NR1D1 Antibody (monoclonal) (M05)
- Known as:
- NR1D1 Antibody (mab) (M05)
- Catalog number:
- AT3094a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- NR1D1 Antibody (monoclonal) (M05)
Related genes to: NR1D1 Antibody (monoclonal) (M05)
- Gene:
- GATAD1 NIH gene
- Name:
- GATA zinc finger domain containing 1
- Previous symbol:
- -
- Synonyms:
- ODAG, RG083M05.2, FLJ22489
- Chromosome:
- 7q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-31
- Date modifiied:
- 2019-04-23
- Gene:
- LRRC17 NIH gene
- Name:
- leucine rich repeat containing 17
- Previous symbol:
- -
- Synonyms:
- P37NB, H_RG318M05.3
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-08-07
- Date modifiied:
- 2014-11-18
- 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
- Gene:
- TJP1 NIH gene
- Name:
- tight junction protein 1
- Previous symbol:
- -
- Synonyms:
- ZO-1, MGC133289, DKFZp686M05161
- Chromosome:
- 15q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-04-26
- Date modifiied:
- 2016-10-05
Related products to: NR1D1 Antibody (monoclonal) (M05)
Related articles to: NR1D1 Antibody (monoclonal) (M05)
- Rhodiola crenulata (Hook. f. et Thoms.) H. Ohba is a traditional Tibetan medicine that has long been used in China for its cardioprotective, Qi-tonifying, and mind-calming properties. It is traditionally indicated for conditions such as irritability, restlessness, and agitation. Among its major active constituents are two naturally occurring small-molecule phenols-salidroside (SAL) and its aglycone tyrosol (TYR). While SAL has been reported to exert neuropsychiatric effects including anxiolytic activity, the underlying mechanisms remain incompletely understood, and whether TYR shares similar anxiolytic properties has yet to be clarified. - Source: PubMed
Publication date: 2026/08/19
Cui JunboJia ChunxueWang ZixinSun YuhanLiang YuluLiu ChuanxinHuang Jianmei - Succinate (SUC), a dietary feed additive, is known to influence muscle fiber structure and lipid metabolism, thereby enhancing meat quality in livestock. This study evaluated the effects of SUC supplementation on growth performance, meat quality, muscle fiber morphology, and transcriptomic profiles of the liver and longissimus thoracis (LT) muscle in Tan sheep. Thirty 5-month-old male Tan sheep (31.48 ± 0.25 kg) were randomly allocated to three dietary treatments ( = 10 per group): control (CON) group (basal diet), SUC1 group (basal diet + 1.0% SUC), and SUC2 group (basal diet + 2.0% SUC). The trial lasted for 60 d. During d 1 to 15, adding SUC to the diet linearly increased average daily gain (ADG) ( = 0.003) and dry matter intake (DMI) ( < 0.001). During d 46 to 60, both ADG ( = 0.002) and DMI ( < 0.001) increased linearly. Over the overall period, DMI increased linearly ( < 0.001), and the feed to gain ratio (F/G) decreased linearly ( < 0.001). Carcass weight ( < 0.001) and dressing percentage ( = 0.004) increased linearly with SUC inclusion. Meat quality improved in both SUC groups, with significantly lower shear force ( = 0.004) and cooking loss ( < 0.001), and higher intramuscular fat (IMF) ( = 0.004) content and LT redness (a∗) value ( = 0.036). Succinate supplementation reduced muscle fiber diameter and cross-sectional area of type I and IIa fibers, while increasing type I and IIa fiber density ( < 0.05). Transcriptomic analyses revealed that SUC altered the expression of genes involved in muscle development, fiber-type transition, lipid metabolism, and circadian rhythm in both liver and LT tissues. Notably, the circadian rhythm pathway was enriched in both tissues, with differential expression of , , and . Molecular docking demonstrated strong binding affinity of SUC to NPAS2 via stable hydrogen bonding, suggesting regulatory roles in circadian and muscle-related pathways. In conclusion, dietary SUC promotes metabolic and muscular adaptations in Tan sheep, improving feed efficiency and meat quality. Under the conditions of this experiment, considering growth performance, feed efficiency, and meat quality, a 1% dietary inclusion of SUC appears to be a practical optimum. - Source: PubMed
Publication date: 2026/07/03
