BMAL1 _ ARNTL
- Known as:
- BMAL1 _ ARNTL
- Catalog number:
- Y214226
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BMAL1 _ ARNTL
Related genes to: BMAL1 _ ARNTL
- Gene:
- ARNTL NIH gene
- Name:
- aryl hydrocarbon receptor nuclear translocator like
- Previous symbol:
- -
- Synonyms:
- MOP3, JAP3, BMAL1, PASD3, bHLHe5
- Chromosome:
- 11p15.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-06
- Date modifiied:
- 2017-08-18
Related products to: BMAL1 _ ARNTL
Related articles to: BMAL1 _ ARNTL
- Circadian and sleep-wake dysregulation have been implicated in episode recurrence and clinical heterogeneity in bipolar disorder (BD), supporting peripheral circadian markers as candidates for further investigation. This study examined the peripheral expression of selected circadian rhythm-related gene mRNAs and antisense long non-coding RNAs (lncRNAs), alongside corresponding serum protein levels and self-report-based rhythm phenotyping, in euthymic patients with BD. Sixty euthymic patients with BD (20 BD-1, 20 BD-2, and 20 with antidepressant-associated hypo/manic switch [ASHH], treated as an exploratory group) and 20 healthy controls were enrolled. Euthymia was verified by HAM-D < 7 and YMRS < 6, and chronotype and rhythm phenotypes were assessed using the MEQ, SRM-5, and BRIAN. Morning fasting blood was collected (08:00-10:00) with the morning medication dose withheld; because sampling was confined to a single morning window, the reported values represent morning transcript abundance rather than circadian rhythmicity, amplitude, or phase position. Three core clock gene mRNAs () and two antisense lncRNAs () were quantified by qRT-PCR (2^-ΔΔCt, β-actin reference), and serum CIART, CRY1, PER2, and ARNTL proteins were measured by ELISA. Between-group comparisons used nonparametric tests (Mann-Whitney U; Kruskal-Wallis H with Bonferroni post hoc), and correlations used Spearman's coefficient with Benjamini-Hochberg FDR correction. Compared with healthy controls, patients showed statistically significantly higher expression of the lncRNAs (r = 0,57) and (r = 0,49) and the mRNAs (r = 0,35) and (r = 0,29), all p ≤ 0,007, whereas mRNA did not differ (p = 0,654). In exploratory subgroup analyses, differences were concentrated in BD-2 and ASHH: BD-2 showed the highest expression and BD-1 the lowest, with BD-1 not differing from controls for any marker. Serum protein levels did not differ between groups or subgroups, and MEQ, BRIAN, and SRM-5 scores did not differ; however, a sensitivity analysis excluding shift workers revealed a chronotype difference masked in the full sample. Across 174 correlational tests, none survived FDR correction (lowest q = 0,063); nominal uncorrected associations are reported as preliminary only. In euthymic BD, peripheral expression of selected circadian rhythm-related markers-particularly the antisense lncRNAs and and the mRNAs of and - differed from healthy controls, whereas corresponding serum protein levels and behavioral rhythm phenotypes did not. This divergence across measurement levels can be considered a substantive finding, and the subgroup patterns are exploratory and hypothesis-generating. Longitudinal, episode-inclusive, and subtype-stratified studies incorporating objective circadian phase markers and repeated sampling are needed to establish the significance of peripheral transcript-level differences in BD.HIGHLIGHTS Peripheral circadian gene mRNAs and antisense lncRNAs are profiled in euthymic bipolar subtypes. and lncRNAs and and mRNAs are higher in patients than controls.Exploratory analyses: transcript differences concentrate in BD-2 and ASHH; not BD-1.Serum CIART, CRY1, PER2, and ARNTL protein levels by ELISA do not differ by group.Behavioral rhythm scores do not differ; correlations do not survive FDR correction. - Source: PubMed
Publication date: 2026/09/04
Gümüşlü Ağcabay AslıhanDemir BahadırKorkmaz MuratYumrutaş PınarSancaktar MuhammetElboğa GülçinBülbül FeridunAltındağ Abdurrahman - Successful embryo development transpires far before fertilization inside the meticulously regulated microenvironment of the ovarian follicle. Increasing data indicates that circadian regulatory systems influence several processes that define oocyte competence, including mitochondrial activity, oxidative balance, meiotic development, and cellular metabolism. Brain and muscle ARNT-like protein 1 (BMAL1), an essential transcription factor in circadian regulation, has garnered significant interest due to its crucial involvement in ovarian physiology and reproductive function. Dysregulated BMAL1 signaling has been linked to compromised folliculogenesis, diminished steroidogenesis, mitochondrial dysfunction, elevated oxidative stress, and irregularities in meiotic spindle organization, all of which may negatively impact oocyte quality and early embryo development. Recent experimental and clinical findings indicate that results of assisted reproduction may be influenced by circadian disruption, sleep problems, obesity, ageing, and metabolic dysfunction. - Source: PubMed
