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Alterations in liver and epididymal white adipose tissue (eWAT) gene expression in mice with a global ablation of the NcoRω splice isoform of the corepressor Ncor1

ABSTRACT: Alterations in liver and epididymal white adipose tissue (eWAT) gene expression in mice with a global ablation of the NcoRω splice isoform of the corepressor Ncor1

PROVIDER: PRJNA671875 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12899074.fastq.gz	Fastqsanger.gz
	SRR12899075.fastq.gz	Fastqsanger.gz
	SRR12899076.fastq.gz	Fastqsanger.gz
	SRR12899077.fastq.gz	Fastqsanger.gz
	SRR12899078.fastq.gz	Fastqsanger.gz

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Alterations in liver and epididymal white adipose tissue (eWAT) gene expression in mice with a global ablation of the NcoRω splice isoform of the corepressor Ncor1

Project description:A knockin mouse line created that contains a point mutation that elminates the requisite GT in the 5' donor site of each of the NCoRω splice variants, thus preventing splicing at that site and forcing splicing of the reciprocal NcoRδ splice variant.

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NCoR1 limits angiogenic capacity by altering Notch signaling

Project description:Corepressors negatively regulate gene expression by chromatin compaction. Targeted regulation of gene expression could provide a means to control endothelial cell phenotype. We hypothesize that by targeting corepressor proteins, endothelial angiogenic function can be improved. To study this, the expression and function of nuclear corepressors in human umbilical vein endothelial cells (HUVEC) and in murine organ culture was studied. RNA-seq revealed that nuclear receptor corepressor 1 (NCoR1), Silencing Mediator of Retinoid and Thyroid hormone receptors (SMRT) and repressor element-1 silencing transcription factor (REST) are the highest expressed corepressors in HUVECs. Knockout and knockdown strategies demonstrated that the depletion of NCoR1 increased the angiogenic capacity of endothelial cells, whereas depletion of SMRT or REST did not. Interestingly, the effect was VEGF signaling independent. NCoR1 depletion significantly upregulated angiogenesis-associated genes, especially tip cell genes, including ESM1, DLL4 and NOTCH4, as observed by RNA- and ATAC-seq. Confrontation assays comparing cells with and without NCoR1-deficiency revealed that loss of NCoR1 promotes a tip-cell position during spheroid sprouting. Moreover, a proximity ligation assay identified NCoR1 as a direct binding partner of the Notch-signaling-related transcription factor RBPJk. Luciferase assays showed that siRNA-mediated knockdown of NCoR1 promotes RBPJk activity. Furthermore, NCoR1 downregulation prompts upregulation of several elements in the Notch signaling cascade. Downregulation of NOTCH4, but not NOTCH1, prevented the positive effect of NCoR1 knockdown on spheroid outgrowth. Collectively, these data indicate that decreasing NCOR1 expression is an attractive approach to promote angiogenic function. This SuperSeries is composed of the SubSeries listed below.

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NCoR1 limits angiogenic capacity by altering Notch signaling [RNA]

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Nuclear Receptor Corepressor 1 (NCoR1) deletion changed the expression profile in cardiomyocytes

Project description:Nuclear Receptor Corepressor 1 (NCoR1) deletion changed the expression profile in cardiomyocytes

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The eWAT proteomics of wild type mice and Mdm2 adipocyte-specific knock-in mice fed high-fat diet

Project description:The epididymal adipose tissue (eWAT) samples from wild type mice fed high-fat diet for 12 weeks (H_WT_E) and Mdm2 adipocyte-specific knock-in mice fed high-fat diet for 12 weeks (H_KI_E) were mixed separately, and subjected to proteomic study by Label-free quantitative techniques and mass spectrometry-based proteomics techniques, etc. The proteomics of mixed eWAT samples were performed in Jingjie PTM BioLab (Hangzhou) Co. Ltd (www.ptm-biolab.com.cn). The difference was determined by 1.5-fold-change criterion, FDR < 0.01.

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