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Nuclear orphan receptor TLX affects gene expression in pancreatic beta cells

ABSTRACT: Using Illumina’s digital gene expression (DGE) system, we investigated the transcriptional response to TLX overexpression in beta cells. Finally, an average of 13,791,918 and 12,476,623 reads of high quality clean tags were obtained from control and TLX-overexpressing beta cells, respectively. Results reveals that overexpression of TLX resulted in suppression of 176 genes by ≥50%, and also results in ≥2-fold upregulation of 49 genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE66551 | GEO | 2015/03/06

SECONDARY ACCESSION(S): PRJNA277312

REPOSITORIES: GEO

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Nuclear orphan receptor TLX affects gene expression in pancreatic beta cells

Project description:Using Illumina’s digital gene expression (DGE) system, we investigated the transcriptional response to TLX overexpression in beta cells. Finally, an average of 13,791,918 and 12,476,623 reads of high quality clean tags were obtained from control and TLX-overexpressing beta cells, respectively. Results reveals that overexpression of TLX resulted in suppression of 176 genes by ?50%, and also results in ?2-fold upregulation of 49 genes. Expression profiling of stable TLX overexpressing MIN6 cells and control cells by high throughput sequencing

2015-03-06 | E-GEOD-66551 | biostudies-arrayexpress

Tumorigenic effects of TLX over-expression in HEK 293T cells

Project description:Transcriptomic profiling to investigate the effect of TLX overexpression with an inducible vector system in the HEK 293T cell line

2021-01-21 | GSE120893 | GEO

A Gain-of-Function Genomic Screen Identifies the Orphan Nuclear Receptor TLX as an Enhancer of STAT1-mediated Transcription and Immunity to Toxoplasma gondii: TLX siRNA

Project description:The protozoan parasite Toxoplasma gondii is a highly successful intracellular pathogen, owing in part to its ability to subvert the host immune system. In particular, parasite infection suppresses STAT1 signaling in a variety of cell types, including IFN-γ activated macrophages, via a block within the nucleus. A high-throughput screen to identify genes able to overcome parasite-mediated suppression of STAT1 activity identified 9 transcription factors as enhancers of STAT1 signaling in T. gondii infected cells, including the orphan nuclear hormone receptor TLX. Expression profiling revealed that TLX is a transcriptional regulator that drives the steady-state expression of STAT1-independent genes involved brain function and development, while enhancing the output of a subset of IFN-γ-dependent target genes. Infection of TLX deficient mice with Toxoplasma results in impaired production of interleukin-12 by dendritic cells and increased parasite burden in the brain during chronic infection. These results demonstrate a previously unrecognized function for this orphan nuclear hormone receptor in regulating STAT1 signaling and host defense, and reveal that STAT1 activity can be modulated in a context-specific manner by such ‘modifiers’.

2015-05-29 | GSE55750 | GEO

A Gain-of-Function Genomic Screen Identifies the Orphan Nuclear Receptor TLX as an Enhancer of STAT1-mediated Transcription and Immunity to Toxoplasma gondii: TLX overexpression

2015-05-29 | GSE55749 | GEO

Tlx (nr2e1)-dependent gene expression in adult neural stem cells

Project description:Tlx (nr2e1) is an orphan nuclear receptor that is highly expressed in proliferating neural stem cells (NSCs) in the adult mouse forebrain. The goal was to identify Tlx-regulated genes in this specific cell population. Two populations of Tlx-positive neural stem cells were isolated from 2-month-old male mice based on a LacZ marker that was knocked into the Tlx locus. The first population, Tlx(f/Z;CreER), contains a floxed allele of Tlx (f), the LacZ marker (Z), and a CreER fusion transgene. Addition of tamoxifen (4OH-tamoxifen) into this NSC population leads to Cre-mediated deletion of the floxed allele of Tlx. The second NSC population, Tlx(f/Z), does not contain a CreER transgene; thus it does not respond to tamoxifen treatment and was used as a control. Keywords: Nuclear receptor-dependent gene expression

2008-12-01 | GSE9981 | GEO

The nuclear receptor TLX (NR2E1) inhibits growth and progression of triple-negative breast cancer

