Project description:Affymetrix GeneChip Mouse Gene 1.0 ST Array was used to study gene expression profiles in three groups of mice: with thyroid hormone receptor ThrbPV (ThrbPV/PV) mutation only, with RAS mutation (KrasG12D) only, and with both ThrbPV/PV and KrasG12D mutations. Three groups mice: with thyroid hormone receptor ThrbPV (ThrbPV/PV) mutation only, with RAS mutation (KrasG12D) only, and with both ThrbPV/PV and KrasG12D mutations. Each group has three biological replicates.
Project description:Affymetrix GeneChip Mouse Gene 1.0 ST Array was used to study gene expression profiles in three groups of mice: with thyroid hormone receptor ThrbPV (ThrbPV/PV) mutation only, with RAS mutation (KrasG12D) only, and with both ThrbPV/PV and KrasG12D mutations.
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.
Project description:To investigate the effect of thyroid hormone and its receptor on glucose and lipid metabolism in white adipose tissue (WAT), and the effect of thyroid hormone and its receptor on WAT regulation on glucose metabolism and obesity. We constructed mice with adipose tissue-specific knockout of thyroid hormone receptor beta（ATRβKO mice）. ATRβKO mice were given T3 stimulation or high-fat feeding. We then performed gene expression profiling analysis using data obtained from RNA-seq of White adipose tissue from knockout ATRβKO mice treated with T3 or HFD feeding.
Project description:Characterization of Directly Regulated Thyroid Hormone Mediated Gene Expression Following Short-Term Perturbations in Thyroid Hormone Levels in Juvenile Mice
