NPAS2 EMSA Probe Set
- Known as:
- NPAS2 EMSA Probe Set
- Catalog number:
- AY1129P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- NPAS2 EMSA Probe Set
Related genes to: NPAS2 EMSA Probe Set
- Gene:
- NPAS2 NIH gene
- Name:
- neuronal PAS domain protein 2
- Previous symbol:
- -
- Synonyms:
- MOP4, PASD4, bHLHe9
- Chromosome:
- 2q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-29
- Date modifiied:
- 2015-08-25
Related products to: NPAS2 EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: NPAS2 EMSA Probe Set
- This study investigated the relationship between periodontitis and metabolic dysfunction-associated steatotic liver disease (MASLD), with a specific focus on the role of Porphyromonas gingivalis peptidylarginine deiminase (PPAD) carried by P. gingivalis-derived outer membrane vesicles (OMVs) in hepatic lipid metabolism. Clinical analyses revealed a positive correlation between periodontal disease severity and the fatty liver index (OR = 6.18, 95% CI: 2.36-16.13), a predictor of MASLD. In an obese mouse model of periodontitis, P. gingivalis-induced periodontitis accelerated MASLD progression, promoted hepatic lipid accumulation and increased inflammation. Since P. gingivalis OMVs had the advantage of traveling through the blood to the liver, we found that they demonstrated liver-specific accumulation, impairing fatty acid oxidation and increasing lipid deposition in hepatocytes, when injected into MASLD model mice via the tail vein. The critical role of PPAD was confirmed using the P. gingivalis and P. gingivalis strains, from which OMVs were isolated. The results of the in vivo and in vitro experiments indicated that PPAD-enriched OMVs mediated hepatic metabolic dysregulation via suppression of the circadian regulator NPAS2 and downstream inhibition of CYP4A10 expression, revealing a previously unrecognized PPAD-liver communication pathway. These findings highlight the urgent need for effective PPAD inhibitors and a deeper understanding of the interactions of PPAD with host proteins implicated in systemic diseases, underscoring the broader health impacts of periodontal disease. - Source: PubMed
Publication date: 2026/05/09
Liu YanqingXue XiaomengLi ZhaorongGe ZimingJiang MuzhouLiu JingboPan YapingLin Li - BMAL1 is a bHLH-PAS transcription factor complex that utilizes its bHLH (basic helix-loop-helix) domains to bind E-box motifs in DNA and tandem PAS (PER-ARNT-SIM) domains to heterodimerize and interact with regulatory proteins to generate circadian rhythms. PAS domains are evolutionarily conserved modules that frequently bind small molecule ligands within buried cavities to perform sensory and signal transduction functions. CLOCK and BMAL1 PAS domains have cavities that could be leveraged to regulate the transcription factor, and consequently, the circadian clock. Using NMR spectroscopy, we identified small molecules that bind within a cavity inside the PAS-A domain of CLOCK and its paralog NPAS2, which sits at an important flexible junction in the structured core of the heterodimer. We identified a gatekeeping mutant in the core of CLOCK PAS-A that significantly decreased ligand binding affinity. High-pressure NMR studies showed that ligand binding or the gatekeeping mutant significantly stabilized the domain. Finally, we showed that ligands induced dose-dependent displacement of CLOCK:BMAL1 from DNA . Together, these data demonstrate that small molecules can regulate DNA binding by the circadian transcription factor CLOCK:BMAL1 through occupancy of a PAS domain cavity. - Source: PubMed
Publication date: 2026/04/14
Sharma DikshaBoral SoumenduWest EthenKressman McClainFranco IreneTripathi SarvindLee Hsiau-WeiAmezcua Carlos AFavaro Denize CGardner Kevin HPartch Carrie L - Background / HypothesisHeadache attacks are reported to occur with circadian rhythmicity by 2/3 of individuals with cluster headache, hinting to potential dysfunctions of the molecular clock. The aim of this study was to investigate the contribution of genetic markers in core clock genes, alone or in combinations, to the genetic risk for cluster headache.MethodsSeven markers in core clock genes and were genotyped using TaqMan qPCR in 707 individuals with cluster headache and 682 controls. Genetic data from eleven additional markers located in six other core clock genes (, , and ) was obtained from the database of the Centre for Cluster Headache at Karolinska Institutet. Genotype analysis was applied for risk analysis for combinations of up to three markers. For validation we used a cluster headache cohort from the National Hospital for Neurology and Neurosurgery, London, UK.Results and interpretationSingle marker