-
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.
-
BMAL1 Deficiency Contributes to Mandibular Dysplasia by Upregulating MMP3.
-
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 findings indicate that BMAL1 deregulation is a feature of the mTOR-activated state and suggest a molecular mechanism for mitigating circadian phenotypes in a neurodevelopmental disorder.
-
Data show that CRY1 binds directly to the PAS domain core of CLOCK:BMAL1, driven primarily by interaction with the CLOCK PAS-B domain.
-
Data suggest that BMAL1 protein expression in the SCN (suprachiasmatic nucleus) is higher in night-time compared to day-time in both chow-fed and fcHFHS-fed mice; the same pattern is found in the LHb (epithalamic lateral habenula) for BMAL1 expression, being higher at night. (fcHFHS = free choice high-fat high-sugar diet)
-
PTEN ablation led to downregulation of BMI-1, a critical regulator of adult stem cell self-renewal, and elevated senescence, suggesting the presence of a protective system that prevents transformation. Short- and long-term PTEN depletion followed by activated BMAL1, a core clock protein, contributed to accumulation of hair follicle stem cells.
-
These findings indicate that the expressions of two key clock genes, Per1 and Bmal1, in the SCN are regulated in such a way that they may adopt different phases and free-running periods relative to each other and are respectively associated with the expression of activity onset and offset.
