Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Prolonged STAT1 activation in neurons drives a pathological transcriptional response

ABSTRACT: Prolonged STAT1 activation in neurons drives a pathological transcriptional response

PROVIDER: PRJNA971582 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24511805_1.fastq.gz	Fastqsanger.gz
	SRR24511805_2.fastq.gz	Fastqsanger.gz
	SRR24511806_1.fastq.gz	Fastqsanger.gz
	SRR24511806_2.fastq.gz	Fastqsanger.gz
	SRR24511807_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 120

Similar Datasets

Prolonged STAT1 activation in neurons drives a pathological transcriptional response

Project description:To investigate the effects of pathological IFN-γ stimulation on neurons in the context of subsequent activation, we established cell cultures of primary mouse neurons receiving pathological priming or no priming. We then performed RNA-Seq on these cells after vehicle, physiological, and pathological IFN-γ restimulation.

2023-08-22 | GSE232304 | GEO

Prolonged STAT1 activation in neurons drives a pathological transcriptional response.

Project description:Neurons require physiological IFN-γ signaling to maintain central nervous system (CNS) homeostasis, however, pathological IFN-γ signaling can cause CNS pathologies. The downstream signaling mechanisms that cause these drastically different outcomes in neurons has not been well studied. We hypothesized that different levels of IFN-γ signaling in neurons results in differential activation of its downstream transcription factor, signal transducer and activator of transduction 1 (STAT1), causing varying outcomes. Using primary cortical neurons, we showed that physiological IFN-γ elicited brief and transient STAT1 activation, whereas pathological IFN-γ induced prolonged STAT1 activation, which primed the pathway to be more responsive to a subsequent IFN-γ challenge. This is an IFN-γ specific response, as other IFNs and cytokines did not elicit such STAT1 activation nor priming in neurons. Additionally, we did not see the same effect in microglia or astrocytes, suggesting this non-canonical IFN-γ/STAT1 signaling is unique to neurons. Prolonged STAT1 activation was facilitated by continuous janus kinase (JAK) activity, even in the absence of IFN-γ. Finally, although IFN-γ initially induced a canonical IFN-γ transcriptional response in neurons, pathological levels of IFN-γ caused long-term changes in synaptic pathway transcripts. Overall, these findings suggest that IFN-γ signaling occurs via non-canonical mechanisms in neurons, and differential STAT1 activation may explain how neurons have both homeostatic and pathological responses to IFN-γ signaling.

| S-EPMC10527980 | biostudies-literature

Prolonged Crowding Drives Cancer Cell Invasiveness

Project description:Our study found that prolonged crowding drives cancer cell invasiveness with memory retention. To further characterize gene expression regulated by prolonged crowding, RNA sequencing was performed in crowding-primed cells (20 days) followed by sparse culture for different times (0, 1, 3, or 10 days).

2024-12-01 | GSE281770 | GEO

STAT1 independent control of a neurotropic measles virus challenge in primary neurons and infected mice

Project description:The objective of this study was to compare the ability of mice that lack STAT1 to resolve a neurotropic viral challenge, and to assess the ability of neurons obtained from these mice to be effectively cleared of virus by interferon gamma For the array, primary neurons were isolated from embryonic mice, grown as pure cultures, exposed to recombinant interferon gamma for 3, 6 or 24 hours and harvested for microarray analysis to identify and compare the gene profiles between wild type and STAT1 knockout neurons.

2012-03-14 | E-GEOD-33057 | biostudies-arrayexpress

Genes induced by IFN-beta, IFN-gamma or unphosphoraylted STAT1 in human fibroblasts

Project description:A single high dose of IFN? activates powerful cellular responses in which many antiviral, pro-apoptotic, and anti-proliferative proteins are highly expressed. Since some of these proteins are deleterious, cells down-regulate this initial response rapidly. However, the expression of many antiviral proteins that do no harm is sustained, prolonging a substantial part of the initial antiviral response for days and also providing resistance to DNA damage. While the transcription factor ISGF3 (IRF9 and tyrosine-phosphorylated STATs 1 and 2) drives the first rapid response phase, the related factor un-phosphorylated ISGF3 (U-ISGF3), formed by IFN?-induced high levels of IRF9 and STATs 1 and 2 without tyrosine phosphorylation, drives the second prolonged response. The U-ISGF3-induced antiviral genes that show prolonged expression are driven by distinct interferon stimulated response elements (ISREs). Continuous exposure of cells to a low level of IFN?, often seen in cancers, leads to steady-state increased expression of only the U-ISGF3-dependent proteins, with no sustained increase of other IFN?-induced proteins, and to constitutive resistance to DNA damage. We classified genes into U-ISGF3-induced genes and classical ISGF3-induced genes using microarray data. We identified 150 genes that are up-regulated by IFN? after 6 h. Among these IFN?-induced genes, only 29 (20%) were induced by the up-regulation of Y701F-STAT1, indicating that these are induced by U-ISGF3. Among the remaining 121 IFN?-induced genes (150 minus 29), 73 are induced by IFN? as well as IFN?, and 48 are induced only by IFN?. Total 5 RNA samples were analyzed in duplicate on microarray chips. Untreated cells and empty vector-transfected cells were the control of IFN treated cells and Y701F-STAT1-transfected cells, respectively.

2013-09-18 | E-GEOD-50954 | biostudies-arrayexpress

STAT1 independent control of a neurotropic measles virus challenge in primary neurons and infected mice

2012-03-14 | GSE33057 | GEO

Pathological effects of SARS-CoV-2 on hESC-derived peripheral neurons

Project description:Pathological effects of SARS-CoV-2 on hESC-derived peripheral neurons

| PRJNA676120 | ENA

Glycogen Metabolism Drives Sensory Activation of Pomc Neurons

Project description:Glycogen Metabolism Drives Sensory Activation of Pomc Neurons

| PRJNA930442 | ENA

Estrogen Drives Melanocortin Neurons To Reduce Sedentary Behavior

Project description:Estrogen Drives Melanocortin Neurons To Reduce Sedentary Behavior

| PRJNA593491 | ENA