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Compound PIP-RBPJ-1 treated human neural stem cells

ABSTRACT: The study of the compond PIP-RBPJ-1‘ function on neural stem cell. Synthetic DNA-binding inhibitors capable of gaining precise control over neurogenesis factors could obviate the current clinical barriers associated with small molecule use in regenerative medicine. Here, we show the design and bio-efficacy of a synthetic ligand PIP-RBPJ-1 to cause promoter-specific suppression of neurogenesis-associated HES1, and its downstream genes. Furthermore, PIP-RBPJ-1 alone could alter the neural system-associated notch signaling factors and remarkably induce neurogenesis with an efficiency that is comparable to a conventional approach. Here is one day treatment of the PIP-RBPJ-1 on neural stem cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE109916 | GEO | 2018/07/19

REPOSITORIES: GEO

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Compound PIP-RBPJ-1 treated human neural stem cells

Project description:Compound PIP-RBPJ-1 treated human neural stem cells

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Project description:Here we performed a ChIP-seq experiment on a sample of adherent cultures of mouse neural stem cells (NS5 cell line) under normal growth conditions. This resulted in the generation of a genome-wide map of RBPJ binding to chromatin.

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A functional and regulatory network associated with PIP expression in human breast cancer

Project description:Background The PIP (prolactin-inducible protein) gene has been shown to be expressed in breast cancers, with contradictory results concerning its implication. As both the physiological role and the molecular pathways in which PIP is involved are poorly understood, we conducted a combined gene expression profiling and network analysis studies on selected breast cancer cell lines presenting distinct PIP expression levels and hormonal receptor status, to explore the functional and regulatory network of PIP co-modulated genes. Results Microarray analysis allowed identification of genes co-modulated with PIP independently of modulations resulting from hormonal treatment or cell line heterogeneity. Relevant clusters of genes that can discriminate between [PIP+] and [PIP-] cells were identified. Functional and regulatory network analyses based on knowledge database revealed a master network of PIP co-modulated genes, including many interconnecting oncogenes and tumor suppressor genes, half of which were detected as differentially expressed through high-precision measurements. The networks identified appear associated with an inhibition of proliferation coupled with an increase of apoptosis and an enhancement of cell adhesion in breast cancer cell lines. Finally, the STAT5 motif was identified in promoters of an important part of genes belonging to the PIP networks. Conclusion Our global exploratory approach was found to be an effective strategy to identify the biological pathways modulated along with the PIP expression, thus supporting good prognostic value of disease-free survival time in breast cancer based on previous reports focusing on PIP’s favorable signature. Moreover, our data allowed us to provide the first insight in its regulatory subnetwork in which STAT5 appears as a potential key regulator.

2009-03-06 | GSE11627 | GEO

Activation of a neural stem cell transcriptional program in parenchymal astrocytes

Project description:Neural stem cells, located in discrete niches in the adult brain, generate new neurons throughout life. These stem cells are specialized astrocytes, but astrocytes in other brain regions (parenchymal astrocytes) do not generate neurons under physiological conditions. After stroke, however, astrocytes in the mouse striatum undergo neurogenesis, triggered by decreased Notch signaling. Notch signaling can be experimentally depleted in mice by deleting the Notch-mediating transcription factor Rbpj. This dataset consists of single-cell RNA sequencing data of astrocytes isolated from the striatum (where astrocytes undergo neurogenesis in response to Rbpj deletion) or somatosensory cortex (where astrocytes don't complete neurogenesis in response to Rbpj deletion) of 4 mice. Cells were isolated from Cx30-CreER; R26-tdTomato; Rbpj(fl/fl) mice at three time points after tamoxifen-induced Rbpj deletion (2, 4, 8 weeks), and from Cx30-CreER; R26-tdTomato mice with intact Rbpj 3 days after tamoxifen. These time points span the transition from astrocyte through transit-amplifying cells to neuroblasts. The dataset contains 1) astrocytes from the striatum that initiate a neurogenic transcriptional program in response to Rbpj deletion and generate transit-amplifying cells and neuroblasts, and 2) astrocytes from the somatosensory cortex that initiate a neurogenic program in response to Rbpj deletion but fail to generate transit-amplifying cells or neuroblasts.

