Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Natural killer cell proliferation requires canonical IRE1 function during viral infection (RNA-Seq)

ABSTRACT: Natural killer cell proliferation requires canonical IRE1 function during viral infection (RNA-Seq)

PROVIDER: PRJNA992481 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25204600_1.fastq.gz	Fastqsanger.gz
	SRR25204600_2.fastq.gz	Fastqsanger.gz
	SRR25204601_1.fastq.gz	Fastqsanger.gz
	SRR25204601_2.fastq.gz	Fastqsanger.gz
	SRR25204602_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 30

Similar Datasets

Natural killer cell proliferation requires canonical IRE1 function during viral infection

Project description:Natural killer cell proliferation requires canonical IRE1 function during viral infection

| PRJNA992477 | ENA

Natural killer cell proliferation requires canonical IRE1 function during viral infection (CITE-Seq)

Project description:Natural killer cell proliferation requires canonical IRE1 function during viral infection (CITE-Seq)

| PRJNA992482 | ENA

Natural killer cell proliferation requires canonical IRE1 function during viral infection (CITE-Seq)

Project description:The unfolded protein response (UPR) aims to restore ER homeostasis under conditions of high protein folding load, a function primarily serving secretory cells. Additional, non-canonical UPR functions have recently been unraveled in immune cells. We addressed the function of the inositol-requiring-enzyme 1 (IRE1) signaling branch of the UPR in NK cells in homeostasis and microbial challenge. Cell-intrinsic compound deficiency (DKO) of IRE1 and its downstream transcription factor XBP1 in NKp46 + NK cells, did not affect basal NK cell homeostasis, or overall outcome of viral MCMV infection. However, mixed bone marrow chimeras revealed a competitive advantage in the proliferation of IRE1 sufficient Ly49H + NK cells after viral infection. CITE-Seq analysis confirmed strong induction of IRE1 early upon infection, concomitant with the activation of a canonical UPR signature. Therefore, we conclude that cell-intrinsic IRE1/XBP1 activation is required for NK cell proliferation early upon viral infection, as part of a canonical UPR response.

2023-10-27 | GSE236820 | GEO

Natural killer cell proliferation requires canonical IRE1 function during viral infection (RNA-Seq)

2023-10-27 | GSE236819 | GEO

Natural killer cell proliferation requires canonical IRE1 function during viral infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-27 | GSE236822 | GEO

IRE1-dependent transcriptional change under a canonical endoplasmic-reticulum stressing stimulus and upon diauxic shift in Saccharomyces cerevisiae cells

Project description:Ire1 is an endoplasmic reticulum (ER)-located transmembrane protein that triggers the unfolded protein response. I recently noticed that Ire1 is activated not only in response to ER accumulation of unfolded proteins but also alongside diauxic shift in yeast Saccharomyces cerevisiae cells. I thus asked how different the Ire1-target genes upon two distinct scenes, a canonical ER -stressing stimuli and diauxic shift. Thus NGS transcriptome analysis was performed by using IRE1+ and ire1-delta mutant yeast cells under these conditions.

2019-03-01 | E-MTAB-6923 | biostudies-arrayexpress

The IRE1-XBP1 pathway promotes natural killer cell responses against viral infection and cancer by regulation of c-Myc

Project description:Natural killer (NK) cells are critical mediators of host immunity against infectious disease and cancer. The intrinsic regulators of NK cells are not fully understood. Here, we demonstrate that the ER stress sensor inositol-requiring enzyme 1 (IRE1α) and its substrate transcription factor X-box-binding protein 1 (XBP1) critically drive NK cell-mediated responses against viral infection and tumors. IRE1α and XBP1 were essential for the robust expansion of activated mouse and human NK cells. Transcriptome analysis revealed the transcription factor c-Myc as a novel and direct target of XBP1 for downstream regulation of NK cell proliferation. Genetic ablation or pharmaceutical blockade of IRE1α downregulated c-Myc, whereas overexpression of XBP1 resulted in c-Myc hyperactivation. NK cells lacking c-Myc demonstrated a functional deficit comparable to IRE1α or XBP1 deficiency. Overall, our study identifies a novel IRE1-XBP1-cMyc axis in NK cell immunity, providing new insight into the host immune response against infection and cancer.

2019-04-01 | GSE113214 | GEO

Novel Bioinformatics Method for Identification of Genome-Wide Non-Canonical Spliced Regions using RNA-Seq Data

Project description:We developed a bioinformatics approach called the Read-Split-Walk (RSW) pipeline, and evaluated it using two Ire1? heterozygous and two Ire1?-null samples. The 26nt non-canonical splice site in Xbp1 was detected as the top hit by our RSW pipeline in heterozygous samples but not in the negative control Ire1? knockout samples. We compared the Xbp1 results from our approach with results using the alignment program BWA, STAR, Exonerate and the Unix “grep” command. We then applied our RSW pipeline to RNA-Seq data from the SKBR3 human breast cancer cell line. RSW reported a large number of non-canonical spliced regions for 108 genes in chromosome 17, which were identified by an independent study. Identification of non-canonical spliced regions for mouse MEF samples (two Ire1? heterozygous and two Ire1?-null samples)

2014-07-29 | E-GEOD-54631 | biostudies-arrayexpress

Targeting canonical and non-canonical STAT3 signaling by WB737, a novel potent STAT3 inhibitor, in natural killer/T-cell lymphoma

Project description:Activating mutations of STAT3 were frequently found in patients with natural killer/T-cell lymphoma (NKTL), suggesting that targeted inhibition of STAT3 is a potential therapeutic option for NKTL patients. Here, we have developed a novel and potent STAT3 inhibitor WB737 that directly binds to the STAT3-SH2 domain with high affinity. WB737 selectively inhibits cell growth of NKTL harbored STAT3 mutations through inducing apoptosis and blocking colony formation. Mechanistically, WB737 inhibits both canonical and non-canonical STAT3 signaling via suppression of STAT3 phosphorylation at Tyr705 and Ser727 sites, respectively. Moreover, the activity of WB737 has a more potent inhibition on STAT3 compared to Sttatic, resulting in a significant anti-tumor effect followed by almost complete tumor regression in a NKTL xenograft model harboring STAT3 activating mutation. Collectively, these findings provide a preclinical proof-of-concept for WB737 as a novel therapeutic strategy for the treatment of NKTL patients with STAT3-activating mutations.

2023-06-21 | GSE202944 | GEO

Expression profiling of Natural killer B cells

Project description:Investigation of global gene expression levels between B cells, Natural killer cells and Natural killer B cells Gene expression profiling using sorted B cells, Natural killer cells and Natural killer B cells from WT mouse spleen. Total RNA extracted from WT cells were quantified by the NanoDrop ND-1000 and RNA integrity was assessed by standard denaturing agarose gel electrophoresis. The sample preparation and microarray hybridization were performed based on the NimbleGenâs standard protocols.

2016-05-17 | E-GEOD-80063 | biostudies-arrayexpress

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