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Changes in the chromatin accessibility landscape of mouse embryonic endocardial cells after Notch pathway manipulation

ABSTRACT: Changes in the chromatin accessibility landscape of mouse embryonic endocardial cells after Notch pathway manipulation

PROVIDER: PRJNA927979 | ENA |

REPOSITORIES: ENA

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Changes in the chromatin accessibility landscape of mouse embryonic endocardial cells after Notch pathway manipulation

Project description:Analysis by ATAC-seq of the changes in chromatin accessibility in MEEC due to the activity of Notch ligands.

2023-12-08 | GSE223733 | GEO

Changes in gene expression in mouse embryonic endocardial cells after Notch pathway manipulation

Project description:Changes in gene expression in mouse embryonic endocardial cells after Notch pathway manipulation

| PRJNA928078 | ENA

Transcriptional regulation in the embryonic endocardium after NOTCH pathway manipulation

Project description:We have manipulated the NOTCH signaling pathway in mouse embryonic endocardial cells by the co-culture with OP9 stromal cells expressing Jag1 and Dll4, the culture over recombinant JAG1 and DLL4, and the use of the γ-secretase inhibitor RO4929097. We have performed RNA-seq and ATAC-seq to define the transcriptional profile and the chromatin accessibility landscape specific for each condition.

2023-12-08 | GSE223735 | GEO

Changes in gene expression in mouse embryonic endocardial cells after Notch pathway manipulation

Project description:Analysis by RNA-seq of the changes in gene expression in MEEC due to the activity of Notch ligands.

2023-12-08 | GSE223734 | GEO

Transcriptional regulation in the embryonic endocardium after NOTCH pathway manipulation

Project description:Transcriptional regulation in the embryonic endocardium after NOTCH pathway manipulation

| PRJNA927818 | ENA

Endocardial Notch Signaling Promotes Cardiomyocyte Proliferation in the Regenerating Zebrafish Heart through Wnt Pathway Antagonism

Project description:Endocardial Notch Signaling Promotes Cardiomyocyte Proliferation in the Regenerating Zebrafish Heart through Wnt Pathway Antagonism

| PRJNA419372 | ENA

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

Endocardial Notch Signaling Promotes Cardiomyocyte Proliferation in the Regenerating Zebrafish Heart through Wnt Pathway Antagonism

Project description:The goal of this study is to understand the molecular mechanisms underlying this Notch-induced muscle cell proliferation defect, we sequenced the transcriptome of control ventricles and Notch-suppressed ventricle at 5 days post-injury, when cardiomyocyte proliferation is normally robust.

2019-01-01 | GSE107228 | GEO

Reduced chromatin accessibility correlates with resistance to Notch activation

Project description:The Notch signalling pathway is a master regulator of cell fate transitions in development and disease. In the brain, Notch promotes neural stem cell (NSC) proliferation, regulates neuronal migration and maturation and can act as an oncogene or tumour suppressor. How NOTCH and its transcription factor RBPJ activate distinct gene regulatory networks in closely related cell types in vivo remains to be determined. Here we use Targeted DamID (TaDa), requiring only thousands of cells, to identify NOTCH and RBPJ binding in NSCs and their progeny in the mouse embryonic cerebral cortex in vivo. We find that NOTCH and RBPJ associate with a broad network of NSC genes. Repression of NSC-specific Notch target genes in intermediate progenitors and neurons correlates with decreased chromatin accessibility, suggesting that chromatin compaction may contribute to restricting NOTCH-mediated transactivation.

2022-01-07 | GSE152207 | GEO

Mutations in the NOTCH pathway regulator MIB1 cause left ventricular noncompaction cardiomyopathy

Project description:Left ventricular noncompaction (LVNC) Causes prominent ventricular trabeculations and reduces cardiac systolic function. The clinical presentation of LVNC ranges from asymptomatic to heart failure. We show that germline mutations in human MIB1 (mindbomb homolog 1), which encodes an E3 ubiquitin ligase that promotes endocytosis of the NOTCH ligands DELTA and JAGGED, cause LVNC in autosomal-dominant pedigrees, with affected individuals showing reduced NOTCH1 activity and reduced expression of target genes. Functional studies in cells and zebrafish embryos and in silico modeling indicate that MIB1 functions as a dimer, which is disrupted by the human mutations. Targeted inactivation of Mib1 in mouse myocardium causes LVNC, a phenotype mimicked by inactivation of myocardial Jagged1 or endocardial Notch1. Myocardial Mib1 mutants show reduced ventricular Notch1 activity, expansion of compact myocardium to proliferative, immature trabeculae and abnormal expression of cardiac development and disease genes. These results implicate NOTCH signaling in LVNC and indicate that MIB1 mutations arrest chamber myocardium development, preventing trabecular maturation and compaction. RNA was isolated from the ventricles of 16 WT and 16 Mib1flox; CTnT-cre hearts at E14.5 and then pooled into four replicates.

2015-08-10 | E-GEOD-71912 | biostudies-arrayexpress

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