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Rbpj expression in regulatory T cells is critical for restraining TH2 responses [spleen Rbpj WT and Rbpj KO ATAC-seq]

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FBXO42 facilitates Notch signaling activation and global chromatin relaxation by promoting K63-linked polyubiquitination of RBPJ

Project description:Dysregulation of the Notch-RBPJ signaling pathway has been found associated with various human diseases including cancers; however, precisely how this key signaling pathway is fine-tuned via its interactors and modifications is still largely unknown. In this study, using a proteomic approach, we identified FBXO42 as a novel RBPJ interactor. FBXO42 promotes RBPJ polyubiquitination on lysine (K) 175 via K63 linkage, which enhances the association of RBPJ with chromatin remodeling complexes and induces a global chromatin relaxation. Genetically depleting FBXO42 or pharmacologically targeting its E3 ligase activity attenuates the Notch signaling-related leukemia development in vivo. Taken together, our findings not only revealed FBXO42 as a critical regulator of the Notch pathway by modulating RBPJ-dependent global chromatin landscape changes, but also provide insights into the therapeutic intervention of the Notch pathway for leukemia treatment.

2022-10-13 | PXD034938 | Pride

Transcriptomics analysis of neurogenesis by striatal astrocytes upon Rbpj-K deletion

Project description:We achieved local recombination of striatal astrocytes and silenced Notch signalling activity through Rbpj-K depletion. Recombined astrocytes and neural progenitors generated from the striaral glia were FAC sorted and their molecular profile investigated in a scRNAseq experiment performed 5 wpi.

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RBPJ deficiency sensitizes pancreatic acinar cells to Kras-mediated PanIN initiation

Project description:Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis and is among the most common causes of cancer death worldwide. KrasG12D mutation is the main driver mutation but insuffi-cient for progression of invasive cancer on its own indicating that other pathways, such as Notch signaling may participate in that process. RBPJ, the only transcription factor in Notch signaling, is frequently lost in human cancers and associated with more aggressive breast cancer phenotype. Notch-independently, in complex with P48, RBPJ initiates transcription of its paralogue RBPJL ensuring acinar differentiation. The RBPJ knockout has an embryonic lethal effect. Mice with pancreas-specific deletion of RBPJ presented with less acinar tissue and large duct-like structures suggesting a relevance of RBPJ for acinar to ductal reprogramming and even pancreatic neoplasia. Here, we found reduced RBPJ expression level in the human PDAC specimens. Analyses of transgenic mouse models of an inducible P48-dependent RBPJ knockout revealed that it is dispensable for the maintenance adult acinar cells. In the context of oncogenic KRAS expression, the RBPJ deficiency facilitated the development of PanIN lesions with massive fibrotic stroma. Interestingly, RNA seq data revealed corresponding transcription pattern prior to phenotypic alterations.

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Effect on small molecule RBPJ inhibitor (RIN1) on gene expression in Jurkat cells compared to gamma secretase inhibition and siRNA knockdown of RBPJ

Project description:We discovered a new class of small molecule inhibitor that disrupts the interaction between NOTCH and RBPJ, which is the main transcriptional effector of NOTCH signaling. RBPJ Inhibitor-1 (RIN1) also blocked the functional interaction of RBPJ with SHARP, a scaffold protein that forms a transcriptional repressor complex with RBPJ in the absence of NOTCH signaling. RIN1 induced changes in gene expression resembled siRNA silencing of RBPJ rather than inhibition at the level of NOTCH itself. RIN1 inhibits RBPJ in its repressing and activating contexts.

2019-07-18 | GSE134401 | GEO

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