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Cis inhibition of NOTCH1 through JAGGED1 sustains embryonic Hematopoietic stem cell fate

ABSTRACT: Cis inhibition of NOTCH1 through JAGGED1 sustains embryonic Hematopoietic stem cell fate

PROVIDER: PRJNA962569 | ENA |

REPOSITORIES: ENA

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Cis inhibition of NOTCH1 through JAGGED1 sustains embryonic Hematopoietic stem cell fate [scRNA-seq]

Project description:Cis inhibition of NOTCH1 through JAGGED1 sustains embryonic Hematopoietic stem cell fate [scRNA-seq]

| PRJNA962580 | ENA

Cis inhibition of NOTCH1 through JAGGED1 sustains embryonic Hematopoietic stem cell fate [RNA-seq]

Project description:Cis inhibition of NOTCH1 through JAGGED1 sustains embryonic Hematopoietic stem cell fate [RNA-seq]

| PRJNA962584 | ENA

Cis inhibition of NOTCH1 through JAGGED1 sustains embryonic Hematopoietic stem cell fate [RNA-seq]

Project description:Hematopoietic stem cells (HSCs) develop from the hemogenic endothelium (HE) in the aorta- gonads-and mesonephros (AGM) region and reside within Intra-aortic hematopoietic clusters (IAHC) along with hematopoietic progenitors (HPC). The signalling mechanisms that distinguish HSCs from HPCs are unknown. Notch signaling is essential for arterial specification, IAHC formation and HSC activity, but current studies on how Notch segregates these different fates are inconsistent. We now demonstrate that Notch activity is highest in a subset of, GFI1+, HSC-primed HE cells, and is gradually lost with HSC maturation. We uncover that the HSC phenotype is maintained due to increasing levels of NOTCH1 and JAG1 interactions on the surface of the same cell (cis) that renders the NOTCH1 receptor from being activated. Forced activation of the NOTCH1 receptor in IAHC activates a hematopoietic differentiation program. Our results indicate that NOTCH1-JAG1 cis-inhibition preserves the HSC phenotype in the hematopoietic clusters of the embryonic aorta.

2024-01-22 | GSE230790 | GEO

Cis inhibition of NOTCH1 through JAGGED1 sustains embryonic Hematopoietic stem cell fate [scRNA-seq]

2024-01-22 | GSE230792 | GEO

Cis inhibition of NOTCH1 through JAGGED1 sustains embryonic Hematopoietic stem cell fate

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-22 | GSE230794 | GEO

Notch-Jagged signaling complex defined by an interaction mosaic

Project description:The Notch signaling system links cellular fate to that of its neighbors, driving proliferation, apoptosis, and cell differentiation in metazoan organisms, whereas dysfunction leads to debilitating developmental disorders and cancers. Here we probe the molecular architecture of mammalian Notch1 full ectodomain in complex with the canonical ligand Jagged1 using cross-linking mass spectrometry (XL-MS). Our data reveals that three Jagged1 sites, C2-epidermal growth factor (EGF) 1, EGF10 and cysteine-rich domain (CRD), are in proximity to the Notch1 negative regulatory region (NRR) in the Notch1-Jagged1 full ectodomain complex. We verified direct interactions and identified additional interacting regions by quantitative-binding experiments. In addition, XL-MS and structural analysis reveal Notch1 and Jagged1 ectodomain intramolecular interactions and structural flexibility that support the formation of backfolded architectures. Together the data suggest a direct and intricate role for the different extracellular regions of Notch1 and Jagged1 in the activation and regulation of Notch1 signaling.

2021-07-08 | PXD023072 | Pride

Jagged1 regulates miRNA expression profile

Project description:miRNA expression profiles of HMECs treated with 40mM Jagged1 (JAG1) or the control peptide for 1 day Genome-wide miRNA PCR array analysis was performed using human miRNA PCR arrays (MIHS216Z, SABiosceinces) acccording to the manufacturer's instructions

2014-05-30 | E-GEOD-56801 | biostudies-arrayexpress

Tumor-derived Jagged1- and Notch-dependent transcription changes in MC3T3-E1 osteoblasts

Project description:Transcriptional profiling of MC3T3-E1 osteoblasts that were flow cytometry-separated from cocultures with control or Jagged1-overexpressing tumor cells and treated with either DMSO control or 1μM MRK-003 (gamma-secretase inhibitor). One cell line (MC3T3-E1) cells: four different experimental conditions: cultured with (1) control tumor cells + DMSO; (2) Jagged1-overexpressing tumor cells + DMSO; (3) control tumor cells + MRK-003; (4) Jagged1-overexpressing tumor cells + MRK-003. Each experiment has two biological replicates. Total, 8 samples.

2010-08-15 | E-GEOD-20517 | biostudies-arrayexpress

Endothelial Jagged1 levels and distribution are post-transcriptionally controlled by ZFP36 decay proteins

Project description:Vascular morphogenesis requires a delicate gradient of Notch signaling that is controlled, at least in part, by the distribution of ligands (Dll4 and Jagged1). How jagged1 (JAG1) expression is compartmentalized in the vascular plexus remains unclear. Here we showed that Jag1 mRNA is a direct target of zinc finger protein 36 (ZFP36), an RNA-binding protein involved in mRNA decay that we found robustly induced by VEGF. Endothelial cells lacking ZFP36 displayed high levels of JAG1 and increased angiogenic sprouting in vitro. Similarly, mice lackingZfp36in endothelial cells display mispatterned and increased levels of JAG1 in the developing retinal vascular plexus. Abnormal levels of JAG1 at the sprouting front altered NOTCH1 signaling, increasing the number of tip cells; a phenotype that was rescued by imposing haploinsufficiency ofJag1. Our findings reveal an important feedforward loop, whereby VEGF stimulates ZFP36, consequently suppressing Jag1 to enable adequate levels of Notch signaling during sprouting angiogenesis.

2023-12-04 | GSE235462 | GEO