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The thyroid hormone receptors regulate the expression of microRNAs with key roles in skin homeostasis

ABSTRACT: The thyroid hormone receptors regulate the expression of microRNAs with key roles in skin homeostasis

PROVIDER: PRJNA418948 | ENA |

REPOSITORIES: ENA

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The thyroid hormone receptors regulate the expression of microRNAs with key roles in skin homeostasis

Project description:The role of the nuclear receptors (TRs) of thyroid hormones in cutaneous miRNA has been studied using RNAseq in a mice model

2018-06-08 | GSE107065 | GEO

Digital Gene Expression (DGE) of thyroid hormone (T3)-responsive genes in C17.2 cells stably transfected with thyroid hormone receptors alpha and beta

Project description:Tagged versions of thyroid hormone receptors alpha (TRa) and beta (TRb) were stably transfected in two C17.2 cell lines, C17.2a and C17.2b, respectively. Cells were treated with 10-7 M T3 for 6, 12 or 24h or left untreated. We performed DGE by sequencing all polyA RNA according to a SAGE-derived method. Differential gene expression after T3 treatment was computed and the T3 responses induced by the two receptors were compared. We could conclude that, in a similar environment, target genes are only partially shared and that a significant proportion show receptor preference and even selectivity. Examination of thyroid hormone target genes over time in two cell lines (C17.2a, C17.2b), each expressing one of the thyroid hormone receptors (alpha, beta).

2012-12-31 | E-GEOD-38539 | biostudies-arrayexpress

Genome-wide cistromes of thyroid hormone receptors alpha and beta in C17.2 cells

Project description:Tagged versions of thyroid hormone receptors alpha (TRa) and beta (TRb) were stably transfected in two C17.2 cell lines, C17.2a and C17.2b, respectively. We performed an affinity-based purification of chromatin (ChAP), and high-throughput sequencing was used to assess binding sites of both receptors (ChAP-Seq). Standard ChIP-Seq for RXR was also performed in C17.2a cells. These data allow us to compare binding sites for both receptors and to conclude that they were only partially redundant, with co-existence of receptor-specific sites. Examination of binding sites of the two thyroid hormone receptors (alpha, beta) in two cell lines (C17.2a, C17.2b), each expressing one of the receptors. Examination of RXR binding sites in C17.2a cells.

2012-12-31 | E-GEOD-38347 | biostudies-arrayexpress

Genome-wide cistromes of thyroid hormone receptors alpha and beta in C17.2 cells

Project description:Tagged versions of thyroid hormone receptors alpha (TRa) and beta (TRb) were stably transfected in two C17.2 cell lines, C17.2a and C17.2b, respectively. We performed an affinity-based purification of chromatin (ChAP), and high-throughput sequencing was used to assess binding sites of both receptors (ChAP-Seq). Standard ChIP-Seq for RXR was also performed in C17.2a cells. These data allow us to compare binding sites for both receptors and to conclude that they were only partially redundant, with co-existence of receptor-specific sites.

2012-12-31 | GSE38347 | GEO

Digital Gene Expression (DGE) of thyroid hormone (T3)-responsive genes in C17.2 cells stably transfected with thyroid hormone receptors alpha and beta

2012-12-31 | GSE38539 | GEO

Next Generation Sequencing to assess pesticides capacity in vitro to act as agonists/antagonists of the thyroid hormone nuclear receptors

Project description:We combined in vitro tests to fully assess the capacity of pesticides to act as thyroid hormone disruptors (THD). Pesticides which were active in these tests were selected for a transcriptome analysis of neural cells. We took advantage of this technique to decipher what were the transcriptomic effects of these chemical in vitro. We also compared the expression of thyroid hormone responsive genes in presence or absence of the pesticides to determine if the transcriptomic changes could impact thyroid hormone receptor signaling. Although some pesticides elicit a cellular response, which sometimes interferes with thyroid hormone signaling, we found no evidence that they can act as TRα1 agonists or antagonists. We conclude that their neurodevelopmental toxicity in mammals is not explained by an alteration of the neural cell response to thyroid hormone.

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Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.

Project description:Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.

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Thyroid hormone receptor alpha is required for thyroid hormone-dependent neural cell proliferation during tadpole metamorphosis

Project description:Using tadpoles mutant for thyroid hormone receptor alpha (thra), we show that TRa is required for thyroid hormone (T3) induction of cell proliferation in the brain. RNA-sequencing showed that the TRa is required for 95% of the gene regulation responses to T3.

2019-05-13 | GSE130816 | GEO

Isoform-specific transcriptional activity of overlapping targets that respond to thyroid hormone receptors a1 and b1

Project description:Thyroid hormone receptors (TRs) are hormone-regulated transcription factors that control multiple aspects of physiology and development. TRs are expressed in vertebrates as a series of distinct isoforms that exert distinct biological roles. We wished to determine if the two most widely expressed isoforms, TRa1 and TRb1, exert their different biological effects by regulating different sets of target genes. Using stably transformed HepG2 cells and a microarray analysis, we were able to demonstrate that TRa1 and TRb1 regulate a largely overlapping repertoire of target genes in response to T3 hormone. However, these two isoforms display very different transcriptional properties on each individual target gene, ranging from a much greater T3-mediated regulation by TRa1 than by TRb1, to near equal regulation by both isoforms. We also identified TRa1 and TRb1 target genes that were regulated by these receptors in a hormone-independent fashion. We suggest that it is this gene-specific, isoform-specific amplitude of transcriptional regulation that is the likely basis for the appearance and maintenance of TRa1 and TRb1 over evolutionary time. In essence, TRa1 and TRb1 adjust the magnitude of the transcriptional response at different target genes to different levels; by altering the ratio of these isoforms in different tissues or at different developmental times, the intensity of T3 response can be individually tailored to different physiological and developmental requirements. TRa1, TRb1, or empty plasmid control stably transfected HepG2 cells were treated with 100 nM T3 or with ethanol carrier alone for 6h. Three independent biological repeats were analyzed for each of the three transformant pools (empty plasmid control, TRa1, and TRb1).

2009-08-08 | E-GEOD-17561 | biostudies-arrayexpress

NCoR1 and SMRT play unique roles in thyroid hormone signaling in the liver

Project description:NCoR1 (Nuclear receptor Co-Repressor) and SMRT (Silencing Mediator of Retinoid and Thyroid hormone receptor) are well-recognized coregulators of nuclear receptor (NR) action. However, their unique roles in the regulation of thyroid hormone (TH) signaling in specific cell types have not been determined. To accomplish this we generated a mouse model that lacked function of either NCoR1 or SMRT or both in the liver only. Despite both corepressors being present in the liver, SMRT had no ability to regulate TH signaling when deleted in either euthyroid or hypothyroid animals. In contrast, disruption of NCoR1 action confirmed that it is the principal mediator of TH sensitivity in vivo. While SMRT played little role in TH signaling alone, when disrupted in combination with NCoR1 it greatly accentuated the activation of hepatic lipogenesis regulated by NCoR1. Thus, corepressor specificity exists in vivo and NCoR1 is the principal regulator of TH action in the liver. However, both NCoR1 and SMRT collaborate to control hepatic lipogenesis and lipid storage, which likely reflects their cooperative activity in regulating the action of multiple NRs including the thyroid hormone receptor (TR). RNA was extracted from livers from 3 individual mice for each group (Double-floxed, Liver specific-SMRT knock out, and Liver specific-double knock out); all were euthyroid, female mice

2014-11-21 | E-GEOD-54192 | biostudies-arrayexpress

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