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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE223734 | GEO | 2023/12/08

REPOSITORIES: GEO

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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

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

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

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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

Transcriptional regulation in the embryonic endocardium after NOTCH pathway manipulation

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

| PRJNA927818 | 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.

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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

NOTCH signaling pathway is required for bovine early embryonic development

Project description:The NOTCH signaling pathway plays an important role in regulating various biological processes, including cell proliferation, lineage specification and apoptosis. Multiple components of the NOTCH pathway have been identified in mammalian preimplantation embryos. However, the precise role of NOTCH pathway in early embryonic development is poorly understood, especially in domestic animals. Here, we show that key transcripts of the NOTCH pathway exhibit a dynamic pattern throughout early embryonic development with an abundant level before embryonic genome activation in cattle. We also confirmed the presence of active NOTCH1 and RBPJ. By using pharmacological and RNAi tools, we demonstrated that the NOTCH pathway is required for the proper development of bovine early embryos. This functional consequence could be partly attributed to the major transcriptional mediator-RBPJ, whose deficiency also compromised the embryo quality. Indeed, we observed a significant increase of histone H3 serine 10 phosphorylation (pH3S10, a mitosis marker) positive blastomeres in not only NOTCH1 depleted embryos but RBPJ depleted ones. Importantly, RNA-seq analysis revealed that either NOTCH1 or RBPJ depletion triggers a reduction in H1FOO that encodes the oocyte-specific linker histone H1 variant. Interestingly, depleting H1FOO also results in detrimental effects on the developmental competence of early embryos, similar with NOTCH1 inhibition. Overall, our results reveal a crucial role for NOTCH pathway in regulating bovine preimplantation development, likely by controlling cell proliferation and maintaining H1FOO expression.

2021-01-31 | GSE158679 | GEO

Effect of depletion of Notch signaling genes in C2C12 cells on the activation of Notch pathway activity in response to stimulation by plated ligand

Project description:To obtain a Notch-depleted base cell line into which we could integrate specific ligands or receptors for quantitative analysis of Notch signaling interactions, we conducted 2 rounds of transfection with RNPs (ribonucleoproteins) consisting of gRNAs targeting Notch2 and Jagged1 complexed with Cas9 protein. After antibiotic selection and screening of monoclonal colonies, we obtained the C2C12-Nkd clone, which showed loss of Notch2 protein and Jag1 transcript.

2023-06-02 | GSE233573 | GEO

Notch pathway mutants do not equivalently perturb mouse embryonic retinal development.

Project description:In the vertebrate eye, Notch ligands, receptors, and ternary complex components determine the destiny of retinal progenitor cells in part by regulating Hes effector gene activity. There are multiple paralogues for nearly every node in this pathway, which results in numerous instances of redundancy and compensation during development. To dissect such complexity at the earliest stages of eye development, we used seven germline or conditional mutant mice and two spatiotemporally distinct Cre drivers. We perturbed the Notch ternary complex and multiple Hes genes to understand if Notch regulates optic stalk/nerve head development; and to test intracellular pathway components for their Notch-dependent versus -independent roles during retinal ganglion cell and cone photoreceptor competence and fate acquisition. We confirmed that disrupting Notch signaling universally blocks progenitor cell growth, but delineated specific pathway components that can act independently, such as sustained Hes1 expression in the optic stalk/nerve head. In retinal progenitor cells, we found that among the genes tested, they do not uniformly suppress retinal ganglion cell or cone differentiation; which is not due differences in developmental timing. We discovered that shifts in the earliest cell fates correlate with expression changes for the early photoreceptor factor Otx2, but not with Atoh7, a factor required for retinal ganglion cell formation. During photoreceptor genesis we also better defined multiple and simultaneous activities for Rbpj and Hes1 and identify redundant activities that occur downstream of Notch. Given its unique roles at the retina-optic stalk boundary and cone photoreceptor genesis, our data suggest Hes1 as a hub where Notch-dependent and -independent inputs converge.

| S-EPMC10522021 | biostudies-literature

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