Project description:Development of targeted therapies will be a critical step towards reducing the mortality associated with triple-negative breast cancer (TNBC). To achieve this, we searched for targets that met three criteria: (1) pharmacologically targetable, (2) expressed in TNBC, and (3) expression is prognostic in TNBC patients. Since nuclear receptors have a well-defined ligand-binding domain and are thus highly amenable to small-molecule intervention, we focused on this class of protein. Our analysis identified TLX (NR2E1) as a candidate. RNA-Seq analysis revealed that TLX reduced the expression of genes implicated in the pro-proliferative KRAS signaling pathway as well as epithelial-mesenchymal transition (EMT), a cellular program known to drive metastatic progression. Indeed, TLX overexpression significantly decreased cell proliferation, migration and invasion, and robustly decreased the metastatic capacity of TNBC cells in murine models. Taken together, our work indicates that TLX retards the progression of TNBC. Several ligands have been shown to regulate the transcriptional activity of TLX, providing a framework for the future development of this receptor for therapeutic intervention.

2022-07-11 | GSE196105 | GEO

Transcription profiling of mouse Tlx-positive neural stem cells isolated from 2-month-old male to investigate Tlx (nr2e1)-dependent gene expression in adult neural stem cells

Project description:Tlx (nr2e1) is an orphan nuclear receptor that is highly expressed in proliferating neural stem cells (NSCs) in the adult mouse forebrain. The goal was to identify Tlx-regulated genes in this specific cell population. Two populations of Tlx-positive neural stem cells were isolated from 2-month-old male mice based on a LacZ marker that was knocked into the Tlx locus. The first population, Tlx(f/Z;CreER), contains a floxed allele of Tlx (f), the LacZ marker (Z), and a CreER fusion transgene. Addition of tamoxifen (4OH-tamoxifen) into this NSC population leads to Cre-mediated deletion of the floxed allele of Tlx. The second NSC population, Tlx(f/Z), does not contain a CreER transgene; thus it does not respond to tamoxifen treatment and was used as a control. Experiment Overall Design: Total RNA samples from two biological replicates were collected at 36 hr or at 60 hr after tamoxifen or vehicle treatment. Total of 16 samples were used to analyze the global gene expression changes using Affymetrix chips.

2009-01-13 | E-GEOD-9981 | biostudies-arrayexpress

Genome-wide analysis of the function of Tlx in regulating mouse brain glioma gene expression

Project description:Analysis of the function of Tlx in regulating brain tumor stem cells (BTSCs) at the gene expression level. Based on our knowledge, we know that Tlx is specifically expressed in the neural stem cells in mouse brain. It also functionally regulates neurogenesis during the postnatal stages. The hypothesis tested in the present study is that Tlx influences the maintenance and progression of mouse brain gliomas through regulating the self-renewal of BTSCs and it is also a specific marker of brain tumor stem cells (BTSCs). Results provide important information about the function of Tlx in brain gliomas. Brain gliomas were initiated from the Nestin-CreERT2;Tlx flox/flox;Nestin-Tva transgenic mouse line. After 2.5 weeks, when the brain gliomas were fully developed, tamoxifen was administered through intraperitoneal injection. Tlx was knocked-out from the Cre-expressing littermates, but the littermates without Cre expression maintained intact Tlx function. Then, total RNA was obtained from mouse brain gliomas with severe neurological symptoms from the Tlx knockout and Tlx intact groups.

2013-04-17 | E-GEOD-46125 | biostudies-arrayexpress

Genome-wide analysis of the function of Tlx in regulating mouse brain glioma gene expression

2013-04-17 | GSE46125 | GEO

Ectopic TLX expression skews lineage commitment toward a myeloid fate and promotes an inflammatory phenotype

Project description:We previously showed that the orphan nuclear hormone receptor, TLX (also known as NR2E1), selectively modifies the output of IFN-gamma-driven, STAT1-dependent gene expression. Since IFN-gamma and STAT1 are also known to regulate myeloid cell development and function, we tested whether ectopic expression of TLX or COUPTF2 (a closely related orphan nuclear receptor) might influence hematopoietic differentiation. Indeed, TLX promotes lineage commitment toward myeloid development and suppresses erythropoiesis, phenocopying IFN-gamma treatment. Moreover, TLX expression in our assay is sufficient to activate a proinflammatory transcriptional program with two hallmarks: differential regulation of STAT1-dependent genes, and suppression of an anti-inflammatory program in favor of a fatty acid signature – a process known to be essential for cellular remodeling during macrophage maturation and phagocytosis. These results demonstrate an important role for a new nuclear hormone receptor in STAT1 signaling, and link TLX to myeloid lineage commitment and function.

2016-09-21 | GSE87126 | GEO

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