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)
- 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 - The incidence of ulcerative colitis (UC) and obesity has risen in recent years, potentially linked through metabolic dysregulation and chronic inflammation. The nuclear receptor NR1D1 is pivotal in regulating circadian rhythms and plays a significant role in inflammation and metabolism. This study investigates the therapeutic effects and mechanisms of the NR1D1 agonist SR9009 on obesity-related UC. - Source: PubMed
Publication date: 2026/07/23
Zheng ZhixueCai XuanLiu YaqiBi Jingtao - By integrating transcriptomics and network pharmacology, we systematically investigated the potential hemostatic mechanism of (BS). - Source: PubMed
Yang TaoXiong YanYang LingWang Xing-GangHuang YongFu Zhi-Li - Rheumatoid arthritis (RA) is a persistent systemic disorder of autoimmune origin, with its core pathological manifestation being inflammation of the synovial tissue. The excessive growth of fibroblast-like synoviocytes (FLS) represents a critical pathological mechanism in RA, actively driving the advancement of the condition. Dictamnus dasycarpus Turcz. (D. dasycarpus) exhibits prominent anti-inflammatory effects and shows favorable therapeutic efficacy against RA. Dictamnine (Dic) is a major active component of D. dasycarpus, however, its therapeutic effectiveness and underlying mechanisms in RA have yet to be fully elucidated. This study investigated the effect of Dic on synovial hyperplasia in RA and elucidated the underlying mechanisms. Using a TNF-α-induced human fibroblast-like synoviocyte (HFLS-RA) model and a collagen-induced arthritis (CIA) mouse model, Dic was found to effectively inhibit synovial cell proliferation and pathological hyperplasia. Proteomics analysis was employed to clarify its potential mechanism in ameliorating the disease, and the findings were further validated through hematoxylin and eosin (H&E) staining, immunofluorescence (IF), ROS detection, JC-1 staining, cellular thermal shift assay (CETSA), drug affinity responsive target stability (DARTS) analysis, quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting (WB). The results suggested that the anti-RA activity of Dic is associated with its interaction with the nuclear receptor NR1D1. Moreover, the NR1D1 antagonist SR8278 reversed Dic's effects on Nrf2 and cytoprotection, confirming that Dic functions through NR1D1. This activation consequently influences the Keap1/Nrf2/ARE cascade, leading to decreased intracellular reactive oxygen species (ROS) accumulation and an improvement in compromised mitochondrial membrane potential. siRNA knockdown experiments further confirmed that NR1D1 is a target of Dic and regulates the downstream Keap1/Nrf2/HO-1 signaling pathway, through which Dic ameliorates RA both in vitro and in vivo by upregulating NR1D1 expression to activate the Keap1/Nrf2/ARE antioxidant pathway, thereby mitigating oxidative stress, inhibiting synovial cell proliferation, and ultimately alleviating pathological synovial hyperplasia. - Source: PubMed
Publication date: 2026/07/26
Wang YueGuan WeiZhuang Lei-XinHao Zhi-ChaoChen Qing-ShanZhang Li-LiLiu ShuKuang Hai-XueHuang Li-LiLiu Yan