Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNASeq of Drosophila intestinal progenitor cells upon Notch knockdown or microbiome alterations

ABSTRACT: RNASeq of Drosophila intestinal progenitor cells upon Notch knockdown or microbiome alterations

PROVIDER: PRJNA576370 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10244315_1.fastq.gz	Fastqsanger.gz
	SRR10244315_2.fastq.gz	Fastqsanger.gz
	SRR10244316_1.fastq.gz	Fastqsanger.gz
	SRR10244316_2.fastq.gz	Fastqsanger.gz
	SRR10244317_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 34

Similar Datasets

RNASeq of Drosophila intestinal progenitor cells upon Notch knockdown or microbiome alterations

Project description:We sequenced the transcriptome of the proliferative progenitor cells of the intestine to determine how the microbiome was affecting growth in wild-type intestines and those with Notch-deficient tumors

2019-10-09 | GSE138555 | GEO

Genome wide analysis of differential gene expression of PFKFB3 under- or overexpression upon inhibition or activation of notch signaling in endothelial cells

Project description:Analysis of gene expression profiles upon PFKFB3 under- or overexpression during inhibition or activation of notch signaling. With this experiment we aimed to identify whether alterations in PFKFB3 could influence the expression pattern of angiogenic genes in conditions that favor a tip- or stalk cell gene signature. Total RNA was collected of human umbilical vein endothelial cells either under- or overexpressing PFKFB3 and/ or have inhibited or activated notch signaling respectively. Cells were harvested 48h after manipulation of PFKFB3 and notch levels.

2013-08-01 | E-GEOD-45750 | biostudies-arrayexpress

Differential Notch target genes expression profile upon GSI washout.

Project description:The Notch signaling pathway regulates several processes including development and differentiation and its aberrant regulation leads to several diseases. Here, we analyzed the gene expression profile upon washout of the Notch inhibitor DAPT in mouse pre-T (Beko) cells.

2024-03-24 | GSE235982 | GEO

Differential Notch target genes expression profile upon GSI washout.

Project description:Differential Notch target genes expression profile upon GSI washout.

| PRJNA988121 | ENA

Differential Notch target genes expression profile upon HDAC3 loss-of-function.

Project description:The Notch signaling pathway regulates several differentiation and developmental processes in both pre- and post-natal life and its aberrant regulation leads to diseases, including cancer. Here, we investigated the role of histone deacetylase 3 (HDAC3) on the regulation of the Notch-dependent gene expression program in mouse pre-T (Beko) cells. We first defined Notch target genes as those genes that are downregulated upon inhibition of the Notch pathway using DAPT, a gamma-secretase inhibitor (GSI). Subsequently, we investigated the role of HDAC3 in the regulation of Notch target genes by shRNA- and pharmacologically (apicidin)-mediated loss-of-function of HDAC3.

2020-02-04 | GSE106361 | GEO

IER5 is a novel Notch target gene that contributes to the effects of Notch on breast cancer stem / progenitor cells

Project description:The Notch signalling pathway has been implicated in the development and progression of numerous malignancies, including breast cancer. In breast cancer, the transcriptional programs elicited by Notch activation and the target genes responsible for mediating the downstream effects of the pathway remain poorly understood. Here, we characterise the immediate cellular consequences of Notch activation in breast cancer cells and identify a panel of direct Notch targets with potential relevance in the disease. One key direct transcriptional target of Notch in this context is IER5. Functionally, IER5 activation in breast cancer contributes to the effects of Notch signalling on the self-renewal and proliferative potential of breast cancer stem and progenitor cells. High levels of IER5 mRNA may be an important biomarker indicative of Notch activation in the disease.

2018-01-08 | GSE30288 | GEO

Genome wide analysis of differential gene expression of PFKFB3 under- or overexpression upon inhibition or activation of notch signaling in endothelial cells

2013-08-01 | GSE45750 | GEO

Acinetobacter baumannii transcriptome-level alterations upon omega76 exposure

Project description:Acinetobacter baumannii transcriptome-level alterations upon omega76 exposure

| PRJNA477852 | ENA

Paneth cells acquire multi-potency upon Notch activation after irradiation

Project description:Paneth cells acquire multi-potency upon Notch activation after irradiation

| PRJNA451469 | ENA

Cancer-associated Notch receptor variants lead to O-fucosylation defects that can deregulate Notch signaling

Project description:NOTCH1 is a transmembrane receptor that initiates the Notch signaling pathway involved in embryonic development and maintenance of adult tissue homeostasis. The extracellular part of NOTCH1 is composed largely of EGF-like domains (EGFs) many of which can be O-fucosylated by protein O-fucosyltransferase 1 (POFUT1). O-fucosylation of NOTCH1 is necessary for its function. The Notch pathway is deregulated in many cancers, and alteration of POFUT1 has been reported in some cancers. Using the Biomuta and COSMIC databases, we selected 9 NOTCH1 variants that could cause a change in O-fucosylation of key EGFs. Cell-based N1 signaling assays, Notch ligand-binding assays and cell surface N1 analysis were used to determine the effect of each mutation on Notch activation. Then mass spectral glycoproteomic site mapping was used to identify alterations in the O-fucosylation of EGFs containing the selected mutation. One of the variants had few effects, two lead to a gain of function (GOF) and six to a loss of function (LOF). Most GOF and LOF could be associated with a change in O-fucosylation. Finally, by comparing our results with known NOTCH1 alterations in cancers from which our mutations originated, we were able to establish a correlation between our results and the known GOF or LOF of NOTCH1 in these cancers. This study shows that point mutations in NOTCH1 can lead to alterations in O-fucosylation that deregulate the Notch pathway and be associated with cancer processes.

2022-10-21 | PXD036345 | Pride

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