Ren WenyiZhang NingCheng YuchenYang ShuangmingLiu XiaonvLiu MiaoKong WeihaoXu XiaofengZhang Lili - Calcium oxalate (CaOx) kidney stone disease is common and highly recurrent, but the upstream mechanisms that predispose renal tubules to crystal deposition remain unclear. This study investigated whether disruption of environmental light-dark cycles promotes CaOx crystal deposition through NR1D1-dependent metabolic and redox regulation. Mouse models of light-cycle disruption were established with or without glyoxylate-induced hyperoxaluria, and NR1D1-deficient mice were used for in vivo validation. Oxalate-injured HK-2 cells were used for pharmacological and genetic experiments. Transcriptomics, histology, biochemical assays, ROS and mitochondrial membrane potential analyses, crystal adhesion assays, ChIP-qPCR, and dual-luciferase reporter assays were performed. Disrupted lighting conditions promoted renal CaOx crystal deposition and further exacerbated glyoxylate-induced crystal accumulation, accompanied by tubular injury, oxidative stress, reduced antioxidant capacity, and altered circulating insulin and melatonin levels. NR1D1 expression was suppressed, whereas IRS1 signaling and crystal adhesion-related proteins were increased. SR9009 treatment and NR1D1 overexpression alleviated oxalate-induced mitochondrial dysfunction, ROS accumulation, and crystal adhesion, whereas NR1D1 deficiency aggravated renal injury in vivo. Mechanistically, NR1D1 directly bound the IRS1 promoter and repressed IRS1 transcription, thereby preserving FOXO1/GPX4-mediated antioxidant defense. These findings identify an NR1D1-IRS1-FOXO1/GPX4 axis linking light-cycle disruption and circadian-associated dysregulation to oxidative tubular injury and CaOx crystal deposition. - Source: PubMed
Publication date: 2026/08/14
Gao ShunyuHuang KeWan SichengWang JiaWang JiahaoBai Yunjin - Germline deletion of the core circadian transcription factor Bmal1 has been shown to reduce blood-spinal cord barrier (BSCB) disruption and tissue loss following moderate T9 contusive spinal cord injury (SCI) in mice. Therefore, effects of conditional Bmal1 deletions were tested using the same model. A strong reduction of Bmal1 expression in the brain or spinal cord followed tamoxifen treatment of Bmal1 young adult mice who carried the broadly expressed Cag-CreERT2 recombinase transgene. Supporting functional consequences of such a deficit, canonical BMAL1 target genes Nr1d1 and Dbp were also downregulated. However, only few tissue damage markers were moderately reduced at 3 days post SCI. Furthermore, neither locomotor recovery nor long-term white matter sparing was improved. Similar SCI phenotype was observed in endothelia-selective Bmal1 mice (Cdh5-Cre:Bmal1) including modest attenuation of few acute injury markers, but no significant effects on functional recovery or long-term tissue sparing. These data suggest that germline deletion of Bmal1 is protective against SCI due to compensatory changes in gene expression that originate during development and involve cells beyond endothelia. Therefore, a direct role for BMAL1 in secondary injury cascades that are activated after SCI is unlikely. - Source: PubMed
Publication date: 2026/08/11
Slomnicki Lukasz PArmstrong Christine DMorehouse Johnny RAndres KarienaMusiek Erik SOhri Sujata SaraswatHetman Michal - Targeting iron-dependent ferroptosis represents a promising strategy to limit myocardial infarction (MI) injury. Wang et al. recently demonstrated that silencing the circadian receptor NR1D2 (REV-ERBβ) preserves ischemic myocardium by activating the Nrf2/GPX4 antioxidant axis. While their mechanistic rigor is commendable, translating NR1D2 modulation to the clinic reveals a pharmacological paradox. Prior studies show that NR1D2 agonists also prevent post-MI heart failure via metabolic remodeling, contrasting with the benefits of NR1D2 inhibition reported here. We argue this discrepancy hinges on temporal specificity: acute knockdown likely halts immediate ferroptotic damage and subsequent DAMP-driven sterile inflammation, whereas subacute agonism supports metabolic recovery. Moving beyond the bench, systemic Nrf2 hyperactivation poses oncogenic risks, and compensatory NR1D1 upregulation may undermine long-term efficacy. Consequently, realizing the therapeutic potential of the NR1D2/Nrf2 axis requires mapping its dynamic post-MI expression to define exact intervention windows, alongside engineering cardiac-homing nanocarriers to bypass systemic toxicity and ensure precise myocardial salvage. - Source: PubMed
Publication date: 2026/08/11
Zhao Minxia