NR1D1 Antibody (monoclonal) (M02)
- Known as:
- NR1D1 Antibody (mab) (M02)
- Catalog number:
- AT3093a
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- NR1D1 Antibody (monoclonal) (M02)
Related genes to: NR1D1 Antibody (monoclonal) (M02)
- Gene:
- EMC10 NIH gene
- Name:
- ER membrane protein complex subunit 10
- Previous symbol:
- C19orf63
- Synonyms:
- INM02, HSS1, HSM1
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2007-07-17
- Date modifiied:
- 2016-12-01
- Gene:
- MRPL1 NIH gene
- Name:
- mitochondrial ribosomal protein L1
- Previous symbol:
- -
- Synonyms:
- BM022
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-28
- Date modifiied:
- 2015-08-25
- 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:
- PMS2 NIH gene
- Name:
- PMS1 homolog 2, mismatch repair system component
- Previous symbol:
- PMSL2
- Synonyms:
- H_DJ0042M02.9, HNPCC4, MLH4
- Chromosome:
- 7p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-13
- Date modifiied:
- 2019-04-23
- Gene:
- SESN2 NIH gene
- Name:
- sestrin 2
- Previous symbol:
- -
- Synonyms:
- SES2, DKFZp761M0212, HI95, SEST2
- Chromosome:
- 1p35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-03
- Date modifiied:
- 2016-10-05
Related products to: NR1D1 Antibody (monoclonal) (M02)
Related articles to: NR1D1 Antibody (monoclonal) (M02)
- Adipocyte lipid metabolism is coordinated by circadian rhythms, diet, and environmental temperature, but how these diverse signals are molecularly integrated remains unknown. We showed that these cues converge on the orphan mitochondrial transporter SLC25A34 to orchestrate lipid cycling. During the sleep phase, the adipocyte clock suppresses expression through the REV-ERB transcriptional repressors. Entering the active phase, consuming lipid-rich diets, or exposure to cold abolishes REV-ERB repression, and lipolytic signals stimulate transcription through the peroxisome proliferator-activated receptors. SLC25A34 is proposed to import oxaloacetate into mitochondria, dually supporting the tricarboxylic acid cycle and cytosolic acetyl-coenzyme A (acetyl-CoA) production. Elevated cytosolic acetyl-CoA then fuels the synthesis of lipids and promotes the transcription of genes enhancing mitochondrial oxidation. Thus, SLC25A34 confers circadian, dietary, and temperature control of adipocyte lipid metabolism. - Source: PubMed
Publication date: 2026/10/01
Karavaeva IuliiaBasse Astrid LindeTrammell Samuel A JHussain Mohammed FaizMarkussen Lasse KruseHavelund Jesper FIsidor Marie SophieChatoff AdamAndress Huacachino AndreaRichter Hannah JBirla MeghnaChubanava SabinaDeleye YannArianti RiniTandio DavidUtzon Sarah EKaiser ZafirShen YachenNeess DitteEmbring HannesMenon DilipConway Olivia JSass FrederikeFinger FabianArgemi-Muntadas LidiaMa TaoSustarsic Elahu GKristensen Cecilie KyndingMcIntyre Rebecca LMartinez Genesee JHusted Anna SofieEmmett Matthew JKipp Zachary AFrost MikkelJedrychowski Mark Pvan Weeghel MichelMajd HomaZhuravleva EkaterinaMcGarrah Robert WPlucińska KajaMidha Mohit KProkesch AndreasCohen PaulGranneman James GSeale PatrickHoutkooper Riekelt HHansen Jacob BGygi Steven PSchwartz Thue WGillum Matthew PHinds Terry DSoccio Raymond EWhite Phillip JKunji Edmund R SMoritz ThomasTreebak Jonas TKristóf EndreMandrup SusanneEmanuelli BriceSnyder Nathaniel WFazakerley Daniel JKazak LawrenceFærgeman Nils JLazar Mitchell AGerhart-Hines Zachary - Kidney metabolism and physiology exhibit circadian oscillations, which are governed by the internal circadian clock. Intracellular lipid accumulation is known to play a critical role in the pathogenesis of kidney fibrosis. However, whether and how circadian disruption accelerates the progression of kidney fibrosis remains poorly understood. - Source: PubMed
Publication date: 2026/09/28
