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GLIS3

ABSTRACT: GLIS3

PROVIDER: PRJNA1002242 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR25517300_1.fastq.gz	Fastqsanger.gz
	SRR25517300_2.fastq.gz	Fastqsanger.gz
	SRR25517301_1.fastq.gz	Fastqsanger.gz
	SRR25517301_2.fastq.gz	Fastqsanger.gz
	SRR25517302_1.fastq.gz	Fastqsanger.gz

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GLIS3 ChIP-seq

Project description:Define the DNA targets of fibroblast GLIS3 in response to fibrotic stimuli.

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Regulation of GLIS3 in neonatal kidney development

Project description:Loss of transcription factor GLIS3 function in humans and mice leads to the development of neonatal polycystic kidney disease (PKD). To investigate how loss of GLIS3 function in kidney affects postnatal kidney development and PKD, we analyzed the gene expression profiles of kidneys from WT and Glis3-null mice at P7, P14, and P28 by RNA-Seq analysis using Glis3 global KO model Glis3-mCherry.

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GLIS3 ChIP-seq

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GLIS3 RNA-seq

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Identification of GLIS3 and HNF1b target genes in kidney

Project description:Comparison of cistromes from GLIS3 and HNF1b ChIP-Seq analysis using mouse kidney was performed to examine whether there was a significant overlap in target genes between GLIS3 and HNF1b.

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GLIS3 RNA-seq

Project description:Define the transcriptome of fibroblasts perturbed for GLIS3 in response to fibrotic stimuli.

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Regulation of gene expression by GLIS3 during neonatal kidney development

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Induction of insulin gene transcription by Gli-similar KrÃ¼ppel-like zinc finger protein 3, Glis3, in Î±TC1-9 cells

Project description:In this study, we examined the effect of Glis3 on the transcriptional activation of gene expression, including insulin gene, in pancreatic Î±-cell line, Î±TC1-9, which do not express the insulin gene. We demonstrate that Glis3 induces the transcription of the insulin and identified a number of other genes that are induced by Glis3. Using ChIP-Seq we map the genome-wide sites with which Glis3 is associated. From this the consesus Glis3 binding site was calculated. This study shows that Glis3 is recruited to the proximal promoter of the insuln gene inthe pancreatic Î±-cell line, Î±TC1-9.

2016-03-14 | E-GEOD-72566 | biostudies-arrayexpress

Multiomics analyses reveal the role of Glis3 in polycystic kidney disease

Project description:We performed unbiased transcriptional profiling and chromatin accessibility analyses on adult kidney tissues from allelic series of Pkd1 and Glis3 inactivation mouse models. Glis3 is a modifer of cyst progression whose inactivation exacerbates polycystic kidney disease. Through the integration of multiomic datasets, we generated hypotheses to explain the worsening phenotype observed in Pkd1 and Glis3 double mutants.

2025-07-30 | GSE299238 | GEO

GLIS3 is indispensable for TSH/TSHR-dependent thyroid hormone biosynthesis and follicular cell proliferation

Project description:Deficiency in Krüppel-like zinc finger transcription factor, GLI-Similar 3 (GLIS3) in humans is associated with the development of congenital hypothyroidism. However, the functions of GLIS3 in the thyroid gland and by what mechanism GLIS3-dysfunction causes hypothyroidism are unknown. In this study, we demonstrate that GLIS3 acts downstream of thyroid stimulating hormone (TSH)/TSHR and is indispensable for TSH/TSHR-mediated induction of thyroid follicular cell proliferation and thyroid hormone biosynthesis. ChIP-Seq and promoter analysis revealed that GLIS3 is critical for the transcriptional activation of several genes required for thyroid hormone biosynthesis, including the iodide transporters Nis and Pds, indicating that these genes are directly regulated by GLIS3. The repression of cell proliferation regulatory genes is due to the inhibition of TSH-mediated activation of the mTORC1/RPS6 pathway as well as direct transcriptional regulation of several cell division-related genes by GLIS3. Consequently, GLIS3-deficiency prevents the development of goiter as well as the induction of inflammatory and fibrotic genes during chronic elevation of circulating TSH. Our study identifies GLIS3 as a new and key regulator of TSH/TSHR-mediated thyroid hormone biosynthesis and proliferation of thyroid follicular cells, and uncovers a mechanism by which GLIS3-deficiency causes congenital hypothyroidism and prevents goiter development.

2017-08-30 | GSE103297 | GEO

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