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lost BMAL1 and Ki-67 overexpression are associated with poor overall survival of nasopharyngeal carcinoma patients
GSEA assay found that ARNTL was associated with cell cycle and ectopic ARNTL overexpression could induce G2-M phase arrest.
study revealed that TP, as a Bmal1-enhancing natural compound, alleviated redox imbalance via strengthening Keap1/Nrf2 antioxidant defense pathway and ameliorating mitochondrial dysfunction in a Bmal1-dependent manner
This work identifies UBE2O as a critical regulator in the ubiquitin-proteasome system, which modulates BMAL1 transcriptional activity and circadian function by promoting BMAL1 ubiquitination and degradation under normal physiological conditions.
BMAL1 Deficiency Contributes to Mandibular Dysplasia by Upregulating MMP3.
ARNTL rs7107287 was associated with a cyclothymic temperament, depressive and stress symptoms
NR1D1 and BMAL1 mRNA and protein levels were significantly reduced in OA compared to normal cartilage. In cultured human chondrocytes, a clear circadian rhythmicity was observed for NR1D1 and BMAL1.
These results suggest that the circadian clock system can be recovered through BMAL1 expression induced by aza-dC within a day.
Determined a novel role of TNF-alpha in inducing Bmal1 via dual calcium dependent pathways; Roralpha was up-regulated in the presence of Ca(2+) influx and Rev-erbalpha was down-regulated in the absence of that.
results of this study suggest that genetic variability in the ARNTL and CLOCK genes might be associated with risk for multiple sclerosis
PI3K-PTEN upregulated-mTORC1 and mTORC2 complex plays a critical role in controlling BMAL1, establishing a connection between PI3K signaling and the regulation of circadian rhythm, ultimately resulting in deregulated BMAL1 in tumor cells with disrupted PI3K signaling
M. tuberculosis infection caused enhanced MMP-1, -9, and miR-223 expression, with inhibited BMAL1 expression. MiR-223 modulated BMAL1 expression via the direct binding of BMAL1 3'-UTR.
research describes an association between changes in the methylation of the BMAL1 gene with the intervention and the effects of a weight loss intervention on blood lipids levels
Study found rhythmic methylation of BMAL1 was altered in Alzheimer's disease brains and fibroblasts and correlated with transcription cycles. Results indicate that cycles of DNA methylation contribute to the regulation of BMAL1 rhythms in the brain.
TFEB regulates PER3 expression via glucose-dependent effects on CLOCK/BMAL1
found that overexpression of both Clock and Bmal1 suppressed cell growth
our results identified Bmal1 as a novel tumor suppressor gene that elevates the sensitivity of cancer cells to paclitaxel, with potential implications as a chronotherapy timing biomarker in tongue squamous cell carcinoma
The level of BMAL1 expression in granulosa cells the polycystic ovary syndrome (PCOS) group was lower than that of the group without PCOS. We also analyzed estrogen synthesis and aromatase expression in KGN cell lines. Both were downregulated after BMAL1 and SIRT1 knock-down and, conversely, upregulated after overexpression treatments of these two genes in KGN cells.
this study shows that BMAL1 can regulate cellular innate immunity against specific RNA viruses
Bmal1 is a key clock gene to involve in cartilage homeostasis mediated through sirt1.
The results of these experiments showed splice variants that were widely expressed in most tissues. Furthermore, they were highly expressed in cerebellum, heart, and kidney.
xBMAL1 and xNOCTURNIN are associated with somite differentiation and promotion of myogenesis.
the second half of the photolyase homology region (PHR) of CRY is important for repression through facilitating interaction with BMAL1
Results indicated that pBMAL1 cDNA had a coding region of 1,878 bp and shared 94.36, 89.85 and 89.79% identity with human, mouse and rat BMAL1. pBMAL1 expression levels in different tissues were studied.
much of BMAL1 target gene transcription depends on BMAL1 capacity to rhythmically regulate a network of enhancers.
HNF4A strongly transrepresses the transcriptional activity of the CLOCK:BMAL1 heterodimer.
Chronic alcohol consumption and hepatocyte clock protein BMAL1 disruption differentially influence the diurnal rhythm of glycogen and various key glycogen metabolism-related genes in the liver.
Loss of Bmal1 expression is associated with loss in retinal development and accelerates cone photoreceptor degeneration during aging.
BMAL1 is a critical regulator of the muscular fatty acid level under nutrition overloading and that the mechanism involves the control of oxidative capacity.
our data show a sex-dependent difference and a sex-dependent effect of Bmal1-deficiency on infarct core volume during the sub-acute phase after focal cortical ischemia. These effects do not seem to be dependent on proliferation, but activation or recruitment of astrocytes and microglia in the peri-infarct area.
Data suggest that loss of aryl hydrocarbon receptor nuclear translocator-like protein (BMAL1) function in astrocytes results in altered GABA levels, leading to the over-inhibition of the circuits involved in learning and memory and to the uncoupling the suprachiasmatic nucleus (SCN) oscillators.
Circadian clock protein BMAL1 regulates IL-1beta in macrophages via NRF2.
The expression of the clock gene Bmal1 in myeloid cells regulates the innate and adaptive immune responses that mediate autoimmune diseases.
Insulin reduces Bmal1 transcriptional activity by affecting its intracellular localization in mouse liver, which requires Akt-dependent phosphorylation of the Ser42 residue.
Bmal1 modulates lipoprotein production and biliary cholesterol excretion by regulating the expression of Mtp and Abcg5/Abcg8 via Shp and Gata4.
these results suggest a role for bmal1 in the development of asthmatic airway disease via the regulation of lung antiviral responses to common viral triggers of asthma
The daily rhythm of BMAL1 mRNA was completely abolished in the EGR1-deficient mice.
Clock:BMAL1 promotes a transcriptionally permissive chromatin landscape that primes its target genes for transcription activation rather than directly activating transcription. Environmental or pathological conditions can reprogram the rhythmic expression of clock-controlled genes.
Bmal1 and Dio2 are required to maintain cone photoreceptor functional integrity.
Islet cell maturation was also characterized by induction in the expression of circadian transcription factor BMAL1, deletion of which altered postnatal development of glucose-stimulated insulin secretion and the associated transcriptional network.
PML mediates the binding of PER2 to BMAL1 in the BMAL1/CLOCK heterodimer and is an important component in the organization of a functional clock complex in the nucleus.
The results demonstrate that Bmal1 expression in skeletal muscle is both necessary and sufficient to regulate total sleep amount and reveal that critical components of normal sleep regulation occur in muscle.
The protein encoded by this gene is a basic helix-loop-helix protein that forms a heterodimer with CLOCK. This complex binds an E-box upstream of the PER1 gene, activating this gene and possibly other circadian rhythym-associated genes. Three transcript variants encoding two different isoforms have been found for this gene.
ARNT-like protein 1, brain and muscle
, PAS domain-containing protein 3
, aryl hydrocarbon receptor nuclear translocator-like protein 1
, bHLH-PAS protein JAP3
, basic-helix-loop-helix-PAS orphan MOP3
, basic-helix-loop-helix-PAS protein MOP3
, brain and muscle ARNT-like 1
, class E basic helix-loop-helix protein 5
, member of PAS protein 3
, member of PAS superfamily 3
, brain and muscle ARNT-like protein 1
, bHLH-PAS transcription factor BMAL1
, clock protein
, aryl hydrocarbon receptor nuclear translocator-like
, Brain and muscle ARNT-like 1
, aryl hydrocarbon receptor nuclear translocator-like protein 1-like
, brain and muscle Arnt-like protein 1
, bHLH-PAS transcription factor