NR1D1 (Human) Recombinant Protein (P01)
- Known as:
- NR1D1 (Human) Recombinant Protein (P01)
- Catalog number:
- H00009572-P01-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- NR1D1 (Human) Recombinant Protein (P01)
Related genes to: NR1D1 (Human) Recombinant Protein (P01)
- Gene:
- BZW2 NIH gene
- Name:
- basic leucine zipper and W2 domains 2
- Previous symbol:
- -
- Synonyms:
- HSPC028, MST017, MSTP017
- Chromosome:
- 7p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-05
- Date modifiied:
- 2016-10-05
- Gene:
- C2CD3 NIH gene
- Name:
- C2 calcium dependent domain containing 3
- Previous symbol:
- -
- Synonyms:
- DKFZP586P0123
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 2007-10-17
- Date modifiied:
- 2016-06-08
- Gene:
- MBTD1 NIH gene
- Name:
- mbt domain containing 1
- Previous symbol:
- -
- Synonyms:
- SA49P01, FLJ20055
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-15
- Date modifiied:
- 2015-04-21
- 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:
- TMEM63C NIH gene
- Name:
- transmembrane protein 63C
- Previous symbol:
- C14orf171
- Synonyms:
- DKFZp434P0111, CSC1, hsCSC1
- Chromosome:
- 14q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-10
- Date modifiied:
- 2017-10-17
Related products to: NR1D1 (Human) Recombinant Protein (P01)
Related articles to: NR1D1 (Human) Recombinant Protein (P01)
- Chronic spontaneous urticaria (CSU) involves mast cells and multiple immune pathways, yet mechanisms sustaining disease chronicity remain incompletely defined. - Source: PubMed
Publication date: 2026/04/21
Abboud AlexiaOsakwe AdrienMartinez-Jaramillo ElvisKhoury LaurenVu DonChergui MayLefrançois PhilippeXu LiqinBen-Shoshan MosheOsman MohamedGiménez-Arnau Ana MariaLi YueNetchiporouk Elena - Diabetic wounds resent a considerable clinical challenge due to impaired healing, which results from persistent inflammation and dysregulated macrophage polarization. This study identifies CITED2 as a critical regulator of diabetic wound repair, primarily through its role in modulating macrophage plasticity. We demonstrate that CITED2 exhibits phase-specific expression during normal wound healing, and its downregulation in diabetic wounds disrupts the transition from M1 to M2 macrophages. Local administration of recombinant CITED2 protein accelerates wound closure by promoting the shift of macrophages toward the anti-inflammatory M2 phenotype, thereby enhancing re-epithelialization, collagen deposition, and angiogenesis. Transcriptomic analysis reveals that CITED2 potentially mediates the activation of PPAR-γ signaling and the upregulation of anti-inflammatory genes. Further immunofluorescence analysis of wound tissues shows an upregulation of anti-inflammatory genes (IL10, Gpnmb, and Nr1d1) and a downregulation of pro-inflammatory genes (IL-6, IL-1β, and TNF-α). Additionally, in vitro experiments indicate that conditioned medium from CITED2-treated macrophages significantly enhances the proliferation and migration capabilities of endothelial cells and fibroblasts. Notably, short-term CITED2 treatment (3 days) achieves comparable efficacy to a 14-day rhFGF therapy. To facilitate clinical translation, we developed a fibrin-thrombin-PEG hydrogel spray (Fib-Thr-PEG-CITED2) that exhibits favorable anti-inflammatory and hemostatic properties, along with demonstrated biosafety. In diabetic mouse wounds, the Fib-Thr-PEG-CITED2 hydrogel spray shows superior wound healing effects compared to CITED2 alone or Fib-Thr-PEG controls. These findings establish CITED2 as a novel therapeutic target and the Fib-Thr-PEG-CITED2 hydrogel as a potential strategy for diabetic wound management. - Source: PubMed
Publication date: 2026/07/11
Jian XichaoShao JingjieTang ShihanHu XingHe QiWei MiaomiaoDeng YapingZhou YanXiao ShuneQi FangDeng Chengliang - Obstructive sleep apnea is characterized by recurrent intermittent hypoxia (IH), which contributes to neuroinflammation and neurological dysfunction. Microglia are pivotal regulators of inflammatory responses in the central nervous system, but the molecular mechanisms underlying IH-induced microglial activation remain unclear. This study aimed to identify key genes mediating this phenomenon and to elucidate their functional significance. An IH model was established in BV2 cells, with inflammation assessed via western blot for cyclooxygenase-2 (COX2) /inducible nitric oxide synthase (iNOS) and ELISA for Interleukin-6 (IL-6) /Tumour necrosis factor-alpha (TNF-α). RNA sequencing was performed to profile transcriptional changes induced by IH. Differential expression analysis, functional enrichment analysis, protein interaction network analysis, transcription factor prediction, and machine learning-based screening were integrated to identify candidate key genes. Pharmacological modulation of Nr1d1 was then performed to evaluate its role in IH-induced inflammation. IH significantly increased COX2, iNOS, IL-6 and TNF-α levels in BV2 cells. Transcriptomics showed distinct profiles between control and IH groups. Enrichment analyses linked IH-related genes to immune regulation, stress responses, and metabolic pathways. Network analysis highlighted a circadian gene cluster as a prominent component of the IH-responsive transcriptional network. Integrated network and machine learning analyses further identified Nr1d1 as a key candidate. Pharmacological experiments showed that inhibition of Nr1d1 attenuated IH-induced inflammatory responses. IH induces pronounced inflammatory activation and transcriptional reprogramming in BV2 cells. Nr1d1 may represent a circadian-associated candidate regulator involved in IH-induced microglial inflammatory activation. - Source: PubMed
Publication date: 2026/07/11
Sun ZhuoranShen TengqunLi MengfanZhang JinbiaoLi ZhenguangMa Fangzhou - 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