NR1D1
- Known as:
- NR1D1
- Catalog number:
- GTX71891
- Product Quantity:
- 25 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- NR1D1
Related genes to: NR1D1
- 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
Related articles to: NR1D1
- Chronic kidney disease (CKD) affect about 10% of adults worldwide, with dyslipidemia being a common feature. Abnormalities in renal lipid metabolism have been strongly implicated in CKD progression; however, the mechanisms by which CKD leads to lipid metabolism disturbances remain underexplored. Here we show that following the accumulation of uremic toxins, the synthesis and deposition of lipids, along with the uremic toxin receptor aryl hydrocarbon receptor (AhR), are upregulated in the kidneys. Tubule-specific AhR knockout in male mice alleviates uremic toxin-induced increases in renal fatty acid (FA) synthesis, lipid accumulation and fibrosis. Immunoprecipitation‒mass spectrometry identifies nuclear receptor subfamily 1 group D member 1 (NR1D1) as an AhR-interacting protein. Co-immunoprecipitation confirms that AhR interacts with NR1D1 and promotes its ubiquitin-mediated degradation. As NR1D1 is an FA synthesis suppressor, its reduction relieves the transcriptional repressing effects on sterol regulatory element-binding protein 1 (SREBP1), thereby enhancing SREBP1/fatty acid synthase (FASN) pathway activity and FA synthesis. In summary, by acting on AhR, the accumulation of uremic toxins may accelerate renal fibrosis via the SREBP1/FASN pathway-mediated increase in FA synthesis. - Source: PubMed
Publication date: 2026/07/10
Xie HongyanZhang YitaoLu LiGuo HengjiangSun Xi'angNing MingXie XinLi LuxinNiu YangyangLi JingyaoWang XinWu LehaoZhou LiZhang WeiZhang YingyingXu ChenLu LiminYu Chen - Astrocyte reactivity is a hallmark of neuroinflammatory diseases. Astrocytes contain functional circadian clocks that drive daily homeostatic rhythms, making them potential regulators of the transition from homeostatic to reactive states. However, it remains unclear whether neuroinflammatory conditions alter endogenous astrocyte clocks and whether these clock alterations contribute to pathway changes associated with reactivity. Here, we combined in vivo and in vitro lipopolysaccharide (LPS)-based neuroinflammation models with circadian profiling, chromatin analysis, and bulk RNA-sequencing of purified microglia and astrocytes. In vivo and in vitro, neuroinflammation reduced the amplitude of Bmal1 and Per1 rhythms and changed clock gene expression patterns across circadian time, while reactive markers gained rhythmic expression. In vitro, these clock changes occurred in astrocytes exposed to the inflammatory glial environment, but not after direct LPS treatment, indicating that paracrine glial signaling is the main driver. RNA-sequencing of microglia from the same neuroinflammatory glial cultures identified Il1b and Tnf as strong candidate mediators, and combined IL-1β/TNFα treatment was sufficient to suppress astrocyte clock gene expression and induce reactive marker expression. This clock suppression was accompanied by a modest reduction in BMAL1 protein but a stronger reduction in average BMAL1 occupancy at multiple clock target loci, including Per1 and Nr1d1. To define BMAL1-dependent pathways in astrocytes, we compared gene expression in wild-type and Bmal1-deficient astrocytes, and then compared these changes with those observed under neuroinflammatory conditions. Bmal1 loss alone did not reproduce the full inflammatory response. Instead, it identified a selective subset of the reactive astrocyte transcriptome, mainly involving suppression of cell-cycle and chromosome-segregation pathways with limited innate immune activation. Together, these findings identify astrocytic BMAL1 as a regulator of a selective pathway subset within reactive astrocytes in response to neuroinflammatory conditions. - Source: PubMed
Publication date: 2026/07/08
Meng XingqiChoi Ming HoZhang XuebingKim Jin Young - 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