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ZEB1 represses neural differentiation and cooperates with CTBP2 to dynamically regulate cell migration during neocortex development [RNA-seq]

ABSTRACT: ZEB1 represses neural differentiation and cooperates with CTBP2 to dynamically regulate cell migration during neocortex development [RNA-seq]

PROVIDER: PRJNA525783 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8689260.fastq.gz	Fastqsanger.gz
	SRR8689261.fastq.gz	Fastqsanger.gz
	SRR8689262.fastq.gz	Fastqsanger.gz
	SRR8689259.fastq.gz	Fastqsanger.gz

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ZEB1 represses neural differentiation and cooperates with CTBP2 to dynamically regulate cell migration during neocortex development

Project description:ZEB1 represses neural differentiation and cooperates with CTBP2 to dynamically regulate cell migration during neocortex development

| PRJNA525782 | ENA

ZEB1 represses neural differentiation and cooperates with CTBP2 to dynamically regulate cell migration during neocortex development [ChIP-seq]

Project description:ZEB1 represses neural differentiation and cooperates with CTBP2 to dynamically regulate cell migration during neocortex development [ChIP-seq]

| PRJNA525784 | ENA

ZEB1 represses neural differentiation and cooperates with CTBP2 to dynamically regulate cell migration during neocortex development [ChIP-seq]

Project description:Zinc finger E-box binding homeobox 1 (Zeb1) is a key regulator of epithelial-mesenchymal transition and cancer metastasis. Mutation of ZEB1 is associated with human diseases and defective brain development. Here we show that down-regulation of Zeb1 expression in the embryonic cortical neural progenitor cells (NPCs) is necessary for proper neuronal differentiation and migration. Overexpression of Zeb1 during neuronal differentiation when its expression normally declines blocks NPC lineage progression and disrupts multipolar-to-bipolar transition of differentiating neurons, leading to severe migration defects and subcortical heterotopia bands at the postnatal stage. We found that ZEB1 regulates a cohort of genes involved in cell differentiation and migration, including Neurod1 and Pard6b. Interestingly, interaction between ZEB1 and CTBP2 in the embryonic cerebral cortex is required for ZEB1 to elicit its effect on multipolar-to-bipolar transition but not its suppression of Neurod1. These findings provide insights into understanding the complexity of transcriptional regulation during neuronal differentiation.

2019-05-21 | GSE127913 | GEO

ZEB1 represses neural differentiation and cooperates with CTBP2 to dynamically regulate cell migration during neocortex development [RNA-seq]

2019-05-21 | GSE127912 | GEO

ZEB1 represses neural differentiation and cooperates with CTBP2 to dynamically regulate cell migration during neocortex development

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

2019-05-21 | GSE127914 | GEO

Down-regulation of miR-200a-3p, targeting C-terminal binding protein-2 (CtBP2), is involved in hypoproduction of IL-2 in SLE-derived T cells

Project description:Systemic lupus erythematosus (SLE) damages multiple organs by producing various autoantibodies. Insufficient interleukin-2 (IL-2) production causes decreased regulatory T cells and permits expansion of autoreactive T cells in the development of SLE. We here show that decreased miR-200a-3p causes IL-2 hypoproduction through directly recruiting ZEB1 or ZEB2 and CtBP2 (ZEB1/ZEB2-CtBP2) complex in SLE T cells. First, we performed RNA sequencing with Illumina Hiseq to obtain the candidate miRNAs and mRNAs involved in the pathogenesis of SLE. We found that miR-200a-3p was significantly downregulated, while its putative targets, ZEB2 and CtBP2 were upregulated in CD4+ T cells in MRL/lpr lupus model mice compared with those of C57BL/6J control mice. ZEB1 and ZEB2 compose ZEB family and suppress various genes including IL-2 by recruiting CtBP2. IL-2 plays a critical role in immune tolerance and IL-2 defect has been recognized in SLE pathogenesis. Therefore, we hypothesized that decreased miR-200a-3p cause IL-2 defect through ZEB1/ZEB2-CtBP2 complex in SLE CD4+T cells. Overexpression of miR-200a-3p induced IL-2 production though downregulating ZEB1, ZEB2 and CtBP2 in EL4 cell lines. We further revealed that miR-200a-3p promote IL-2 expression by reducing the bindings of suppressive ZEB1/ZEB2-CtBP2 complex on NRE-A of IL-2 promoter in SLE murine T cells. Interestingly, ZEB1/ZEB2-CtBP2 complex on NRE-A (a negative regulatory element) were significantly upregulated after phorbol-12-myristate-13-acetate and ionomycin (PMA/Iono) stimulation in lupus T cells. Our findings provide a new insight for the epigenetic regulation of IL-2 defect in SLE.

2016-09-23 | GSE87219 | GEO

Liver transcriptome regulated by CtBP2

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2021-09-27 | GSE128145 | GEO

proteome analysis of exosomes from WT CtBP2-HA knock-in and Mut CtBP2-HA knock-in MEF cells

Project description:We prepared two types of MEF cells: one is cells with wild-type CtBP2-HA knock-in and the other is Rossmann fold mutant CtBP2-HA knock-in. We isolated exosomes from those cells with the polymer precipitation method and subjected them to proteome analysis.

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Genome wide expression analysis of Ctbp2 knock down mouse F9 cells

Project description:Using an RNA interference-based genetic screen in mouse F9 cells we identify the transcriptional corepressor CTBP2 as a coactivator critically required for retinoic acid (RA)-induced transcription. Here we perfom a whole genome transcriptome analysis in F9 cells expressing shRNA for Ctbp2 and Rxr in the absence or presence of retinoic acid (RA). A total of 2,754 genes were found to be upregulated (>2 fold) and 1518 genes were downregulated (>2 fold) in response to RA treatment in the control cells. We find that around 52% and 55% of upregulated genes are dependent on Ctbp2 and Rxr for activation respectively suggesting that Ctbp2 is a coactivator of RA signaling. Whole genome RNA-sequencing in F9 cells expressing shGFP or shCtbp2 or shRxr

2013-06-21 | E-GEOD-47708 | biostudies-arrayexpress

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