NR1D1 Pre-design Chimera RNAi
- Known as:
- NR1D1 Pre-design Chimera RNAi
- Catalog number:
- H00009572-R01
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- NR1D1 Pre-design Chimera RNAi
Related genes to: NR1D1 Pre-design Chimera RNAi
- Gene:
- NR1D1 NIH gene
- Name:
- nuclear receptor subfamily 1 group D member 1
- Previous symbol:
- THRAL
- Synonyms:
- ear-1, hRev, Rev-ErbAalpha, THRA1, REVERBA, REVERBalpha
- Chromosome:
- 17q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-16
- Date modifiied:
- 2018-02-14
Related products to: NR1D1 Pre-design Chimera RNAi
Related articles to: NR1D1 Pre-design Chimera RNAi
- Biphenotypic sinonasal sarcoma (BSNS) is a rare, low-grade spindle cell sarcoma of the sinonasal tract. It is characterized by dual neural and myogenic differentiation and classically shows fusions involving PAX3. MAML3, a co-activator in the Notch signaling pathway, is the most common fusion partner of PAX3. Here, we describe the first reported case, to our knowledge, of BSNS harboring a novel PAX3::MAML2 fusion in a polypoid lesion arising from the left ethmoid of a 61-year-old man. Microscopically, the tumor demonstrated bland spindle cell morphology. The cells were arranged in small fascicles and a vaguely whorled pattern without mitotic activity or cellular atypia. Immunohistochemistry displayed characteristic co-expression of S100 and smooth muscle actin as well as patchy nuclear positivity for beta-catenin. SOX10, AE1/AE3, EMA, and CD34 were negative. Ki-67 was expressed in less than 1% of tumor cells, consistent with a low-grade lesion. The RNA sequencing identified a novel PAX3::MAML2 fusion transcript. MAML2 fusion is commonly associated with other head and neck neoplasms, including mucoepidermoid carcinoma and NR1D1-rearranged tumors. These findings highlight the value of comprehensive fusion testing in BSNS and emphasize the evolving fusion landscape in this entity and related tumors. - Source: PubMed
Uemura MayuGoh Anna Fong NaKumar AmitQuagliotto GaryDorwal Pranav - Excessive exposure to artificial blue light has been associated with circadian disruption and metabolic disorders; however, its role in hepatic lipid metabolism under dietary stress remains poorly defined. This study investigated how blue light exposure modulates Western diet-induced nonalcoholic fatty liver disease (NAFLD) and the underlying molecular mechanisms involving the NR1D1-SIRT1 metabolic axis. Male C57BL/6J mice were fed either a control or Western diet and exposed to blue light or sham illumination for 12 weeks. Hepatic morphology was evaluated by hematoxylin-eosin and Masson's trichrome staining, whereas macrophage infiltration and expression of NR1D1 and SIRT1 were assessed by immunohistochemistry. Untargeted LC-TOFMS-based metabolomic profiling and pathway enrichment analysis were conducted to characterize global metabolic alterations across experimental groups. The results showed that blue light exposure markedly aggravated Western diet-induced hepatic steatosis, ballooning, and lobular inflammation without evidence of fibrosis. Immunohistochemical staining revealed increased F4/80 positive macrophages and downregulation of NR1D1 and SIRT1 in blue light exposed, Western diet-fed (WDBL) mice, suggesting impaired mitochondrial homeostasis. Metabolomic profiling identified 113 hepatic metabolites, revealing distinct clustering by diet and light exposure. Blue light synergistically amplified Western diet-driven accumulation of long-chain and unsaturated acylcarnitines and polyunsaturated fatty acids, indicative of incomplete β-oxidation and oxidative lipid remodeling. Pathway enrichment analysis highlighted disruptions in glycerophospholipid, sphingolipid and bile acid metabolism, accompanied by reduced antioxidant cofactors (retinol and tocopherols). In conclusion, chronic blue light exposure accelerates Western diet-induced NAFLD progression by suppressing the SIRT1-NR1D1 axis, disrupting mitochondrial lipid oxidation, and promoting redox imbalance and macrophage-mediated inflammation. These findings identify environmental blue light as a metabolic stressor that synergizes with dietary lipid overload to drive hepatic injury, offering new mechanistic insight into light-associated metabolic liver disease. - Source: PubMed
Publication date: 2026/06/26
