Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Before and after fecal microbiota transplantation in ulcerative colitis patients

PROVIDER: PRJNA647221 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12326900_1.fastq.gz	Fastqsanger.gz
	SRR12326900_2.fastq.gz	Fastqsanger.gz
	SRR12326901_1.fastq.gz	Fastqsanger.gz
	SRR12326901_2.fastq.gz	Fastqsanger.gz
	SRR12326902_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 136

Similar Datasets

Project description:Fecal Microbiota Transplantation for Ulcerative Colitis

| PRJNA388210 | ENA

Fecal Microbiota Transplantation for Ulcerative Colitis.

Project description:Fecal Microbiota Transplantation for Ulcerative Colitis.

| PRJEB46777 | ENA

human gut metagenome

Project description:Microbiome sequencing of ulcerative colitis patients receiving fecal microbiota transplantation

| PRJNA737472 | ENA

human gut metagenome

Project description:Fecal microbiota transplantation (FMT) for ulcerative colitis

| PRJNA285502 | ENA

Impact of fecal microbiota transplantation (FMT) in 3 days-ABX-treated recipient mice using feces from 6 NSCLC patients at diagnosis.

Project description:This study aimed to analyze changes in gut microbiota composition in mice after transplantation of fecal microbiota (FMT, N = 6) from the feces of NSCLC patients by analyzing fecal content using 16S rRNA sequencing, 10 days after transplantation. Specific-pathogen-free (SPF) mice were used for each experiments (N=4) as controls.

2023-07-01 | E-MTAB-12812 | biostudies-arrayexpress

OTUD3 prevents ulcerative colitis by modulating microbiota-mediated STING activation (part 5)

Project description:Ulcerative colitis (UC) develops through a complicated interaction between the host and microbiota. Intestinal fibroblasts are suggested to play crucial roles in the pathogenesis of UC. However, the influences of the host-microbiota interaction on the pathophysiology of intestinal fibroblasts remain poorly understood. Here, we reveal that OTUD3 suppresses pathologic activation of fibroblasts exposed to microbial cyclic GMP-AMP (3’3’-cGAMP) by deubiquitinating stimulator of interferon genes (STING) in the colon. Sting deficiency ameliorated dextran sodium sulfate-induced colitis in Otud3-/- mice. In addition, mice harboring an UC risk missense variant in the Otud3 gene showed pathological features of UC in the colon after transplantation of a fecal microbiome with the potential to produce excessive cGAMP from UC patients. Collectively, these results demonstrate the critical role of OTUD3 in the maintenance of intestinal homeostasis and highlight one mechanism of the interaction between the host (OTUD3 in fibroblasts) and microbiota (STING agonist) in UC development.

2025-05-12 | GSE244080 | GEO

OTUD3 prevents ulcerative colitis by modulating microbiota-mediated STING activation (part 4)

2025-05-12 | GSE244079 | GEO

OTUD3 prevents ulcerative colitis by modulating microbiota-mediated STING activation (part 1)

2025-05-12 | GSE244076 | GEO

OTUD3 prevents ulcerative colitis by modulating microbiota-mediated STING activation (part 2)

2025-05-12 | GSE244077 | GEO

OTUD3 prevents ulcerative colitis by modulating microbiota-mediated STING activation (part 3)

2025-05-12 | GSE244078 | GEO