Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans

ABSTRACT: The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans

PROVIDER: PRJNA607243 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11100814_1.fastq.gz	Fastqsanger.gz
	SRR11100814_2.fastq.gz	Fastqsanger.gz
	SRR11100815_1.fastq.gz	Fastqsanger.gz
	SRR11100815_2.fastq.gz	Fastqsanger.gz
	SRR11100816_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 92

Similar Datasets

The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans (LPS dataset)

Project description:The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans (LPS dataset)

| PRJNA607247 | ENA

The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans (IAV and HSV dataset)

Project description:The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans (IAV and HSV dataset)

| PRJNA607248 | ENA

The long non-coding RNA LUCAT1 is a negative feedback regulator of interferon responses in humans.

Project description:Long non-coding RNAs are important regulators of biological processes including immune responses. The immunoregulatory functions of lncRNAs have been revealed primarily in murine models with limited understanding of lncRNAs in human immune responses. Here, we identify lncRNA LUCAT1 which is upregulated in human myeloid cells stimulated with lipopolysaccharide and other innate immune stimuli. Targeted deletion of LUCAT1 in myeloid cells increases expression of type I interferon stimulated genes in response to LPS. By contrast, increased LUCAT1 expression results in a reduction of the inducible ISG response. In activated cells, LUCAT1 is enriched in the nucleus where it associates with chromatin. Further, LUCAT1 limits transcription of interferon stimulated genes by interacting with STAT1 in the nucleus. Together, our study highlights the role of the lncRNA LUCAT1 as a post-induction feedback regulator which functions to restrain the immune response in human cells.

| S-EPMC7733444 | biostudies-literature

The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans (LPS dataset)

Project description:Long non-coding RNAs (lncRNAs) are important regulators of biological processes including immune responses. In the immune system, the immunoregulatory functions of lncRNAs have been revealed in murine studies with limited understanding of lncRNAs and the immune response in humans. Here, we identified lncRNA LUCAT1 as amongst the most dynamically regulated non-coding transcripts in human myeloid cells stimulated with lipopolysaccharide (LPS) and other activators of the innate immune response.

2020-02-19 | GSE145450 | GEO

The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans (IAV and HSV dataset)

2020-02-19 | GSE145449 | GEO

The long non-coding RNA LUCAT1 is a negative feedback regulator of the Interferon Response in humans

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

2020-02-19 | GSE145451 | GEO

The Cul5 E3 Ligase Complex Is a Key Negative Feedback Regulator of TCR/IL2 Signaling and Anti-Tumor Activity in CD8+ T Cells

Project description:To help advancing cancer immunotherapies, we developed a step-wise CRISPR knockout (KO) screening strategy under the selection of TGF-beta, and identified Cul5 as a core negative-feedback regulator of CD8+ T cell differentiation and persistence.

2023-09-01 | GSE213921 | GEO

A Negative Feedback Loop Between TET2 and Leptin in Adipocyte Regulates Body Weight

Project description:Ten-eleven translocation (TET) 2 is an enzyme that catalyzes DNA demethylation to regulate gene expression by oxidizing 5-methylcytosine to 5-hydroxymethylcytosine, functioning as an essential epigenetic regulator in various biological processes. However, the regulation and function of TET2 in adipocytes during obesity are poorly understood. In this study, we demonstrate that leptin, a key adipokine in mammalian energy homeostasis regulation, suppresses adipocyte TET2 levels via JAK2-STAT3 signaling. Adipocyte Tet2 deficiency protects against high-fat diet-induced weight gain by reducing leptin levels and further improving leptin sensitivity. By interacting with C/EBPα, adipocyte TET2 increases the hydroxymethylcytosine levels of the leptin gene promoter, thereby promoting leptin gene expression. A decrease in adipose TET2 is associated with obesity-related hyperleptinemia in humans. Inhibition of TET2 suppresses the production of leptin in mature human adipocytes.Our findings support the existence of a negative feedback loop between TET2 and leptin in adipocytes and reveal a novel compensatory mechanism for the body to counteract the metabolic dysfunction caused by obesity.

2024-02-29 | GSE252186 | GEO

Negative feedback of IFN-I signaling through IFN-competent RIG-I-like receptor-induced HSPA6

Project description:The RIG-I-like receptors (RLRs) form filaments to activate type-I interferon (IFN-I) and NF-KB signaling through their adaptor protein MAVS and downstream cascades. These filaments are recognized and regulated by cell-encoded machinery for correct activation. Here, we identified the stress-sensitive heat shock protein, HSPA6, was induced to express upon RLR-MAVS activation to act as a negative regulator of IFN-I signaling. Interestingly, by using MAVS-KO cells, we showed that HSPA6 was upregulated dependent on the presence of IFN-competent RLRs but not MAVS. Gene knockout (KO) tests indicated that the E3 ligases, stress granules (SGs), and transcription factors IRF1 and AP1 were all shared to induce HSPA6 and the canonical IFNb. Kinetic analysis showed that HSPA6 upregulated slower than IFNb, implicating these two genes competed machinery for transcription activation. Further tests suggested the induced HSPA6 bound to IFN-competent MDA5 to dissolve the filaments and downregulated IFN induction. Thus, our study uncovered a new gene activation mechanism by the IFN-competent RLRs to serve as negative feedback, arguing for a gene regulatory role of functional filaments of innate immunity.

2024-01-01 | GSE252140 | GEO

PLC-γ1 Can Regulate T-Cell Activation by Positive and Negative Feedback via Lck

Project description:Phospholipase C gamma 1 (PLC-γ1) occupies a critically important position in the T cell signaling pathway. While its functions as a regulator of both Ca2+ signaling and PKC-family kinases are well characterized, PLC-γ1’s role in the regulation of early T cell receptor signaling events is incomplete. Activation of the T cell receptor leads to the formation of a signalosome complex between SLP-76, LAT, PLC-γ1, Itk, and Vav1. Recent studies have revealed the existence of both positive and negative feedback pathways from components of the signalosome complex to the apical kinase in the pathway, Lck. To determine the role, if any, of PLC-γ1 in these feedback networks, we performed a quantitative phosphoproteomic analysis of the PLC-γ1-deficient T cells. These data revealed a previously unappreciated role for PLC-γ1 in the positive regulation of Zap-70 and T cell receptor tyrosine phosphorylation. Conversely, PLC-γ1 negatively regulated the phosphorylation of signalosome associated proteins including previously established Lck substrate phosphorylation sites within this complex. While the positive and negative regulatory phosphorylation sites on Lck were largely unchanged, Tyr192 phosphorylation was elevated in Jgamma1. The data supports a model wherein Lck’s targeting, but not its kinase activity is altered by PLC-γ1, possibly through Lck Tyr192 phosphorylation.

2017-06-28 | PXD005165 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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