Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Breast cancer derived Evs cause liver fibrosis. [I]

ABSTRACT: Breast cancer derived Evs cause liver fibrosis. [I]

PROVIDER: PRJNA1093377 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28496017_1.fastq.gz	Fastqsanger.gz
	SRR28496017_2.fastq.gz	Fastqsanger.gz
	SRR28496018_1.fastq.gz	Fastqsanger.gz
	SRR28496018_2.fastq.gz	Fastqsanger.gz
	SRR28496019_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Inosine suppresses liver A-to-I RNA editing to promote cancer-associated cachexia in a riboswitch-like manner.

Project description:Cancer-associated cachexia (CAC) is a devastating syndrome and a major cause of morbidity and mortality in advanced cancer patients while liver is emerging as a key organ during CAC progression1. However, how tumor dysregulates liver function to promote CAC remains largely unknown. Here, we employ NMR spectrometry to detect that the elevation of 13C-inosine availability, attributed to the tumor-induced cytosolic 5'-nucleotidase II (NT5C2) protein accumulation, decreases the abundance of adenosine deaminase act on RNA 1 p150 isoform in a riboswitch-like manner. Intriguingly, reduced liver A-I mRNA editome enhances the stability of Cathepsin L mRNA to aggravate liver autophagy, triggering the secretion of serum amyloid A1, while CTSL-/- mice fail to develop cachectic phenotype upon inosine treatment. Strikingly, NT5C2 inhibitor CRCD2, a frontline leukemia treatment drug, greatly attenuates CAC progression. Conclusively, our finding reveals that inosine-mediated liver A-to-I mRNA editome alteration promotes CAC progression in a riboswitch-like manner, shedding light on the clinical applications for early CAC diagnosis and intervention.

2026-04-21 | GSE262917 | GEO

Inosine suppresses liver A-to-I RNA editing to promote cancer-associated cachexia in a riboswitch-like manner

2026-04-21 | GSE262782 | GEO

Inosine suppresses liver A-to-I RNA editing to promote cancer-associated cachexia in a riboswitch-like manner.

Project description:Inosine suppresses liver A-to-I RNA editing to promote cancer-associated cachexia in a riboswitch-like manner.

| PRJNA1094904 | ENA

DANCE-MaP probing of the adenine riboswitch

Project description:We show that DANCE-MaP permits measurement of state-specific per-nucleotide reactivities, direct secondary structure PAIRs, and tertiary RINGs for RNA structural ensembles. Here, we demonstrate DANCE-MaP on the V. vulnificus add riboswitch.

2022-03-23 | GSE182552 | GEO

Inosine monophosphate and inosine differentially regulate endotoxemia and bacterial sepsis

Project description:Inosine monophosphate and inosine differentially regulate endotoxemia and bacterial sepsis

| PRJNA762272 | ENA

Testicular adenosine to inosine RNA editing in the mouse

Project description:Adenosine to inosine (A-to-I) RNA editing occurs in a wide range of tissues and cell types and can be catalyzed by one of two adenosine deaminase acting on double stranded RNA enzymes, ADAR and ADARB1. Editing can impact both coding and non-coding regions of RNA, and in higher organisms, has been proposed to function in adaptive evolution. Neither the prevalence of A-to-I editing nor the role of either ADAR or ADARB1 has been examined in the context of germ cell development in mammals. Computational analysis of whole testis and cell type specific RNA-sequencing data followed by molecular confirmation demonstrated that A-to-I RNA editing occurs in both the germ line and in somatic Sertoli cells in two targets, Cog3 and Rpa1. Expression analysis demonstrated both Adar and Adarb1 were expressed in both Sertoli cells and in a cell-type dependent manner during germ cell development. Conditional ablation of Adar did not impact testicular RNA editing in either germ cells or Sertoli cells. Additionally, Adar ablation in either cell type did not have gross impacts on germ cell development or male fertility. In contrast, global Adarb1 knockout animals demonstrated a complete loss of A-to-I RNA editing in spite of normal germ cell development. Taken together, these observations demonstrate ADARB1 mediates A-to-I RNA editing in the testis and these editing events are dispensable for male fertility in an inbred mouse strain in the lab.

2016-12-24 | GSE92870 | GEO

A dual T-box riboswitch in Enterococcus faecium binds two tRNAs

Project description:A set of small RNAs was identified in Vancomycin-resistant Enterococcus faecium, a leading cause of MDR infections. We described here the function of srn_2050, acting as a T-box riboswitch to regulate expression of downstream genes encoding the HisRS and AspRS aminoacyl-tRNA synthetases. Comparative RNAseq between Aus0004 and isogenic srn_2050 mutant identified the genes whose expression is impacted by the RNA. srn_2050 structure in its ‘off state’ was deciphered by in-line probing, containing T-box consensus sequences, a pseudoknot, a specifier loop and a terminator. Transcription binding assays between the riboswitch and either tRNAAsp or tRNAHis indicate that each deacylated tRNA interacts with the T-box. Their anticodons bind to a GACAC sequence within the specifier loop (GAC and CAC are Asp and His codons, respectively), whereas tRNATyr (UA/C-U) does not. A pioneering evaluation of E. faecium amino acid auxotrophy, with emphasis on E. faecium strain Aus0004, revealed auxotrophy for Histidine but not for Aspartic acid. Based on comparative growths and RNAseq between Aus004 and Aus004-srn2050, the riboswitch is shown essential for growth under aspartate starvation. This is the first example of a functional riboswitch in E. faecium with two overlapping codons allowing a dual tRNA-dependent regulation at transcriptional level.

2020-11-16 | GSE161499 | GEO

Microbiota-derived Inosine Suppresses Systemic Autoimmunity via Restriction of B Cell Differentiation and Migration

Project description:The role of gut microbiota dysbiosis in systemic lupus erythematosus (SLE) pathogenesis remains elusive. Here, we show that fecal microbiota transplantation (FMT) from healthy mice to lupus mice ameliorated lupus-like symptoms. Microbiota reconstitution effectively reduced systemic class switch recombination and elevated IGH naïve isotype. Microbiota profiling revealed an enrichment of Lactobacillus johnsonii post-FMT, with a significant correlation to purine metabolites. Importantly, the Lactobacillus johnsonii-derived inosine, an intermediate metabolite in purine metabolism, effectively alleviated lupus-like symptoms by impeding B cell differentiation and reducing renal B cell infiltration. We further demonstrated that inosine reprograms B cells through the ERK-HIF-1α signaling pathway. Overall, our study highlights the discovery of a novel microbial metabolite modulating autoimmunity and suggests its potential for innovative microbiome-based therapeutic approaches.

2024-03-31 | GSE255441 | GEO

Leukemia inhibitory factor suppresses hepatic de novo lipogenesis and induces cachexia in mice

Project description:To investigate the role of LIF in cachexia, we performed gene expression profiling analysis using data obtained from RNA-seq of liver tissues from TgLC mice with Tamoxifen injection and TgL mice with Tamoxifen injection

2023-11-29 | GSE245198 | GEO

Inosine enhances mitochondria respiration to promote cancer survival under starvation

Project description:To investigate mechanism of inosine promotes the survival and metabolism of MDA-MB-231 cells under starvation conditions, MDA-MB-231 cells were treated with inosine and glucose for 12h under starvation conditions. We then performed gene expression profiling analysis using data obtained from RNA-seq of MDA-MB-231 cells under three different treatments（-G-Q,Inosine,Glucose）.

2023-07-17 | GSE225643 | 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