Chang Shu-JyuanChen Wan-TzuChen Yi-TingYu SebastianYu Hsin-SuChai Chee-Yin - Obesity remains a global health concern, and personalized prevention strategies that consider genetic predispositions can enhance existing strategies. Research suggests that variation in circadian rhythm-related genes, or clock genes, may influence obesity risk, in part through effects on dietary behaviour. However, associations between single-nucleotide polymorphisms (SNPs) in clock genes and dietary outcomes remain understudied, particularly in children. Therefore, we investigated cross-sectional associations between clock gene SNPs and dietary outcomes using baseline data from 226 adults (138 females, 88 males) aged 26-50 y and 168 children (90 females, 78 males) aged 2-6 y from the Guelph Family Health Study. DNA was extracted from saliva and genotyped using the Illumina Global Diversity Array, and dietary intake was assessed using the Automated Self-Administered 24 h Dietary Assessment Tool. Nine SNPs representing 8 clock genes were selected based on prior associations with dietary and obesity-related outcomes. Generalized Estimating Equations were used to test associations, adjusted for multiple comparisons with the Benjamini-Hochberg false discovery rate (FDR) procedure. Ten nominal associations were identified ( < 0.05), and 2 remained significant after FDR correction (P < 0.05); among children, rs2314339-T () was associated with a lower percentage of energy from protein (β = -2.4%, P = 0.003) and rs11605924-A () with higher energy intake (β = 118.0 kcal, P = 0.044). Findings suggest that clock gene SNPs may influence dietary habits from early childhood. Future longitudinal and functional studies are needed to clarify whether these variants can inform precision nutrition strategies for obesity prevention. - Source: PubMed
Publication date: 2026/06/12
Ribau Zachary JSubedi SanjeenaVallis Lori AnnCoyle-Asbil Hannah JAnnis AngelaNixon MadelineHillyer LynDuncan Alison MHaines JessMa David W L - Salivary gland hypofunction is a common adverse effect in patients after radiotherapy for head and neck cancers, resulting in the dry mouth syndrome called xerostomia. Previous studies suggested that the functionality of the salivary gland is under the regulation of the circadian clock, however, the extent and scope of this regulation remains unexplored. Here, we profiled the diurnal fluctuation of gene expression in the mouse submandibular gland, and found that about 6% of the transcriptome showed rhythmic expression. We further analyzed the regulatory role of key circadian transcription factors BMAL1, NR1D1 (REV-ERBA), and DBP, which revealed a wide range of potential down-stream target genes. The circadian rhythmic transcription was disrupted upon irradiation in a process related to p53 activation and the increased production of reactive oxygen species. Modulation of the circadian clock by chemical agents including Nobiletin and SR1078 can reduce the damaging effect and improve saliva production. We propose that the salivary gland hypofunction after radiotherapy involves perturbation of the circadian rhythmic transcription, which can be partially rescued by chemical agents that improve the circadian rhythm. - Source: PubMed
Publication date: 2026/06/25
Song Shi-TingYang Kai-BinChen Xiao-QiChen Zi-YuXu Xing-ZhiZhang Guo-YiHuang ZhenYue Zhi-Cao - Emerging evidence links environmental exposures and circadian dysregulation to autism spectrum disorder (ASD), yet whether circadian phase modulates vulnerability to developmental toxicants remains unclear. Here, we investigated whether embryonic bisphenol A (BPA) exposure induces circadian phase-dependent ASD-related behavioral alterations via disruption of rhythmicity in zebrafish. In control larvae, exhibited significant circadian oscillation, whereas BPA exposure reduced expression levels and dampened oscillation amplitude. Two-way ANOVA revealed significant treatment × phase interactions in expression. Pharmacological activation of Nr1d1 partially restored rhythmic expression. Behavioral assessments conducted at defined circadian phases demonstrated a significant treatment × phase interaction in social preference. BPA-exposed larvae exhibited reduced social preference selectively at circadian time 15 (CT15), corresponding to the trough phase of expression, whereas no differences were observed at circadian time 3 (CT3). In contrast, tactile hyper-responsiveness showed a significant treatment effect but no phase interaction. BPA exposure also induced phase-dependent alterations in ASD-related genes, including and with significant treatment × phase interactions. At the molecular level, BPA increased reactive oxygen species, impaired antioxidant defense, enhanced neuroinflammatory responses, and disrupted excitatory-inhibitory balance. Several of these endpoints exhibited phase-dependent modulation and were partially attenuated by Nr1d1 activation. These findings indicate that circadian phase modulates embryonic susceptibility to BPA-induced ASD-related behavioral and molecular alterations. Disruption of nr1d1 rhythmicity may contribute to time-of-day-specific neurodevelopmental vulnerability following environmental exposure. - Source: PubMed
Publication date: 2026/05/31
Wu YingLiu JianjunChen PinyiWang XinweiWang YutingSong XiaoyaoZhang Jie