Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ecto-5’-Nucleotidase (Nt5e/CD73)-Mediated Adenosine Signaling Attenuates TGFβ-2 Induced Elastin and Cellular Contraction

ABSTRACT: Ecto-5’-Nucleotidase (Nt5e/CD73)-Mediated Adenosine Signaling Attenuates TGFβ-2 Induced Elastin and Cellular Contraction

PROVIDER: PRJNA895057 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22069800_1.fastq.gz	Fastqsanger.gz
	SRR22069800_2.fastq.gz	Fastqsanger.gz
	SRR22069801_1.fastq.gz	Fastqsanger.gz
	SRR22069801_2.fastq.gz	Fastqsanger.gz
	SRR22069802_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Novel microRNAs modulating ecto-5′-nucleotidase expression

Project description:Novel microRNAs modulating ecto-5′-nucleotidase expression

| PRJNA950915 | ENA

Novel microRNAs modulating ecto-5′-nucleotidase expression [MaMel]

Project description:Novel microRNAs modulating ecto-5′-nucleotidase expression [MaMel]

| PRJNA950919 | ENA

Ecto-5’-Nucleotidase (Nt5e/CD73)-Mediated Adenosine Signaling Attenuates TGFβ-2 Induced Elastin and Cellular Contraction

Project description:To investigate the broad transcriptional consequences of Nt5e knock-out on mice vascular smooth cells in culture at baseline.

2022-11-01 | GSE216727 | GEO

Novel microRNAs modulating ecto-5′-nucleotidase expression [SK-Mel-28]

Project description:Novel microRNAs modulating ecto-5′-nucleotidase expression [SK-Mel-28]

| PRJNA950920 | ENA

Novel microRNAs modulating ecto-5′-nucleotidase expression [MDA-MB-231]

Project description:Novel microRNAs modulating ecto-5′-nucleotidase expression [MDA-MB-231]

| PRJNA950921 | ENA

Ecto-5'-nucleotidase (CD73) inhibits nociception by hydrolyzing AMP to adenosine in nociceptive circuits.

Project description:Ecto-5'-nucleotidase (NT5E, CD73) is a membrane-anchored protein that hydrolyzes extracellular adenosine 5'-monophosphate (AMP) to adenosine in diverse tissues but has not been directly studied in nociceptive neurons. We found that NT5E was located on peptidergic and nonpeptidergic nociceptive neurons in dorsal root ganglia (DRG) and on axon terminals in lamina II (the substantia gelatinosa) of spinal cord. NT5E was also located on epidermal keratinocytes, cells of the dermis, and on nociceptive axon terminals in the epidermis. Following nerve injury, NT5E protein and AMP histochemical staining were coordinately reduced in lamina II. In addition, AMP hydrolytic activity was reduced in DRG neurons and spinal cord of Nt5e(-/-) mice. The antinociceptive effects of AMP, when combined with the adenosine kinase inhibitor 5-iodotubericidin, were reduced by approximately 50% in Nt5e(-/-) mice and were eliminated in Adenosine A(1) receptor (A(1)R, Adora1) knock-out mice. Additionally, Nt5e(-/-) mice displayed enhanced sensitivity in the tail immersion assay, in the complete Freund's adjuvant model of inflammatory pain and in the spared nerve injury model of neuropathic pain. Collectively, our data indicate that the ectonucleotidase NT5E regulates nociception by hydrolyzing AMP to adenosine in nociceptive circuits and represents a new molecular target for the treatment of chronic pain. Moreover, our data suggest NT5E is well localized to regulate nucleotide signaling between skin cells and sensory axons.

| S-EPMC2826808 | biostudies-literature

CD73+ memory CD4 T cells are a long-lived population with elevated effector function and prone to differentiate into TRM-like cells [RNA-seq]

Project description:The understanding of heterogeneity of human memory T cells will help to know the function, development and maintenance of memory population, then to improve the recall response or effective immunotherapy. Ecto-5’-nucleotidase CD73 expression in four subsets of memory T cells decreases with aging. The resistance to apoptosis and high expression of IL7R entitle CD73+ memory T cells to be long-lived population. We found antigen-specific memory T cells have overwhelming CD73 expression. The transcriptional and chromatin accessibility profiles indicate the elevated effector functions in CD73+ memory CD4 T cells comparing to CD73- counterparts. Homer analysis and Transcriptional factor (TF)-regulatory element-target gene triplet network clearly show the crucial role of RUNT and NR family TFs in CD73+ cells. Furthermore, CD73+ memory CD4 T cells were prone to differentiate into TRM-like cells under in-vitro sequential TCR and TGF/IL-15 signaling. The decreased percentage of CD73+ memory T cells with age leads to the less replenishment of TRM cells from peripheral blood.

2021-08-28 | GSE157163 | GEO

CD73+ memory CD4 T cells are a long-lived population with elevated effector function and prone to differentiate into TRM-like cells [ATAC-seq]

2021-08-28 | GSE157162 | GEO

Fluorescent Probes for Ecto-5'-nucleotidase (CD73).

Project description:Ecto-5'-nucleotidase (CD73) catalyzes the hydrolysis of AMP to anti-inflammatory, immunosuppressive adenosine. It is expressed on vascular endothelial, epithelial, and also numerous cancer cells where it strongly contributes to an immunosuppressive microenvironment. In the present study we designed and synthesized fluorescent-labeled CD73 inhibitors with low nanomolar affinity and high selectivity based on N 6 -benzyl-α,β-methylene-ADP (PSB-12379) as a lead structure. Fluorescein was attached to the benzyl residue via different linkers resulting in PSB-19416 (14b, K i 12.6 nM) and PSB-18332 (14a, K i 2.98 nM) as fluorescent high-affinity probes for CD73. These compounds are anticipated to become useful tools for biological studies, drug screening, and diagnostic applications.

| S-EPMC7667873 | biostudies-literature

CD73 Immune Checkpoint Defines Inducible Regulatory NK cells in the Tumor Microenvironment

Project description:High levels of ecto-5'-nucleotidase (CD73) have been implicated in immune suppression and tumor progression. Elevated levels of CD73 has also been observed in patients who progress on anti–PD-1 immunotherapy. While regulatory T cells can express CD73 and inhibit T cell responses via the production of adenosine, less is known if conventional T cells and natural killer (NK) cells can express CD73. We found that the expression of CD73 is restricted to tumor-infiltrating NK cells and the frequency of these cells correlate with larger tumor size in patients with breast cancer. In addition, the expression of other immune checkpoint receptors including LAG-3 and VISTA was significantly higher in CD73 positive NK cells than on CD73 negative NK cells. Furthermore, the prognostic value of CD73 gene expression was influenced by NK cell signature expressed in patients with breast cancer and sarcoma. Mechanistically, upon engagement of 4-1BBL on tumor cells, NK cells transport CD73 in intracellular vesicles to the cell surface and extracellular space via actin polymerization-dependent exocytosis. These CD73 positive NK cells undergo transcriptional reprogramming and upregulate IL10 production via STAT3 transcriptional activity and suppress CD4 T cell activity. Altogether, our results support that tumors can hijack NK cells as a means to escape immunity and that CD73 expression defines an inducible population of NK cells with immune regulatory properties within the tumor microenvironment.

2020-06-10 | GSE125119 | 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