Wang Xiao-LanCheng JiaZhu YutingXiang HuilingYuan QianMeng XianfangZhang Chun - Sleep and circadian disturbances are common in neurodevelopmental conditions, yet the developmental cortical programs linking clock-related transcriptional regulators to disease vulnerability remain unclear. Here, we integrated human developmental brain transcriptomes, weighted gene co-expression network analysis (WGCNA), human and mouse cortical single-cell atlases, prenatal immune activation transcriptomes, and ASD postmortem brain datasets to characterize the developmental architecture of BrainSpan-derived cortical programs and examine their behavior in perturbational and disease contexts. In the BrainSpan frontal cortex, canonical clock-related genes followed structured but heterogeneous developmental trajectories rather than behaving as a coordinated oscillator-like unit. WGCNA identified a postnatal-rising BrainSpan-derived primary developmental module that was strongly associated with developmental age and enriched for synaptic signaling, neurotransmitter transport, ion transport, membrane excitability, cellular respiration, metabolic regulation, and proteostatic processes. Network analysis placed multiple canonical clock-related and clock-regulatory genes, including NPAS2, BHLHE40, BHLHE41, PER family members, RORA, NR1D1/2, and CLOCK, within a broader neuronal and homeostatic co-expression architecture, although their module-membership strengths varied substantially. Projection onto a human cortical developmental single-cell atlas revealed a non-uniform distribution of the corrected BrainSpan-derived developmental signature, with relatively higher scores in excitatory and inhibitory neuronal populations and lower scores in neuroblast and radial glial populations. A mouse cortical developmental single-cell atlas provided a comparative view of the stage- and cell-type-dependent expression of clock-related genes and the transferred developmental signature during corticogenesis. In a Poly(I:C)-based maternal immune activation dataset, litter-aware reanalysis identified stage-resolved genome-wide transcriptional responses following E12.5 exposure. However, neither the aggregate core clock-gene expression score nor the independently transferred BrainSpan-derived developmental signature showed a significant overall treatment effect or collection-stage-by-treatment interaction, indicating that this bulk dataset provides a perturbational context rather than evidence for selective disruption of the developmental program. An exploratory region-stratified analysis of GSE28521 yielded near-null effects for the BrainSpan-derived developmental signature, with confidence intervals crossing zero across all examined regions. These ASD postmortem findings were therefore treated as a boundary assessment rather than evidence of ASD-specific convergence. Collectively, these findings position clock-related genes as components of a developmentally regulated cortical maturation program enriched for neuronal signaling, synaptic maturation, metabolic regulation, and stress-response processes. - Source: PubMed
Publication date: 2026/09/12
Wang YilinLi ShanshanJin Xin - Insulin clearance is a key determinant of circulating insulin availability, but its diurnal variation and relationship with circadian metabolic programs in metabolic dysfunction associated steatotic liver disease (MASLD) remain unclear. This study aimed to explore diurnal insulin clearance in humans and examine associated metabolic gene signatures in MASLD. - Source: PubMed
Publication date: 2026/08/29
Guo LinYin YiminSun YanyanZhou HongwenGong Yingyun - Leptin regulates metabolism and is modulated by circadian rhythms and light exposure, which is of fundamental importance for Arctic residents living under conditions of extreme photoperiods. This longitudinal study aimed to investigate the association between morning leptin, seasonal circadian light hygiene, and NR1D1 expression in 64 Arctic residents (aged 18‑54 years; 88.7% women) using 7‑day actigraphy, morning leptin and NR1D1 expression. Better circadian light hygiene, measured as normalized blue light exposure amplitude (NA BLE) was associated with lower morning leptin (β = -0.263; p < 0.001), also after adjusting for photoperiod. This association remained significant after controlling for sex, age, and ethnicity (β = -0.171). Later BLE light onset also predicted elevated leptin (β = 0.162; p = 0.031). In non-natives exclusively, reduced NR1D1 expression correlated with higher leptin (β = -0.276; p = 0.026). - Source: PubMed
Publication date: 2026/09/22
Gubin D GKolomeychuk S NBorisenkov M FPetrov I MMarkov A APetrova Yu AVoronin K AMezhakova M SBoldyreva Y VShigabaeva A U