GEO DataSets

(Submitter supplied) 293T were transfected with plasmids expressing DNA-dependent activator of IFN-regulatory factors (DAI) or retinoic acid-inducible gene 1 (RIG-I). Transfected cells were subsequently infected with influenza A/Puerto Rico/8/34 virus for 12 hours. Cell extract was subjected to FLAG Ab beads, washed, and retained. RNA was sequenced using the Illumina TruSeq Stranded Total RNA Library kit. The input sample represents total RNA from vector-infected cells.

Organism:

Homo sapiens; Influenza A virus (A/Puerto Rico/8/1934(H1N1))

Type:

Expression profiling by high throughput sequencing

Platform:

GPL22483

2 Samples

Download data: TXT

(Submitter supplied) Ripk3-deficient fibroblasts and lung epithelial cells are resistant to influenza-induced cell deaths. However, Ripk3 is required for protection against influenza infection in vivo. Here, we examine the influenza-regulated gene expressions between wild type and knock out MEFs as well as an involvement of kinase activity if any.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL11202

24 Samples

Download data: TXT

(Submitter supplied) Necroptosis is a lytic form of cell death that is mediated by the kinase RIPK3 and the pseudokinase MLKL when caspase-8 is inhibited downstream of death receptors, toll-like receptor 3 (TLR3), TLR4, and the intracellular Z-form nucleic acid sensor ZBP1. Oligomerization and activation of RIPK3 is driven by interactions with the kinase RIPK1, the TLR adaptor TRIF, or ZBP1. In this study, we use immunohistochemistry (IHC) and in situ hybridization (ISH) assays to generate a tissue atlas characterizing RIPK1, RIPK3, Mlkl, and ZBP1 expression in mouse tissues. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

11 Samples

Download data: TXT

(Submitter supplied) The innate immune system recognizes nucleic acids as a signature of microbial infection and initiates host-protective responses, including the production of type I IFN and proinflammatory cytokines. Z-DNA binding protein 1 (ZBP1, also known as DLM-1 or DAI) was previously identified as a dsDNA binding protein, triggering DNA-mediated activation of innate immune responses. However, mice or cells lacking ZBP1 produce normal levels of type I IFN in response to dsDNA. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

4 Samples

Download data: CEL

(Submitter supplied) Keratinocyte-specific RIPK1 deficiency causes skin inflammation due to ZBP1-induced necroptosis. RNA-Seq analysis of the skin from wild type and RIK1E-KO mice was performed to examine how RIPK1 deficiency affects the expression of mRNAs as well as endogenous retroelement-derived transcripts.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL13112 GPL24247

25 Samples

Download data: CSV

(Submitter supplied) Caspase-8 and FADD play key roles in the regulation of cell death by necroptosis. The absence of either protein results in early embryonic lethality due to the activation of the kinase RIPK3 and its phosphorylation of the necroptosis executioner, MLKL. We genetically engineered and characterized a mouse model to monitor MLKL phosphorylation in the absence of necroptosis in vivo. Ablation of caspase-8 or FADD resulted in the transcriptional upregulation in several tissues of ZBP1, a cytosolic nucleic acid sensor capable of activating RIPK3, and ZBP1 was required for spontaneous phosphorylation of MLKL. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

12 Samples

Download data: TAB

(Submitter supplied) Here, we characterize RIPK3-dependent transcriptional responses in cortical neurons following infection with neurotropic flaviviruses. Neurons were infected with either Zika virus (ZIKV) strain MR766 at an MOI of 0.1, West Nile virus (WNV) strain TX 2002-HC at an MOI of 0.001, or a saline mock solution. Neurons were derived from mice lacking RIPK3 expression (Ripk3-/-) or wildtype controls. These studies revealed a number of antiviral genes whose upregulation following viral infection is absent in neurons lacking RIPK3, a subset of which were validated using qRT-PCR.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL7202

18 Samples

Download data: TXT

(Submitter supplied) We hypothesize that human RIPK3 deficiency does not result in impairment of type I IFN mediated antiviral immunity, contrasting with the situation in deficiencies of the TLR3-IFNAR1 circuit. To test the cellular responses to HSV1 at the wide transcriptome level, bulk RNA sequencing was performed with human primary fibroblasts without or with HSV-1 infection for 24 hours, in cells from healthy controls, RIPK3 HSE patient and other patients with recessive TLR3, IFNAR1 or NEMO deficiency.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24676

14 Samples

Download data: TXT

(Submitter supplied) We report that IFI16, which was previously identified as a cytosolic DNA sensor, is essential for the activation of programmed cell death pathways in IAV infected cells. We have identified IFI16 as an innate immune sensor of the influenza A virus. We find that IFI16 recognizes viral genomic RNA upon infection. The activation of IFI16, in turn, triggers the production of type I, III interferons, and also other pro-inflammatory cytokines via the STING-TBK1 and Pro-caspase-1 signalling axis, thereby promoting cell death (apoptosis and pyroptosis in IAV infected cells).

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

4 Samples

Download data: TXT