Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: RNA-Seq shows that HAVCR1 knockdown does not affect JEG3 interferon signaling response

PROVIDER: PRJNA1122927 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29406609_1.fastq.gz	Fastqsanger.gz
	SRR29406609_2.fastq.gz	Fastqsanger.gz
	SRR29406610_1.fastq.gz	Fastqsanger.gz
	SRR29406610_2.fastq.gz	Fastqsanger.gz
	SRR29406611_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

RNA-Seq shows that HAVCR1 knockdown does not affect JEG3 interferon signaling response

Project description:To investigate whether HAVCR1 knockout (KO) affects the response of the interferon signaling pathway in JEG3 cells, RNA-Seq was performed on HAVCR1 KO and control JEG3 cells under both basal conditions and stimulation with double-stranded RNA mimic poly I:C. The results indicated that HAVCR1 knockdown does not affect the interferon signaling pathway response in JEG3 cells. Both groups exhibited comparable activation of the interferon signaling pathway.

2025-03-26 | GSE272065 | GEO

KAT2A and KAT2B prevents double-stranded RNA formation and interferon signaling to maintain intestinal stem cell renewal

Project description:Histone acetyltransferases KAT2A and KAT2B are paralogs highly expressed in the intestinal epithelium, but their functions are not well understood. In this study, double knockout of murine Kat2 genes in the intestinal epithelium was lethal, resulting in diminished H3K9ac expression, loss of stem cells, and robust activation of interferon signaling. Use of pharmacological agents and sterile organoid cultures indicated a cell-intrinsic double-stranded RNA trigger for interferon signaling. Acetyl-proteomics and dsRIP-seq were employed to interrogate the mechanism behind this response, which identified self-derived, mitochondria- encoded double-stranded RNA as the source of intrinsic interferon signaling. KAT2A and KAT2B therefore play an essential role in regulating mitochondrial functions as well as maintaining intestinal health.

2023-07-07 | MSV000092370 | MassIVE

RNA-seq quantification in EPS15 knockdown and scramble-oligo controls in JEG3 cells

Project description:RNA-seq quantification in EPS15 knockdown and scramble-oligo controls in JEG3 cells

| PRJNA767603 | ENA

Homo sapiens

Project description:JEG3 vs BeWo

| PRJNA92683 | ENA

Homo sapiens

Project description:Affect of Interferon Gamma on Chordoma Cells

| PRJNA311327 | ENA

Expression data from primary human keratinocytes upon control or HERC6 knockdown using siRNA and stimulated in vitro with or without cGAMP or Poly(I:C)

Project description:HERC6 is an Interferon stimulated gene and expressed by epidermal keratinocytes, yet its specific role in the skin remains unclear. In this investigation, we employed bulk RNA-sequencing to explore the broader impact of HERC6 in response to sensing of cytosolic DNA mimic, cGAMP or RNA agonist, TLR3. We observed an elevated number of differentially expressed genes in keratinocytes following HERC6 knockdown, and among them, several were associated with the Interferon signaling pathway, such as OAS1, IFIT3, and STAT2, showing increased expression in HERC6 knockdown keratinocytes when stimulated with cGAMP. Additionally, our findings revealed a dysregulation in the HIPPO pathway-related genes, particularly LATS1/2, in HERC6 knockdown keratinocytes. Utilizing bulk RNA-sequencing, we identified enriched Gene Ontology terms associated with the Interferon pathway and cytosolic sensing of foreign DNA in HERC6 knockdown keratinocytes, suggesting HERC6 as a negative regulator of Interferon signaling upon DNA sensing but not RNA. This data was instrumental in elucidating the regulatory functions of HERC6 in keratinocytes during the sensing of exogenous DNA or RNA mimics.

2024-02-14 | GSE253221 | GEO

8c04ed0b-6517-42ab-b510-7a64e9f57129 - samples

Project description:We analyzed baseline and on-therapy tumor biopsies from 101 patients with advanced melanoma treated with nivolumab (anti-PD-1) alone or combined with ipilimumab (anti-CTLA-4). Analysis of whole transcriptome data showed that T cell infiltration and interferon-gamma signaling signatures corresponded most highly with clinical response to therapy, with a reciprocal decrease in cell cycle and WNT signaling pathways in responding biopsies. Clinical outcome differences were likely not due to differential melanoma cell responses to interferon-gamma, as 57 human melanoma cell lines exposed in vitro to this cytokine showed a conserved interferon-gamma transcriptome response unless they had mutations that precluded signaling from the interferon-gamma receptor. Therefore, the magnitude of the antitumor T cell response and the corresponding downstream interferon-gamma signaling are the main drivers of clinical response or resistance to immune checkpoint blockade therapy.

| EGAD00001006284 | EGA

a101f3f6-6af8-4428-9d7f-94d57551d3e3 - samples

| EGAD00001006282 | EGA

Conserved interferon-gamma signaling and decreased immune exclusion programs in responses to immune checkpoint blockade therapy

| EGAS00001004545 | EGA

YTHDF1 suppresses innate immune responses by promoting induction of A-to-I RNA editing

Project description:In this study, we show that the m6A modification promotes translation of the ADAR1 transcript, which encodes an A-to-I RNA editing enzyme, in response to interferon stimulation. We reveal that this translation upregulation is mediated by the YTHDF1-dependent pathway; YTHDF1 is a reader protein that can preferentially bind m6A-modified transcripts and promote translation. Knockdown of YTHDF1 reduces the overall levels of interferon-induced A-to-I RNA editing, which consequently activates dsRNA-sensing pathway and increased expression of various interferon-stimulated genes. These RNA-seq experiments investigate the effect of YTHDF1 knockdown on the interferon-treated A172 cell transcriptome.

2021-05-14 | GSE148542 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data