IRF3 and ZBP1
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA686391 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:ZBP1/IMP1 is an mRNA binding protein that post-transcriptionally regulates the expression of a handful mRNAs, implicated in maintaining cell polarity and adhesion. We have previously shown that ZBP1 was able to inhibit proliferation and invasiveness of breast carcinoma cells in vitro. In the current study, we utilized orthotopic breast fat pad xenografts to further investigate the ZBP1-mediated functions in breast tumorigenesis and metastasis in vivo. We used microarrays to identify important gene for breast tumor growth and metastasis in response to ZBP1 expression Total RNA was extracted from breast tumor generated from ZBP1-expression and ZBP1-nonexpression MDA231 cells and used for hybridization on Affymetrix microarrays. We sought to obtain gene expression profiles from the individual tumors and identify what genes are up-regulated or down-regulated in the presence of ZBP1. The microarray experiments and data analysis were performed in 'Gene Company Limited' in Senzheng, China. G-10 and G-13, Tumors generated from MDA231/GFP cells; I-5 and I-6, tumors generated from MDA231/ZBP1-GFP cells.
2014-10-24 | E-GEOD-62638 | biostudies-arrayexpress
Project description:ZBP1/IMP1 is an mRNA binding protein that post-transcriptionally regulates the expression of a handful mRNAs, implicated in maintaining cell polarity and adhesion. We have previously shown that ZBP1 was able to inhibit proliferation and invasiveness of breast carcinoma cells in vitro. In the current study, we utilized orthotopic breast fat pad xenografts to further investigate the ZBP1-mediated functions in breast tumorigenesis and metastasis in vivo. We used microarrays to identify important gene for breast tumor growth and metastasis in response to ZBP1 expression
2014-10-24 | GSE62638 | GEO
Project description:B-cell lymphomas arising in Zbp1-/-Eu-Myc mice were compared to B-cell lymphomas arising in Zbp1+/+Eu-Myc mice
2014-04-01 | E-MTAB-2354 | biostudies-arrayexpress
Project description:The goal of this study was to compare the gene expression profiles of WT, Tfam+/-, Zbp1-/- and Tfam+/-Zbp1-/- MEFs.
2023-01-28 | GSE223553 | GEO
Project description:The interferon regulatory factors IRF3 and IRF7 are key players in the regulation of type I and III IFN genes. In this study, we analyzed the role of IRF3 and IRF7 for the host response to influenza A virus infections in Irf3-/-, Irf7-/- and Irf3-/-Irf7-/- knock-out mice.
2016-11-02 | GSE77600 | GEO
Project description:The RNA editing enzyme ADAR1 is essential for suppression of innate immune activation and pathology caused by aberrant recognition of self-RNA, a role it carries out by disrupting the duplex structure of endogenous double-stranded RNA species. A point mutation in the Z-nucleic-acid binding domain (ZBD) of ADAR1 is associated with severe autoinflammatory disease. ZBP1 is the only other ZBD-containing mammalian protein and its activation can trigger both cell death and transcriptional responses via the kinases RIPK1 and RIPK3, and the protease caspase-8. Here, we show that the pathology caused by ADAR1 ZBD mutation is driven by activation of ZBP1. We found that ablation of ZBP1 fully rescued the overt pathology caused by ADAR1 mutation, without reversing the underlying inflammatory program caused by this mutation. While loss of RIPK3 partially phenocopied the protective effects of ZBP1 ablation, combined deletion of caspase-8 and RIPK3, or of caspase-8 and MLKL, unexpectedly exacerbated the pathogenic effects of ADAR1 mutation. These findings indicate that ADAR1 is a negative regulator of sterile ZBP1 activation, and that ZBP1-dependent signaling underlies the autoinflammatory pathology caused by mutation of ADAR1.
2022-06-11 | GSE200854 | GEO
Project description:IRF3 is one of the most critical transcription factor in down stream of pattern recognition receptors (such as toll-like receptor and RIG-I-like receptor) signalling pathway. IRF3 is known to induce the expression of type I IFN gene upon virus infection. To furter examine the role of IRF3 in virus-induced gene expression, we preformed microarray analysis in IRF3-/- peritoneal macrophages infected with VSV, and found that IRF3 suppresses the expression of Il12b gene. Peritoneal macrophages from WT of IRF3-/- B6 mice were infected with VSV(1 M.O.I. ) for 6 hous, and then subjected to microarray analysis.
2012-05-19 | E-GEOD-37855 | biostudies-arrayexpress
Project description:Cell death provides host defense and maintains homeostasis. Zα-containing molecules are essential for these processes. ZBP1 activates inflammatory cell death, PANoptosis, while ADAR1 serves as an RNA editor to maintain homeostasis. Here, we identify and characterize ADAR1’s interaction with ZBP1, defining its role in cell death regulation and tumorigenesis. Combining IFNs and nuclear export inhibitors (NEIs) activates ZBP1–dependent PANoptosis. ADAR1 suppresses PANoptosis by interacting with the Zα2 domain of ZBP1 to limit ZBP1 and RIPK3 interactions. Adar1fl/flLysMcre mice are resistant to development of colorectal cancer and melanoma, but deletion of the ZBP1 Zα2 domain restores tumorigenesis in these mice. In addition, treating wildtype mice with IFN-γ and the NEI KPT-330 regresses melanoma in a ZBP1–dependent manner. Our findings suggest that ADAR1 suppresses ZBP1–mediated PANoptosis, promoting tumorigenesis. Defining the functions of ADAR1 and ZBP1 in cell death is fundamental to inform therapeutic strategies for cancer and other diseases.
2021-10-19 | GSE184323 | GEO
Project description:Whole transcriptome of ZBP1-depleted myeloma cells was analysed using a high-throughput RNA-seq approach. ZBP1 was depleted by 2 different shRNAs in MM1.S and H929 cells, and total RNA was isolated on day 4 post-lentiviral transduction. Poly A-tail enriched RNA was sequenced and the analysis of commonly regulated genes by both shRNAs from 2 independent experiments revealed that ZBP1 regulates genes that are involved in cell cycle regulation.
2021-02-28 | GSE163496 | GEO
Project description:The RNA editing enzyme ADAR1 is essential for suppression of innate immune activation and pathology caused by aberrant recognition of self-RNA, a role it carries out by disrupting the duplex structure of endogenous double-stranded RNA species. A point mutation in the Z-nucleic-acid binding domain (ZBD) of ADAR1 is associated with severe autoinflammatory disease. ZBP1 is the only other ZBD-containing mammalian protein and its activation can trigger both cell death and transcriptional responses via the kinases RIPK1 and RIPK3, and the protease caspase-8. Here, we show that the pathology caused by ADAR1 ZBD mutation is driven by activation of ZBP1. We found that ablation of ZBP1 fully rescued the overt pathology caused by ADAR1 mutation, without reversing the underlying inflammatory program caused by this mutation. While loss of RIPK3 partially phenocopied the protective effects of ZBP1 ablation, combined deletion of caspase-8 and RIPK3, or of caspase-8 and MLKL, unexpectedly exacerbated the pathogenic effects of ADAR1 mutation. These findings indicate that ADAR1 is a negative regulator of sterile ZBP1 activation, and that ZBP1-dependent signaling underlies the autoinflammatory pathology caused by mutation of ADAR1.
2022-08-10 | GSE200986 | GEO