Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Knockdown of xenotropic and polytropic retrovirus receptor 1 in thyroid cancer cells

ABSTRACT: Xenotropic and polytropic retrovirus receptor 1 (XPR1), initially identified as a receptor for murine leukemia viruses, has been shown to function as a phosphate exporter, maintaining inorganic phosphate homeostasis in cells. Recently, XPR1 was recognized as a late-stage neoantigen-related gene in thyroid cancer; however, its functions in this context have not been well characterized.

ORGANISM(S): Homo sapiens

PROVIDER: GSE292773 | GEO | 2025/04/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Renal Fanconi syndrome and hypoposphatemic rickets in mice deficient for retroviral receptor XPR1 in the nephron

Project description:Tight control of both extracellular and intracellular inorganic phosphate (Pi) levels is critical to the normal functioning of virtually all biochemical and physiological processes. The kidney participates in Pi homeostasis by controlling Pi reabsorption from the primary urine. Pi is freely filtered at the kidney glomerulus and is reabsorbed in the renal tubule by the action of the apical sodium-dependent phosphate transporters NaPi-IIa/NaPi-IIc/Pit2. The molecular identity of transporter(s) involved in the basolateral Pi efflux remains unknown. Recent evidence has suggested that the retroviral receptor XPR1 might be a candidate for this role. Here we show that conditional inactivation of Xpr1 in the renal tubule in mice results in impaired renal Pi reabsorption associated with a generalized proximal tubular dysfunction, or Fanconi syndrome, characterized by glycosuria, aminoaciduria, calciuria and albuminuria. Bone histomorphometry showed that the Xpr1-deficient mice develop hypophosphatemic osteomalacia secondary to the renal dysfunction. The analysis of Pi transport in primary culture of the proximal tubular cells revealed that the Pi efflux was significantly affected in cells devoid of Xpr1. These results identify XPR1 as a major player in Pi homeostasis and as a potential therapeutic target in bone and kidney disorders.

2016-12-01 | GSE87450 | GEO

Knockdown of xenotropic and polytropic retrovirus receptor 1 in thyroid cancer cells

Project description:Knockdown of xenotropic and polytropic retrovirus receptor 1 in thyroid cancer cells

| PRJNA1241234 | ENA

The phosphate exporter XPR1/SLC53A1 is required for the tumorigenicity of ovarian cancer.

Project description:Ovarian cancer is the fifth cause of cancer-related death in women. Ovarian clear cell carcinoma (OCCC) is a chemotherapy-resistant epithelial ovarian cancer with poor prognosis. As a basis for the development of therapeutic agents that may improve the prognosis of OCCC, we performed a screen for proteins critical for the tumorigenicity of OCCC using the CRISPR/Cas9 system. Here we show that knockdown of the phosphate exporter XPR1/SLC53A1 induces the growth arrest and apoptosis of OCCC cells in vitro. Moreover, we demonstrate that knockdown of XPR1/SLC53A1 inhibits the proliferation of OCCC cells xenografted into immunocompromised mice. These results suggest that XPR1/SLC53A1 plays a critical role in the tumorigenesis of OCCC cells. We speculate that XPR1/SLC53A1 might be a promising molecular target for the therapeutic treatment of OCCC.

2022-07-07 | GSE189552 | GEO

The phosphate exporter XPR1/SLC53A1 is required for the tumorigenicity of ovarian cancer.

Project description:The phosphate exporter XPR1/SLC53A1 is required for the tumorigenicity of ovarian cancer.

| PRJNA783541 | ENA

Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis

Project description:Thyroid hormones are important for homeostatic control of energy metabolism and body temperature. Although skeletal muscle is considered an important site for thyroid action, the contribution of thyroid hormone receptor signaling, in muscle, to whole-body energy metabolism and body temperature has not been resolved. Here, we show that thyroid hormone-induced increase in energy expenditure requires thyroid hormone receptor alpha 1 (TRa1) in skeletal muscle, but that thyroid hormone induced elevation in body temperature is independent of muscle-TRa1. In slow-twitch soleus muscle, ablation of TRa1 leads to an altered fiber type composition toward a more oxidative phenotype, which, however, does not influence running capacity or motivation to voluntary running. RNA-sequencing of soleus muscle from WT mice and TRaHSACre mice revealed differentiated transcriptional regulation of genes associated with muscle thermogenesis, such as sarcolipin and UCP3, thus providing molecular clues pertaining to the mechanistic underpinnings of TRa1-linked control of whole-body metabolic rate. Together, this work establishes a fundamental role for skeletal muscle in thyroid hormone-stimulated increase in whole-body energy expenditure.

2020-09-21 | GSE146336 | GEO

GNPS - Maternal thyroid hormone receptor beta activation sparks brown fat thermogenesis in the offspring

Project description:Metabolomics dataset of serum from T3-treated dams. Related to following publication by Oelkrug et al: "Maternal thyroid hormone receptor beta activation sparks brown fat thermogenesis in the offspring"

2023-01-11 | MSV000091042 | GNPS

Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis

Project description:Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis

| PRJNA610173 | ENA

Thyroid RDC8 versus C57Bl6

Project description:Mutations of the thyrotropin receptor leading to constitutive activation of the cAMP cascade are responsible for the development of hot nodules, if arising in a somatic cell, and non-auto-immune hyperthyroidism, when occurring in a germinal cell. An animal model of constitutive activation of the thyroid cAMP cascade has been obtained by generating transgenic mice expressing the adenosine receptor (Tg-A2aR) under the control of the thyroglobulin promoter. These mice develop huge goiters and die prematurely due to hyperthyroidism induced cardiac failure. To identify new genes involved in the tumorigenic pathway of the thyroid, we designed a protocol using microarray technology to study the differential expression, between normal and transgenic thyroid, of +/- 13.000 genes. 360 genes or EST showed a strong modulation with background corrected values of fluorescence superior to 2 fold change. The modulated genes were classified according to their proposed gene ontology functions. Approximately half of them were upregulated. The function of the majority of these genes in thyroid physiology is still to be determined. Some of them, like IGF-I, IGF-BP3, IGF-BP5, may play an important role in the development of thyroid nodules through paracrine mechanisms. Keywords = Thyroid Keywords = Adenosine Receptor 2a Keywords: parallel sample

2003-11-25 | GSE773 | GEO

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

Thyroid C57Bl6 versus RDC8 (Color Flip)

2003-11-25 | GSE774 | GEO