Publication date: 2026/08/21
Voros CharalamposZagorianakou NektariaMakrydimas StylianosChatzinikolaou FotiosPapadimas GeorgiosKoulakmanidis Aristotelis MariosThomakos NikolaosAntsaklis PanagiotisDaskalakis GeorgiosMakrydimas George - While circadian disturbances are commonly comorbid with schizophrenia (SCZ), whether deficits in clock genes can induce SCZ-like behaviors in mice remains poorly understood. Brain and muscle Arnt-like protein 1 (Bmal1, also known as Mop3 or Arntl), a core circadian clock gene, is implicated in the regulation of circadian rhythms, and its single nucleotide polymorphism rs1982350 has been linked to the pathogenesis of SCZ. - Source: PubMed
Yao Yi-QinGuo Bo-WeiXu Zhi-YiWang CunHong HaoChen Zhi-GangTang Su-Su - The circadian clock controls a vast array of cellular and organismal functions, from the molecular scale to behavior. While each cell is regimented by a cell-autonomous clock, few studies in the brain have dissected the circuit and behavioral contributions of cell-specific clocks. Relatedly, astrocytes are now known to play key roles in regulating synaptic function, circuit activity and behavior, but whether these functions are guided by astrocyte-autonomous clocks is unknown. Here, we report that post-natal deletion of the critical circadian clock gene Bmal1 in astrocytes, which abrogates core clock function in a cell type specific manner, induced expression of genes related to extracellular matrix (ECM) production, maintenance, and remodeling. Circadian variations have been shown in a specific ECM structure, perineuronal nets (PNNs), which are implicated in synaptic function and plasticity. In astrocyte-specific Bmal1 knockouts, hippocampal PNN abundance was decreased, and the circadian rhythm of these structures was also abolished. In line with evidence implicating PNNs, and the ECM in general, in synaptic function and plasticity, we found that astrocyte-specific Bmal1 KO mice had increased synaptic strength but blunted long term potentiation (LTP), as well as impaired learning and memory performance in a novel object recognition task. Taken together, these findings suggest that the astrocyte circadian clock regulates circadian rhythms in perineuronal net abundance as well as synaptic plasticity and behavioral learning and memory. - Source: PubMed
Smith Philip CQuillin Elsa ILefton Katheryn BMcKee Celia ADang BrendanPapouin ThomasMusiek Erik S - Circadian rhythms are endogenous ∼24-h cycles that regulate cardiovascular physiology. Although circadian regulation of the left ventricle (LV) is well established, whether the right ventricle (RV) exhibits intrinsic rhythmicity is not known. Here, we provide the first evidence that the healthy RV exhibits robust rhythms in function and molecular gene expression. Cardiovascular disease is the leading cause of mortality in type 1 diabetes (T1D). T1D disrupts circadian rhythms, yet how T1D alters chamber-specific circadian control remains unclear. We investigated RV and LV function and gene expression across the 24-h light-dark cycle in male streptozotocin-induced T1D and control mice. Echocardiographic assessment of diabetes-induced remodeling at ZT0-4 and ZT12-16 [zeitgeber time (ZT)] revealed time-dependent functional impairment, including reversal of the normal diurnal heart rate pattern. T1D impaired day-night RV and LV systolic function, with loss of day-night difference in LV ejection fraction and impaired active period RV stroke volume. Cosinor analysis of RV and LV gene expression demonstrated preserved 24-h rhythmicity of core clock genes and in both ventricles with T1D, whereas the clock output genes and had dampened amplitude in the RV but amplified expression in the T1D LV. These findings demonstrate that T1D differentially disrupts circadian regulation of the RV and LV, with selective vulnerability of the clock-controlled output genes despite preservation of the core oscillator. Chamber-specific circadian remodeling may contribute to the elevated cardiovascular risk in T1D and has implications for the timing of diagnostic and therapeutic interventions. This study provides the first evidence that the healthy right ventricle (RV), like the left ventricle (LV), possesses an intrinsic circadian clock with robust 24-h rhythmicity. Using a mouse model of type 1 diabetes, we show that diabetes does not uniformly suppress cardiac clocks but instead differentially rewires RV and LV rhythms, dampening clock-output gene amplitude in the RV while amplifying it in the LV. Together, we reveal chamber-specific circadian vulnerability with implications for diabetic cardiomyopathy and chronotherapy. - Source: PubMed
Publication date: 2026/08/07
Bettadapura Sharanya STorres Samantha JSchmitt Marjie PRoberts Brandon LBruns Danielle R