Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA318007 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3355773.fastq.gz | Fastqsanger.gz | |||
| SRR3355774.fastq.gz | Fastqsanger.gz | |||
| SRR3355776.fastq.gz | Fastqsanger.gz | |||
| SRR3355777.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
Project description:Topoisomerase 1 inhibition suppresses inflammatory genes and protects from death by inflammation
| PRJNA318003 | ENA
Project description:Topoisomerase 1 inhibition suppresses inflammatory genes and protects from death by inflammation (RNA-Seq)
| PRJNA318006 | ENA
Project description:The host innate immune response is the first line of defense against pathogens and is orchestrated by the concerted expression of genes induced by microbial stimuli. Deregulated expression of these genes is linked to the initiation and progression of numerous diseases associated with exacerbated inflammation. Here, we identify Topoisomerase 1 (Top1) as a critical positive regulator of RNA polymerase II (RNAPII) transcriptional activity at pathogen-induced genes. Notably, depletion or chemical inhibition of Top1 suppresses the host response against replicating Influenza and Ebola viruses as well as bacterial products. As a result, therapeutic pharmacological inhibition of Top1 protects mice from death in experimental models of chemical- and pathogen-induced lethal inflammation. Our results indicate that Top1 inhibition could be used as therapy against life threatening infections characterized by an acutely exacerbated immune response.
2016-07-11 | GSE80131 | GEO
Project description:The host innate immune response is the first line of defense against pathogens and is orchestrated by the concerted expression of genes induced by microbial stimuli. Deregulated expression of these genes is linked to the initiation and progression of numerous diseases associated with exacerbated inflammation. Here, we identify Topoisomerase 1 (Top1) as a critical positive regulator of RNA polymerase II (RNAPII) transcriptional activity at pathogen-induced genes. Notably, depletion or chemical inhibition of Top1 suppresses the host response against replicating Influenza and Ebola viruses as well as bacterial products. As a result, therapeutic pharmacological inhibition of Top1 protects mice from death in experimental models of chemical- and pathogen-induced lethal inflammation. Our results indicate that Top1 inhibition could be used as therapy against life threatening infections characterized by an acutely exacerbated immune response.
2016-07-11 | GSE80129 | GEO
Project description:The ongoing pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is currently affecting millions of lives worldwide. Large retrospective studies indicate that an elevated level of inflammatory cytokines and pro-inflammatory factors are associated with both increased disease severity and mortality. Targeting these pathways might therefore be a viable therapeutic strategy. Previously, we have reported that chromatin factors such as Topoisomerase I (Top1) play key roles in controlling the induction of inflammatory gene expression programs. Here, by using multidimensional epigenetic, transcriptional, in vitro and in vivo analyses, we show that Topoisomerase 1 (Top1) inhibition in infected cells and animals suppresses lethal inflammation induced by SARS-CoV-2.
2021-02-26 | GSE167528 | GEO
Project description:The ongoing pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is currently affecting millions of lives worldwide. Large retrospective studies indicate that an elevated level of inflammatory cytokines and pro-inflammatory factors are associated with both increased disease severity and mortality. Targeting these pathways might therefore be a viable therapeutic strategy. Previously, we have reported that chromatin factors such as Topoisomerase I (Top1) play key roles in controlling the induction of inflammatory gene expression programs. Here, by using multidimensional epigenetic, transcriptional, in vitro and in vivo analyses, we show that Topoisomerase 1 (Top1) inhibition in infected cells and animals suppresses lethal inflammation induced by SARS-CoV-2.
2021-03-30 | GSE162618 | GEO
Project description:The ongoing pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is currently affecting millions of lives worldwide. Large retrospective studies indicate that an elevated level of inflammatory cytokines and pro-inflammatory factors are associated with both increased disease severity and mortality. Targeting these pathways might therefore be a viable therapeutic strategy. Previously, we have reported that chromatin factors such as Topoisomerase I (Top1) play key roles in controlling the induction of inflammatory gene expression programs. Here, by using multidimensional epigenetic, transcriptional, in vitro and in vivo analyses, we show that Topoisomerase 1 (Top1) inhibition in infected cells and animals suppresses lethal inflammation induced by SARS-CoV-2.
2021-03-30 | GSE162615 | GEO
Project description:The ongoing pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is currently affecting millions of lives worldwide. Large retrospective studies indicate that an elevated level of inflammatory cytokines and pro-inflammatory factors are associated with both increased disease severity and mortality. Targeting these pathways might therefore be a viable therapeutic strategy. Previously, we have reported that chromatin factors such as Topoisomerase I (Top1) play key roles in controlling the induction of inflammatory gene expression programs. Here, by using multidimensional epigenetic, transcriptional, in vitro and in vivo analyses, we show that Topoisomerase 1 (Top1) inhibition in infected cells and animals suppresses lethal inflammation induced by SARS-CoV-2.
2021-03-30 | GSE162612 | GEO
Project description:Death of intestinal epithelial cells (IECs) is important in the pathological process of intestinal inflammatory diseases. TNF acts as one pathogenic driver for inducing IEC death and substantial intestinal inflammation. However, the physiological protective mechanisms for suppressing TNF-induced IEC death remain poorly understood. Here, we report that EF-hand domain-containing protein D2 (EFHD2), highly expressed in normal intestine tissues but decreased in intestinal biopsy samples of ulcerative colitis patients, protects the intestinal epithelium from TNF-induced IEC apoptosis. EFHD2 inhibits TNF-induced apoptosis in primary IECs and intestinal organoids (enteroids). Mice deficient of Efhd2 in IECs exhibit excessive IEC death and exacerbated experimental colitis. Mechanistically, EFHD2 interacts with Cofilin to suppress the phosphorylation of Cofilin, leading to the inhibition of TNF receptor Ⅰ (TNFR1) internalization and TNF-induced apoptosis. Our findings define EFHD2 as an endogenous suppressor of IEC death to protect intestine inflammation, providing new insight to the regulation of death receptor signaling and control of intestinal inflammatory diseases.
2024-01-14 | PXD048587 |
Project description:Nrf2 (NF-E2-related factor-2) transcription factor regulates oxidative/xenobiotic stress response and also represses inflammation. However, the mechanisms how Nrf2 alleviates inflammation are still unclear. Here, we demonstrate that Nrf2 interferes with lipopolysaccharide-induced transcriptional upregulation of proinflammatory cytokines, including IL-6 and IL-1β. ChIP-seq and ChIP-qPCR analyses revealed that Nrf2 binds to the proximity of these genes in macrophages and inhibits RNA Pol II recruitment. Further, we found that Nrf2-mediated inhibition is independent of the Nrf2 binding motif and reactive oxygen species level. Murine inflammatory models further demonstrated that Nrf2 interferes with IL6 induction and inflammatory phenotypes in vivo. Thus, contrary to the widely accepted view that Nrf2 suppresses inflammation through redox control, we demonstrate here that Nrf2 opposes transcriptional upregulation of proinflammatory cytokine genes. This study identifies Nrf2 as the upstream regulator of cytokine production and establishes a molecular basis for an Nrf2-mediated anti-inflammation approach.
2016-05-12 | GSE71263 | GEO