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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.
2023-12-31 | GSE240072 | GEO
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 and kidney specific knockout model Glis3-PAX8Cre.
2023-12-31 | GSE240071 | GEO
Project description:In this study, we examined the effect of Glis3 on the transcriptional activation of gene expression, including insulin gene, in pancreatic α-cell line, αTC1-9, 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 α-cell line, αTC1-9.
2016-03-14 | E-GEOD-72566 | biostudies-arrayexpress
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
Project description:The expression of Glis3 in C3H10T1/2 cells promotes osteoblastic differentiation as indicated by the the induction of increase in alkaline phosphatase activity, an early marker of osteoblast differentiation, and increased expression of osteopontin, a late marker of osteogenesis. Glis3 acts synergistically with bone morphogenic protein 2 (BMP-2). In contrast, expression of Glis3 inhibits the induction of adipocyte differentiation. Microarray analysis identified the fibroblast growth factor 18 (FGF18) as one of the genes induced by Glis3 in C3H10T1/2 cells directly. Keywords: Glis3, osteoblast differentiation, adipocyte differentiation, FGF18, BMP2
2007-05-22 | GSE5379 | GEO
Project description:The serum hormone levels including T3 and T4 were dramatically decreased in Glis3-null mice due to reduced production of thyroid hormones in thyroid. Gene expression profile and EdU incorporation analysis between WT and Glis3-null mice showed that the cell proliferation was greatly reduced in Glis3-null thyroid. Goitergenic diet (low iodine diet; LID) dramatically enhanced serum TSH levels in both WT and Glis3-null mice, however thyroid goiter was observed in WT mice but not in Glis3-null mice. A subset of genes associated with thyroid hormone production including Pendrin (Slc26a4), Nis (Na+/I– symporter, Slc5a5), Duoxa2 (dualoxidase A2), Tpo (thyroperoxidase), and Dio1 (Deiodinase1) was significantly induced in WT but not in Glis3-null mice by LID feeding.
2017-11-06 | GSE86841 | GEO
Project description:RNA sequencing of mouse islets from mice containing a pancreas-specific deletion of Glis3, and control littermates. Also, ChIP-seq analysis of Glis3 binding using a Glis3-eGFP mouse (endogenous Glis3 fused to enhanced GFP) and GFP antibody.
2020-12-01 | GSE122120 | GEO
Project description:Through development and use of a minimal component protocol for derivation of late stage pancreatic progenitors and beta-like cells, we compared WT and GLIS3-/- pancreatic cells at different stages and discovered that GLIS3-/- cells show an ectopic activation of TGF-beta signaling.
2018-05-05 | GSE114051 | GEO
Project description:In this study, we examined the effect of Glis3 on the transcriptional activation of gene expression, including insulin gene, in pancreatic α-cell line, αTC1-9, 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.
2016-03-14 | GSE72566 | GEO
Project description:Glis3 is expressed in pancreatic beta and PP cells. To identify down stream target genes of Glis3, we performed microarray analysis using pancreas total RNAs from 1 week-old WT and Glis3KO2 mice. insulin and pancreatic polypeptide (Ppy) was significantly decreased together with several other β cell markers, Glut2 and MafA by microarray analysis. Immunohistochemistry, QRT-PCR, and transmission electron microscopy indicated that postnatal Glis3KO2 pancreas still contains a large population of β cells that express Pdx-1, Nkx6.1, and Isl-1; however, insulin production and secretory granules were greatly reduced in these cells. In addition, chromogranin A (ChgA) and Urocortin 3, which are associated with mature β cells, was dramatically decreased in Glis3KO2 pancreas. These observations suggest that Glis3 plays a critical role in the maturation of pancreatic β cell phenotype. Pancreatic total RNAs were purified from 4 WT and 4 Glis3KO2 at 1 week old age. Then the samples were applied to Agilent mouse genome chip.
2016-07-01 | E-GEOD-67238 | biostudies-arrayexpress