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Satb2 deletion in colon approach to treat short bowel syndrome

ABSTRACT: Satb2 deletion in colon approach to treat short bowel syndrome

PROVIDER: PRJNA1174226 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31039630_1.fastq.gz	Fastqsanger.gz
	SRR31039630_2.fastq.gz	Fastqsanger.gz
	SRR31039631_1.fastq.gz	Fastqsanger.gz
	SRR31039631_2.fastq.gz	Fastqsanger.gz

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Satb2 deletion in colon approach to treat short bowel syndrome

Project description:Loss of the transcription factor Satb2 converts mouse colonic epithelium into an ileal type. Here, we report that Satb2 gene deletion alleviates SBS by replacing diminished absorptive function and by inducing lymphovascular channels in the proximal colon. Enhanced nutrient absorption following Satb2 loss increased body weight and survival of mice with SBS. Deletion of SATB2 by adeno-associated viral delivery of CRISPR Split Cas9 to human colon organoids, followed by xenotransplantation into mice, resulted in ileal morphology and expression of ileal marker genes. This approach offers a feasible strategy for future treatment of SBS.

2025-03-19 | GSE279770 | GEO

ChIP-seq for Satb2 in E15 cortex

Project description:The goal of the study was to identify the binding site of SATB2 in wild-ype cortex by performing ChIP-seq using SATB2 antibody. E15 cortical tissues were dissected, lysed and fixed. Chromatin was prepared by sonication. Sequences bound by SATB2 protein was precipitated using a SATB2 antibody. Sequencing was performed on Illumina Genome Analyzer II. SATB2 binding peaks were called using MACS. ChIP for Satb2, followed by sequencing on Illumina Genome Analyzer II platform

2015-09-08 | E-GEOD-68910 | biostudies-arrayexpress

Role of Satb1 and Satb2 in embryonic stem cells

Project description:Satb1 and Satb2 are regulators of higher order chromatin in T cells and osteoblasts repectively. We were interested if Satb1 and Satb2 play a role in the regulation of gene expression in ES cells. This SuperSeries is composed of the following subset Series: GSE17487: Expression data in WT and Satb1-/- ES cells GSE17488: Expression data in WT and ES cells overexpressing Satb1 GSE17489: Expression data in WT and ES cells overexpressing Satb2 Refer to individual Series

2009-09-01 | E-GEOD-17490 | biostudies-arrayexpress

ChIP-seq for Satb2 in E15 cortex

2015-09-08 | GSE68910 | GEO

Short bowel syndrome mouse microbiome

Project description:Short bowel syndrome mouse microbiome

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ATAC-seq of Intestine Epithelia (Ileum and Colon) from Satb2-deficient and WT mice

Project description:The goal of this study is to study the chromatin accessibility signature after Satb2 gene loss in the colonic epithelium.

2021-10-05 | GSE148690 | GEO

scRNA-Seq of Intestine Epithelia (Ileum and Colon) from Satb2-deficient and WT mice

Project description:The goal of this study is to study signal cell transcripton level changes after Satb2 gene loss in the colonic epithelium.

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Project description:The goal of this study is to study the consequence of Satb2 gene loss in the colonic epithelium.

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Expression data in WT and ES cells overexpressing Satb2

Project description:Satb1 and Satb2 are regulators of higher order chromatin in T cells and osteoblasts repectively. We were interested if Satb1 and Satb2 play a role in the regulation of gene expression in ES cells. ES cells which can inducibly express Satb1 or Satb2 were generated using the tet-ON system. In this experiment, we compared gene expression in uninduced cells to that in cells which had been induced for 24h to express Satb2 ectopcially at very high levels.

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Project description:During CNS development, the nuclear protein SATB2 is expressed in superficial cortical layers and determines projection neuron identity. In the adult CNS, SATB2 is expressed in pyramidal neurons of all cortical layers and is a regulator of synaptic plasticity and long-term memory. Common variation in SATB2 locus confers risk of schizophrenia whereas rare, de novo structural and single nucleotide variants cause severe intellectual disability and absent or limited speech. To which extent symptoms in SATB2-related human pathologies depend on developmental or adult functions of the protein remains to be established. To characterize differences in SATB2 molecular function in developing vs adult neocortex, we compared SATB2 protein interactomes and SATB2-driven gene expression programs at the two ontogenetic stages by co-IP mass spectrometry and RNAseq analyses, respectively. Our results demonstrated that 1) SATB2 interacts with different protein networks at the two ontogenetic stages, with a switch from transcriptional repression towards organization of chromatin structure and 2) SATB2 determines differential transcriptional programs in neonatal vs adult cortex.

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