Ask about this productRelated genes to: NR1D1 antibody
- 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 antibody
Related articles to: NR1D1 antibody
- Metabolic dysfunction-associated steatotic liver disease (MASLD) is closely linked to circadian rhythm disruption (CRD). While the biological clock coordinates metabolic homeostasis, the rhythmic signaling coupling lipid and bile acid metabolism remains unclear. Bupleuri Radix (BR; Bupleurum chinense DC.) is a traditional Chinese medicine widely used for liver-related disorders and known for its liver-soothing effect. However, whether its bioactive fractions can modulate the "circadian-metabolic coupling" process in MASLD has not yet been elucidated. - Source: PubMed
Publication date: 2026/04/29
Wang ShuhengBai ShuaidongZhou TianhuiWang YukunBai XueWang YimingMa JunwenQin XuemeiGao Xiaoxia - Circadian rhythms-self-sustained, ~24-h oscillations in transcript and protein levels-are generated by a cell-autonomous molecular clock. These rhythms shape how individual cells respond to external signals, influencing key decisions such as differentiation and apoptosis. However, current tools for visualizing circadian rhythms at the single-cell level often rely on genomic engineering and clonal expansion, limiting their accessibility and applicability. We present fluorescent circadian reporters based on the murine gene, delivered via lentiviral transduction and compatible with time-lapse single-cell microscopy. These reporters produce oscillatory signals that depend on a functional circadian clock and can be used to determine a cell's circadian dynamics parameters, such as circadian phase. Their simple and efficient delivery should make them suitable for a wide variety of cell types, greatly expanding opportunities to study single-cell circadian dynamics and their impact across diverse biological processes and systems. - Source: PubMed
Publication date: 2026/04/27
Gabriel Christian HLehmann LuisAhlburg JoanaKramer Achim - Glaucoma is a chronic optic neuropathy characterized by progressive vision loss. A previous study from our group showed that glaucoma-induced retinal degeneration disrupts photic signaling to the suprachiasmatic nucleus (SCN), altering the molecular components of the central circadian clock. Through its hypothalamic projections, the SCN entrains the hypothalamic-pituitary-adrenal (HPA) axis and drives the rhythmic secretion of corticosterone. In this study, we investigated whether central circadian clock disruption in glaucoma impacts the HPA axis and its downstream physiological rhythms. We analyzed the temporal profiles of key genes controlling the HPA axis in mice with glaucoma. The Crh gene expression was reduced in the paraventricular nucleus, while Crh-r1 exhibited a 10-h phase delay in the pituitary in response to glaucoma. Additionally, Pomc in the pituitary and Mc2r in the adrenal lost rhythmicity. The modulation of the daily rhythms of these key genes was associated with alterations in the diurnal rhythms of clock genes in the PVN, pituitary and adrenal gland. Glaucoma-induced phase shifts and amplitude alterations in the rhythmic expression of Per1, Per2, Nr1d1, and Bmal1 in the pituitary and adrenal gland, resulted in a temporal misalignment between the pituitary and adrenal rhythms. These molecular changes were associated with reduced corticosterone amplitude, suggesting impaired communication between central and peripheral clocks. Together, these findings demonstrate that glaucoma alters the temporal coordination of the HPA axis, highlighting how retinal dysfunction can propagate beyond the visual system to disturb systemic circadian and neuroendocrine regulation. - Source: PubMed
