Similar Datasets
Project description:Analysis of third instar eye-antennal Drosophila imaginal discs with forced expression of hth, tsh or hth+tsh in the eye using an eye-specific GAL4 driver (optix2.3-GAL4). Forced maintenance of hth+tsh expression (but not of any of the two alone) results in overgrowth and aberrant cell differentiation. Results provide insight into new targets of hth+tsh.
2017-08-31 | GSE65250 | GEO
Project description:Analysis of third instar eye-antennal Drosophila imaginal discs with forced expression of hth, tsh or hth+tsh in the eye using an eye-specific GAL4 driver (optix2.3-GAL4). Forced maintenance of hth+tsh expression (but not of any of the two alone) results in overgrowth and aberrant cell differentiation. Results provide insight into new targets of hth+tsh.
2017-08-31 | GSE65251 | GEO
Project description:Activation of thyroid stimulating hormone receptor (TSHR) fundamentally leads to hyperthyroidism. To elucidate TSHR signaling, we conducted transcriptome analyses for hyperthyroid mice that we generated by overexpressing TSH. TSH overexpression drastically changed their thyroid transcriptome. In particular, enrichment analyses identified the cell cycle, phosphatidylinositol-3 kinase/Akt pathway, and Ras-related protein 1 pathway as possibly associated with goiter development. Regarding hyperthyroidism, Slc26a4 was exclusively upregulated with TSH overexpression among genes crucial to thyroid hormone secretion. To verify its significance, we overexpressed TSH in Slc26a4 knockout mice. TSH overexpression caused hyperthyroidism in Slc26a4 knockout mice, equivalent to that in control mice. Thus, we did not observe significant changes in known genes and pathways involved in thyroid hormone secretion with TSH overexpression. Our datasets might include candidate genes that have not yet been identified as regulators of thyroid function. Our transcriptome datasets regarding hyperthyroidism can contribute to future research on TSHR signaling.
2024-10-21 | GSE279577 | GEO
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:This study sought to identify the profile of circulating miRNAs and its response to human recombinant TSH in thyroid cancer patients with recurrent disease
2021-04-25 | GSE173248 | GEO
Project description:Thyroid hormone receptor beta (THRB) is post-translationally modified by small ubiquitin-like modifier (SUMO). To investigate the biological role of THRB sumoylation, we generated a mouse model with a mutation that disrupts sumoylation at lysine 146 (K146Q). The THRB K146Q mutant mice had normal serum thyroxine (T4), markedly elevated serum thyrotropin (TSH) (81-fold above control), and enlargement of both the pituitary and the thyroid gland. The marked elevation in TSH, despite a normal serum T4 concentration, indicated blunted feedback regulation of TSH. TH profuction was 10-fold lower (per mg of thyroid tissue) in mutant mice compared to Wt mice.
2021-02-20 | GSE167105 | GEO
Project description:A time-course analysis of TSH-stimulation in two rat thyroid cell lines (FRTL5 and FRT/TSHR) was performed. The expression levels of 8,784 transcripts were measured at three different time points, i.e. before (0), 30 minutes (30m) and 17 hours (17h) after TSH stimulation, by means of Affymetrix RG-U34A arrays. Keywords: Time course
2006-10-01 | GSE5115 | GEO
Project description:A time-course analysis of TSH-stimulation in two rat thyroid cell lines (FRTL5 and FRT/TSHR) was performed. The expression levels of 8,784 transcripts were measured at three different time points, i.e. before (0), 30 minutes (30m) and 17 hours (17h) after TSH stimulation, by means of Affymetrix RG-U34A arrays. Experiment Overall Design: 2 cell lines, 3 time points and 3 biological replicates per time point were analyzed
2008-06-13 | E-GEOD-5115 | biostudies-arrayexpress
Project description:Capture-C was performed on sonicated and amplified 3C libraries generated from nuclei isolated from fixed 3-18h Drosophila whole embryo samples. Capture-C was performed on wildtype and embryos with deletions or insertions at loop anchors/genes at the respective loci (scyl-chrb or tsh-tio). Capture-C was performed using two different Capture probe pools, one indicated as left (scyl, tsh, salm) and one as right (chrb, tio, salr).
2023-12-07 | E-MTAB-13271 | biostudies-arrayexpress
Project description:Background: For thyroid tumorigenesis, two main human in vitro models are available: primary cultures of human thyrocytes treated with TSH or EGF/serum as models for autonomous adenomas (AA) or papillary thyroid carcinomas (PTC) respectively, and human thyroid tumor derived cell lines. Previous works of our group have assessed properties of those models, with a special emphasis on mRNA regulations. It is often assumed that miRNA may be one of the primary events inducing these mRNA regulations. Methods: The purpose of this study was to investigate the representativity of those models to study microRNA regulations and their relation with mRNA expression. To achieve this aim, the miRNA expressions profiles of primary cultures treated with TSH or EGF/serum and of 6 thyroid cancer cell lines were compared to the expression profiles of 35 tumor tissues obtained by microarrays. Results: Our data on primary cultures have shown that the TSH or EGF/serum treatment did not greatly modify the microRNA expression profiles, which is contrary to what is observed for mRNA expression profiles, although they still evolved differently according to the treatment. The analysis of miRNA and mRNA expressions profiles in the cell lines has shown that they have evolved into a common, dedifferentiated phenotype, closer to ATC than to the tumors they are derived from. Conclusions: Long-terms TSH or EGF/serum treatments do not mimic AA or PTC respectively in terms of miRNA expression as they do for mRNA, suggesting that the regulations of mRNA expression induced by these physiological agents occur independently of miRNA. The general patterns of miRNA expression in the cell lines suggest that they represent a useful model for undifferentiated thyroid cancer. Mirna probably do not mediate the rapid changes in gene expression in rapid cell biology regulation.
2014-10-01 | GSE61482 | GEO