse model, we found that IFN-κ was the earliest responding type I interferon among all known members in mice after H9N2 infection, a low-pathogenic Avian Influenza, whereas this early induction did not occur upon highly pathogenic H7N9 infection. IFN-κ can efficiently contain both low- and high-pathogenic influenza replication in cultured human lung cells, and CHD6 was the major effector responsive molecule for IFN-κ, but not for IFN-α/β. Furthermore, we discovered that both IFNAR1 and IFNAR2 subunits of type I interferon receptor and their downstream axis of p38-cFos are engaged in IFN-κ signaling cascade to acti vate CHD6, which didn`t require STAT1 activity. In addition, we showed that the pre-treatment with IFN-κ before IAV challenge protected mice from high mortality. Altogether, our study identified an IFN-κ-specific pathway that suppressed influenza A virus in vitro and in vivo. Thus, IFN-κ may have potential as a new prevention and treatment agents against emerging viruses
2020-04-09 | GSE142707 | GEO
Project description:BRD9 was identified in a genome-wide screen for genes regulating the response to interferon (IFN) in a A549 based reporter cell line. Subsequent experiments determined an involvement of BRD9 in the transcriptional regulation of Interferon-stimulated genes (ISGs) expression following stimulation with IFN-a2. The aim of this proximity-labelling experiments was to gain a more mechanistic understanding of BRD9 recruitment during the IFN signal transduction using A549 cells stably transduced with BRD9-TurboID and mCherry-TurboID fusion proteins. The BRD9 interactome in the absence of IFN- a2 was determined. We found that following IFN-a2 treatment, STAT2 significantly associates with BRD9-TurboID.
2021-08-17 | PXD026926 | Pride
Project description:Type-II interferon or IFN-gamma is a critical cytokine in innate immunity that control multitude of intracellular infections. IFN-gamma binds to interferon gamma receptors to phosphorylate and activate STAT1 mediated transcription of interferon stimulated genes (ISGs). We executed a genome-wide CRISPR-Cas9 screen against ~20,000 human genes to identify IRF-1 and NF2 as significant regulators of Toxoplasma infection in A549 lung epithelial cells. IRF-1 is a key transcription factor immediately downstream of STAT1 induced transcription that amplifies ISG expression in different cell types. NF2 or MERLIN is a tumor suppressor that is known to regulate expression of genes involved with cellular growth and metabolism. Transcriptomic signature of A549 cells lacking IRF-1 and NF2 were measured upon activation with IFN-gamma to find set of genes that may be regulating Toxoplasma infection. A total of 1,046,709,676 reads from 3 independent biological replicates were mapped to human hg38 reference genome. Expression of a ISGs that failed to induced in cells lacking IRF1 were found to be dysregulated in absence of NF2 as well.
2023-12-15 | GSE215771 | GEO
Project description:miRNA profiling of A549 cell line
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Project description:A549 cell line expressing PAX5-flag and performed ChIP-seq
2024-01-15 | GSE164913 | GEO
Project description:Earthworm's celomic fluid has long attracted scientists' interest due to its toxic properties. It has been shown that subjecting it to a short heating at 70 ° C, which effectively reduces the toxicity to healthy cells, and demonstrates the selective action of the obtained Venetin-1 preparation against Candida albicans cells, as well as tumor cells from the A549 line. In order to find out about the molecular mechanisms behind the anti-cancer properties of the preparation, the conducted research investigated the proteome response of A549 cells to the presence of Venetin-1. The sequential window acquisition of all theoretical mass spectra (SWATH-MS) methodology was used for the analysis, which allows for a relative quantitative analysis to be carried out without radiolabelling. The results showed that the formulation did not induce significant proteome responses in healthy BEAS cells. In the case of the tumor line, 31 proteins were up-regulated and 18 proteins down-regulated. Proteins with increased expression in neoplastic cells are mainly associated with the mitochondrion, membrane transport and the endoplasmic reticulum. In the case of altered proteins, Venetin-1 interferes in proteins that stabilize the structures, i.e. keratin, glycolysis / gluconeogenesis and metabolic processes. This information shows the potential of Venetin-1, which may be used in the treatment of lung cancer in the future.
2023-06-02 | PXD034121 | Pride