Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of mouse fetal intestines comparing wildtype littermates with Notch inhibited mutants

ABSTRACT: RNA-seq of mouse fetal intestines comparing wildtype littermates with Notch inhibited mutants

PROVIDER: PRJEB91344 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq experiment of developing mouse forelimbs, comparing Bcl9/9l mutant with control littermates.

Project description:RNA-seq experiment of developing mouse forelimbs, comparing Bcl9/9l mutant with control littermates.

| PRJEB38051 | ENA

Liver transcriptome analysis comparing gene expression between Esr1 knockout mice and wild type littermates

Project description:Liver transcriptome analysis comparing gene expression between Esr1 knockout mice and wild type littermates

| PRJNA730496 | ENA

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

Notch

Project description:Notch

| PRJNA988118 | 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

Transcription profiling of mouse small intestines

Project description:Rb and E2F are thought to play antagonistic roles in celll proliferation. However, this model is based mostly from in vitro cell culture systems. We used small intestines to test this model in vivo. We found that deletion of E2f1-3 in the small intestine of mice suppressed the ectopic expression of E2F targets and cell proliferation caused by Rb-deficiency. Surprisingly, E2f1-3 deletion failed to arrest the proliferation of intestinal cells containing an intact Rb gene, and instead led to E2F target derepression and apoptosis. Experiment Overall Design: Total RNA of crypts and villi from wild-type, Rb-/-, E2f1-/-, E2f2-/-, E2f3-/-, E2f1-/-, E2f2-/-, and E2f3-/- small intestines. Small intestines were harvested 7 days after mice were injected intraperitoneally with beta-napthoflavone.

2010-01-19 | E-GEOD-16454 | biostudies-arrayexpress

Collier1996 - Delta Notch intercellular signalling and lateral inhibition

Project description:ODE model describing how slight variations in Notch and Delta cellular concentrations, through lateral inhibition, lead to cells with different states of differentiation. Lateral inhibition is a process whereby a given cell adopting a given fate prevents its immediate neighbouring cells from doing likewise. Notch and Delta are interacting transmembrane proteins and according to this model, lateral inhibition is due to a process where the inhibited cells (where notch has been activated by Delta) loose their ability to inhibit other cells (by synthesizing Delta). This process creates a feedback loop where cells with more delta proteins on their surface inhibit their immediate neighbours and adopt a different cell fate than those neighbours.

2024-09-02 | BIOMD0000001047 | BioModels

Vismodegib and Gamma-Secretase/Notch Signalling Pathway Inhibitor RO4929097 in Treating Patients With Advanced or Metastatic Sarcoma

Project description:This randomized phase I/II clinical trial is studying the side effects and best dose of gamma-secretase/notch signalling pathway inhibitor RO4929097 when given together with vismodegib and to see how well they work in treating patients with advanced or metastatic sarcoma. Vismodegib may slow the growth of tumor cells. Gamma-secretase/notch signalling pathway inhibitor RO4929097 may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Giving vismodegib together with gamma-secretase/notch signalling pathway inhibitor RO4929097 may be an effective treatment for sarcoma.

| 2091475 | ecrin-mdr-crc

Transcriptomics analysis of C. elegans intestines

Project description:To identify new heme responsive genes, we performed transcriptomics analysis on the intestines isolated from worms that were cultured at different concentrations of heme. Results of SMART-seq and gene expression profiling showed that 578 genes were differentially expressed at different heme concentrations.

2022-08-07 | GSE198848 | GEO

Transcriptomics analysis of C. elegans intestines

Project description:Transcriptomics analysis of C. elegans intestines

| PRJNA817173 | ENA