Barsanele Pietra Souzada Silva Juliano JeffersonCortes Bryan Fellipe da Silvade Oliveira Furtado Eliz MariaCipolla-Neto Joséde Assis Leonardo Vinícius MonteiroPoletini Maristela OliveiraMoraes Maria Nathália - Bisphenol A (BPA) is a widely existing endocrine-disrupting chemical that poses potential threats to human and animal health, including inducing metabolic disorders. Although previous studies have reported the adverse effects of BPA on liver glucose and lipid metabolism, the underlying molecular mechanisms remain incompletely elucidated. This study systematically evaluated the effects of BPA exposure on liver glucose and lipid metabolism in mouse hepatocytes (AML12) and mouse models, and detected its association with circadian clock disruption. In vitro models, BPA exposure for 24 h significantly decreased the mRNA and protein expression levels of BMAL1 in AML12 cells, while significantly up-regulating the mRNA expression of Nr1d1 and Dbp. On the contrary, the expression of Nr1d1 and Dbp decreased significantly after 48 h of BPA exposure. It is worthy to note that both mRNA and protein levels of BMAL1 were significantly increased in forskolin synchronized AML12 cells. In addition, the genes related to glucose and lipid metabolism were also detected after BPA exposure. The results showed that BPA exposure significantly increased the expression of Cd36 and Glut2 in non-synchronized AML12 cells. Meanwhile, the elevation of Hmgcr expression and the reduction of Pparα were detected in forskolin synchronized AML12 cells. In vivo models, the results showed that ICR mice exposed to BPA (50 μg kg) for 42 consecutive days exhibited impaired glucose tolerance, decreased insulin sensitivity, increased liver glycogen storage, and decreased liver triglyceride (TG) levels. Meanwhile, the mRNA expression of Nr1d1 was significantly increased in mouse liver after BPA exposure. In addition, the mRNA expression of two lipid metabolism-related genes (Srebp1c and Elovl6) was significantly decreased in mouse liver after BPA treatment, but the expression level of Cd36 was significantly increased. In conclusion, this study demonstrates that BPA exposure impairs the circadian clock system and glucose and lipid metabolism in AML12 cells and mouse liver, providing important evidence that BPA overload in the environment can lead to the incidence of metabolic disorders in mammals. This study highlights the potential regulatory role of circadian clock system in BPA induced mammalian liver metabolic disorders and suggests that BPA may pose more profound potential risks to human and animal health. - Source: PubMed
Publication date: 2026/04/16
Dong HaoDing WenliXiao BonanLi CuimeiJiang HaizhenYang WanghaoLi DanLi ChaoZhang HaisenGao DengkeWang AihuaJin YapingChen Huatao - Following extensive liver resections, diminished liver regeneration impairs the maintenance or restoration of sufficient functional liver mass. Currently, effective therapies to restore liver regeneration are lacking, rendering liver transplantation the sole treatment option for end-stage liver disease. Therefore, it is imperative to elucidate the regulatory mechanisms underlying liver regeneration. In this study, we employed a multi-omics approach integrating Hi-C, RNA-seq, and ATAC-seq to dissect the early regulatory mechanisms of liver regeneration in rats and mice. Our results indicate that immune and inflammatory processes are markedly enriched during the early phase of regeneration, accompanied by upregulation of glucocorticoids (GCs) and their receptor (GR). First, the expression dynamics of the GC-related circadian gene Nr1d1 and its regulatory network-including Nfκbiα, Arntl, Clock, and Rora-align with chromatin reorganization, leading us to propose that the GC-GR-Nr1d1 axis is involved in maintaining liver homeostasis. Second, the GR-regulated FoxO family is significantly enriched, and the FoxO-associated gene Klf2 exhibits coordinated changes in expression, chromatin accessibility, and chromatin structure. Functional experiments demonstrate that Klf2 negatively regulates hepatocyte proliferation. Hence, we propose the GC-GR-FoxOs-Klf2 axis acts as a checkpoint in hepatocyte proliferation, preventing premature activation of proliferation- and cell cycle-related genes and ensuring orderly and efficient liver regeneration. Our findings on the role of GCs in liver regeneration may further support their future therapeutic application in liver diseases such as liver fibrosis, alcoholic cirrhosis, and hepatocellular carcinoma (HCC). - Source: PubMed
Publication date: 2026/04/13
Ye BingyuXie DejianShen WenlongYue MeijuanJin QinpengGuo XinjieZhang YanLi PingZhao Zhihu