RXRg
- Known as:
- RXRg
- Catalog number:
- 000467A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- RXRg
Related genes to: RXRg
- Gene:
- RXRG NIH gene
- Name:
- retinoid X receptor gamma
- Previous symbol:
- -
- Synonyms:
- NR2B3
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-11-14
- Date modifiied:
- 2016-10-05
Related products to: RXRg
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- This exploratory, hypothesis-generating study aimed to investigate methylation differences in 16 angiogenesis- and fibrosis-related genes across diabetic retinopathy (DR) stages and proliferative diabetic retinopathy (PDR) subtypes (Florid and Gliotic), and to identify potential epigenetic biomarkers for disease progression. - Source: PubMed
Publication date: 2026/03/25
Ren XiaotongCui LijinYao YaoQiu YuzheYu ChenyueGuo Jian - Overcoming remyelination failure is one of the main targets in therapeutic strategies for multiple sclerosis. This process requires the differentiation of oligodendrocyte precursor cells (OPCs) to mature myelinating oligodendrocytes (OLs), a process known to be controlled by thyroid hormone, nuclear receptors, and sonic hedgehog (SHH). Retinoid X receptor gamma (RXRg) is one of the nuclear receptors acting as a positive regulator of remyelination, but little is known about its mechanisms of function. Using transcriptomic and pharmacological analysis of primary neural stem cell-derived OPCs, we show that RXRg is involved in the induction of the thyroid hormone-driven differentiation process and in refining it toward an oligodendrogenic cell fate. RXRg also emerged as an important negative modulator of SHH expression and signaling, as Shh and additional genes from this pathway were found to be strongly upregulated in Rxrg OPCs. An inhibition of SHH signaling by cyclopamine or GANT61 entirely normalized the differentiation deficit of Rxrg OPCs, but also myelination of newly generated Rxrg OLs. Such data indicate a key role of SHH hyperactivity in the oligodendrogenesis block associated with the absence of RXRg. Importantly, hyperactivation of the SHH pathway by purmorphamine or SAG inhibited the oligodendrogenesis and myelination potential of wild-type OPCs, indicating that SHH hyperactivity can also be a sufficient factor to block OPC differentiation. These results point to RXRg as an important regulator of SHH pathway signaling and underline the need of an optimal, fine-tuning of SHH signaling to assure successful oligodendrogenesis. - Source: PubMed
Baldassarro Vito AntonioBrassart QuentinFraulob ValérieCalzà LauraKrezel Wojciech - Eggshell strength is a critical economic trait that declines with hen age, yet the molecular mechanisms distinguishing stable genetic determinants from age-responsive pathways remain unclear. This study implemented a multi-stage comparative framework using uterine transcriptomes from Rhode Island Red hens at peak lay (60 weeks) and late lay (90 weeks) to address this question. At each age, hens were stratified into Weak and Strong shell strength groups based on longitudinal records (5 time points for the 90-week cohort), with 5 individuals per group selected for RNA-seq analysis. Uterine transcriptomic analysis revealed a conserved core of 86 differentially expressed genes associated with shell strength at both ages, with 96.5% exhibiting concordant regulation direction and highly correlated fold-changes (r = 0.84). Weighted gene co-expression network analysis identified two pivotal modules: a stable intrinsic module (MElightcyan) at 60 weeks correlated with peak-lay strength, and an aging-amplified module (MEyellow) at 90 weeks whose correlation with strength progressively increased from mid- to late lay (r = 0.57 at 40 weeks to 0.72 at 90 weeks). Functionally, enriched pathways shifted from cellular structure (MElightcyan) to calcium signaling and hormone regulation (MEyellow) with age. Transcriptional network analysis identified 8 conserved transcription factors (including SATB1 and RXRG) orchestrating this core program. Integrative analysis prioritizing differential expression, longitudinal phenotypic correlation, and QTL mapping highlighted high-confidence candidate genes, including CNTNAP5 (peak-lay) and SLCO1C1 (late-lay). We propose a two-tiered regulatory model wherein a stable core genetic program interacts with dynamic, age-adapted effector networks to determine shell strength. This model provides a dual-strategy framework, distinguishing targets for genetic selection (core program) from pathways for precision management (age-adapted networks) to mitigate age-related decline in shell quality. - Source: PubMed
Publication date: 2026/03/18
Wang LiyuanLiu LeiBai YingWang YanhengZheng ChuanweiWang JinweiChang ShiminMao ZhiqiongLiu XiaohuiGao Yahui - Neurons exert a pivotal role in the preservation of cardiac physiological function. However, there is a lack of explanation about the mechanism of cardiac neurons in the pathogenesis of cardiac dysfunction. Here, we generated a cardiac neuron landscape including 11,026 neuronal cells based on the integration of published single-nucleus RNA sequencing data from 75 patients with heart failure and 45 healthy donors. We determined ten distinct neuronal cell subsets differing in abundances, compositions, and biological functions in the heart. In particular, N4-ALK neurons were significantly enriched in failing hearts relative to healthy controls, and their abundance was associated with the response to left ventricular assist device implantation. RXRG, a transcription factor highly expressed in neuronal cells, participated in the transcriptional regulatory network of N4-ALK neurons and showed a positive correlation with the expression of their marker genes. Notably, in heart failure, the PTN-PTPRZ1 axis mediated specific crosstalk between cardiac fibroblasts and N4-ALK neurons. Finally, we used N4-ALK-related features to develop an optimized prediction model for identifying individuals with heart failure. Overall, our integrative cardiac neuron atlas comprehensively characterizes the molecular and functional diversity of neuronal cells, providing a new perspective for further exploration of the regulatory function of neurons in heart failure. - Source: PubMed
Publication date: 2026/03/20
Zhuang ShupingYang XiuqiZhang NanLiu JiangQiLiu KaidongHan HuimingZhai SongmeiLiu MingyueLiang HaihaiGu YunyanLu Yanjie - Evolutionary adaptation to diurnal vision in ground squirrels has led to the development of a cone-dominant retina, in stark contrast to the rod-dominant retinas of most mammals. The molecular mechanisms driving this shift remain largely unexplored. Here, we perform single-cell RNA sequencing and chromatin accessibility profiling (scATAC-Seq) across developmental retinal neurogenesis in the 13-lined ground squirrel (13LGS) to uncover the regulatory basis of this adaptation. We find that 13LGS cone photoreceptors arise not only from early-stage neurogenic progenitors, as seen in rod-dominant species like mice, but also from late-stage neurogenic progenitors. This extended period of cone generation is driven by a heterochronic shift in transcription factor expression, with cone-promoting factors such as , , and remaining active in late-stage progenitors, and factors that promote cone differentiation such as , , and expressed precociously in late-stage neurogenic progenitors. Functional analyses reveal that and are sufficient to promote cone and repress rod photoreceptor-specific gene expression and act through species-specific regulatory elements that drive their expression in late-stage progenitors. These results demonstrate that modifications to gene regulatory networks underlie the development of cone-dominant retinas and provide insight into mechanisms of sensory adaptation and potential strategies for cone photoreceptor regeneration in vision disorders. - Source: PubMed
Publication date: 2026/02/06
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