Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nuclear translocation of PTH receptor hijacks thyroid hormone signaling for bone mass regulation [ChIP-Seq]

ABSTRACT: After preliminary verification of physical interaction between PTH1R and THR, we next performed chromatin co-immunoprecipitation sequencing (ChIP -seq) to detect the overlapping downstream promoters genome-widely between PTH1R and THR.

ORGANISM(S): Mus musculus

PROVIDER: GSE233174 | GEO | 2023/12/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Nuclear translocation of PTH receptor hijacks thyroid hormone signaling for bone mass regulation [RNA-seq]

Project description:After demonstrating that the bone-forming ability of mice is altered by blocking PTH1R entry into the nucleus, We performed RNA-seq on BMSCs from Pth1rΔNLS individuals and wild-type individuals to explore the mechanism behind this phenomenon.

2023-12-20 | GSE233172 | GEO

Nuclear translocation of PTH receptor hijacks thyroid hormone signaling for bone mass regulation

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-12-20 | GSE233176 | GEO

Kindlin-2 modulates PTH1R to regulate bone mass and PTH actions in bone

Project description:Kindlin-2 modulates PTH1R to regulate bone mass and PTH actions in bone

| PRJNA631725 | ENA

Parathyroid Hormone Receptor-1 Signaling Aggravates Hepatic Fibrosis through Upregulating cAMP Response Element Binding Protein-Like 2 (human)

Project description:Background & Aims Parathyroid hormone receptor-1 (PTH1R) is a class B G protein-coupled receptor central to skeletal development, bone turnover, and calcium homeostasis. However, the role of PTH1R signaling in liver fibrosis is largely unknown. Here, the role of PTH1R signaling in the activation of hepatic stellate cells (HSCs) and hepatic fibrosis was examined. Approach & Results PTH1R was highly expressed in activated HSCs and fibrotic liver by using human liver specimens or carbon tetrachloride (CCl4)-treated or methionine and choline-deficient diet (MCD)-fed C57/BL6 mice. The mRNA level of hepatic PTH1R was positively correlated to α-smooth muscle actin (α-SMA) in patients with liver cirrhosis. Mice with HSCs-specific PTH1R deletion were protected from CCl4, MCD, or western diet plus low-dose CCl4-induced liver fibrosis. Conversely, parathyroid hormone (PTH) aggravated liver fibrosis in CCl4-treated mice. Mouse primary HSCs and LX2 cell lines were used for in vitro experiments. Molecular analyses by luciferase reporter assays and chromatin-immunoprecipitation assays in combination with mRNA sequencing in HSCs revealed that cAMP response element-binding protein-like 2 (Crebl2), a novel regulator in HSCs treated by PTH that interacted with Mothers against decapentaplegic homolog 3 (SMAD3) and increased the transcription of transforming growth factor β (TGFβ) in activating HSCs and collagen deposition. In agreement, HSCs-specific Crebl2 deletion ameliorated PTH-induced liver fibrosis in CCl4-treated mice. Conclusions In both mouse and human models, we found that PTH1R was highly expressed in activated HSCs and fibrotic liver. PTH1R signaling regulated collagen production in the HSCs via Crebl2/SMAD3/TGFβ regulatory circuits. Blockade of PTH1R signaling in HSCs might help mitigate the development of liver fibrosis.

2023-03-29 | GSE227902 | GEO

Parathyroid Hormone Receptor-1 Signaling Aggravates Hepatic Fibrosis through Upregulating cAMP Response Element Binding Protein-Like 2 (mouse)

2023-03-29 | GSE227901 | GEO

Altered selectivity of parathyroid hormone (PTH) and PTH-related protein (PTHrP) for distinct conformations of the PTH/PTHrP receptor.

Project description: Not available

| S-EPMC2194631 | biostudies-literature

Negative regulation of parathyroid hormone (PTH)-activated phospholipase C by PTH/PTH-related peptide receptor phosphorylation and protein kinase A.

Project description: Not available

| S-EPMC2488210 | biostudies-literature

Disruption of ?-catenin binding to parathyroid hormone (PTH) receptor inhibits PTH-stimulated ERK1/2 activation.

Project description: Not available

| S-EPMC4509838 | biostudies-literature

Critical role of parathyroid hormone (PTH) receptor-1 phosphorylation in regulating acute responses to PTH.

Project description: Not available

| S-EPMC3625299 | biostudies-literature

Atlas of target genes of thyroid hormone (TH) in mice

Project description:We gathered in a single database available RNAseq and ChIPseq data to better characterize the target genes of the thyroid hormone receptors in several cell types. This database can serve as a resource to analyze the mode of action of the hormone. Also, it is an easy-handling convenient tool to obtain information on specific genes in regards to T3 regulation, or extract larger list of genes of interest based on the users’ criteria. Overall, this atlas is a unique compilation of recent sequencing data focusing on thyroid hormones, their receptors, mode of action, targets and roles which may profit researchers within the field. A preliminary analysis indicates extensive variations in the repertoire of target genes which transcription is upregulated by chromatin-bound nuclear receptor. Although it has a major influence, chromatin accessibility is not the only parameter that determines the cellular selectivity of hormonal response.

2022-08-12 | GSE210975 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data