analysis of the newly genotyped markers in and found rs3789327 and rs3768984 more frequently among individuals with cluster headache (p < 0.01 and p < 0.05 respectively). Multiallelic analysis revealed that the median number of risk alleles was eight for controls and nine for individuals with cluster headache, which justifies the analysis of combinations of markers. The analysis of combinations of up to three markers identified 258 out of 897 combinations to be associated with significant risk. Further investigation starting from the function of genes in the molecular clock transcription-translation feedback loop (TTFL) found that 80% of the combinations had >50% markers located in the positive arm of the TTFL. The comparison between Swedish and UK cohorts identified 39 concordant combinations, which confirmed the risk associated with rs3768984 (), as well as the enrichment in markers in , , and in combinations associated with significant risk.ConclusionOur data points to molecular clock dysfunction playing a central role in the manifestation of cluster headache. - Source: PubMed
Publication date: 2026/04/12
Sanches Clémence DeborgiesSpulber StefanOlofsgård Felicia JennysdotterFourier CarmenSundholm AnnaLantz MariaSjöstrand ChristinaWaldenlind ElisabetSteinberg AnnaHoulden HenryMatharu ManjitRan CarolineBelin Andrea Carmine - DNA methylation (DNAm) is implicated in age-related disease susceptibility. Some studies have reported alterations in DNAm patterns with sleep deprivation, yet this has not been demonstrated in long-term studies. We aimed to analyze whether prolonged mild sleep restriction (SR) results in differentially methylated loci (DML) in selected candidate circadian genes and explore changes in DML epigenome-wide. We conducted a pooled analysis of two randomized crossover trials of SR. Healthy adults (n=60; 65% women, age ≥20y) habitually sleeping 7-9h/night completed two 6-wk (week) intervention periods (condition): maintenance of habitual adequate sleep (AS, ≥7h/night) and SR (-1.5h/night), separated by a washout interval. We determined DNAm levels in morning fasting blood samples collected at baseline and endpoint using EPICv.2 array and multivariable adjusted models for repeated measures and analyzed the sleep condition x week interaction. Pathways and biological processes from the most significant DML were explored. In the candidate core circadian gene approach, sleep condition x week interactions were at cg02394126 (ARNTL; p˂0.001), cg23506964 (CLOCK; p=0.001), cg03701037 and cg06606972 (NPAS2; both p=0.009). In the exploratory EWAS, suggestive top DML were cg23738833 (SNHG3-RCC1; p=1.34E-06), cg13280380 (FAF1; p=2.25E-05), and cg03179866 (MMP12; p=2.78E-05). All but one (cg23738833) showed hypermethylation after SR vs AS. The most significant pathways associated with SR were aging-related genes involved in TGF-beta signaling, glucagon signaling, and fatty acid degradation. These findings reveal that prolonged mild SR is associated with DNAm in core clock candidate genes and suggests DML in other genes across the epigenome suggesting a potentially plastic epigenetic mechanism. Studies are needed to replicate these preliminary findings. - Source: PubMed
Publication date: 2026/03/21
Barragán RocioDye Christian KAggarwal BrookeJelic SanjaColtell OscarCorella DoloresSt-Onge Marie-Pierre - The biological basis of the afternoon nap, a widespread yet poorly understood phenomenon, has remained elusive. Here we identify NPAS2, among core circadian regulators, as a sex-independent determinant of the nap behavior in mice. Specifically, medial prefrontal cortex (mPFC)-expressed NPAS2 orchestrates nap regulation through circadian modulation of local dopaminergic activity. We demonstrate that tyrosine hydroxylase-positive (TH) neurons in mPFC exhibit time-of-day dependent wake-promoting activity, showing minimal excitation precisely during nap hours. Mechanistically, NPAS2 achieves this circadian suppression through a POU2F2-TH regulatory pathway: 1) transcriptional activation of the transcription repressor POU2F2, and 2) consequent downregulation of TH expression (a rate-limiting enzyme for dopamine synthesis) and dopamine production in mPFC TH neurons. These findings establish an endogenous circadian mechanism where mPFC NPAS2 periodically inhibits wake-promoting dopaminergic activity to drive nap behavior, providing fundamental insights into the neural and molecular regulation of nap biology. - Source: PubMed
Publication date: 2026/03/16
Guo LianxiaCen HaobinHuang YuweiLi ZanjinZeng KengranWu ZicongWeng JiaxianGuo XiaocaoHe DiLiu XinyuYang ZhehanXu HaimanHao TingyingWei BinbinDiao XingxingWu Baojian