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BMAL1Brain and Muscle ARNT-Like 1
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According to timed sleep restriction (TSR) study, sleep timing directly affects clock-controlled genes including ClockD19, BMAL1, Per1, Rev-erba and Dbp, and circadian machinery.
To explore the specific roles of Bmal1 and Per2 in the regulation of bone formation and to determine whether Bmal1 and Per2 have an interaction in this process, we inhibited the expression of Bmal1 or/and Per2 in BMSCs and observed their ability to differentiate into osteoblasts.
Bmal1 is an essential component of the circadian timing system [102], and thus, Bmal1 knockout (KO) mice are completely arrhythmic [102, 103].
Turning Bmal1 off throughout the brain and body in mice, using a molecular genetic technique, impaired their ability to rebound from sleep deprivation, the researchers reported.
The ( study found that while the presence or absence of BMAL1 in mice brain had little effect on their sleep recovery, higher levels of the protein in their muscles helped them recover from sleep deprivation more quickly.
In mammals, circadian rhythm is controlled by hypothalamic suprachiasmatic nucleus (SCN), and regulated by a transcriptional feedback loop with clock genes, such as circadian locomotor cycle kaput ( Clock ), Brain and muscle Arnt-like protein-1 ( Bmal1 ), Period ( Per ), Cryptochrome ( Cry ), Reverse erythroblastosis virus ( Rev-erb ), Retinoic acid receptor-related orphan receptor ( Rora ) genes, and their corresponding proteins.[sup][7] Clock and Bmal1 are two critical transcriptional activators, which stimulate the expression of Per and Cry at the beginning of the day.
Jia et al., "Vascular PPAR[gamma] controls circadian variation in blood pressure and heart rate through Bmal1," Cell Metabolism, vol.
Li et al., "Loss of Bmal1 leads to uncoupling and impaired glucose-stimulated insulin secretion in fi-cells," Islets, vol.
Mouse primary culture of mesenchymal cells responds with oscillatory transcription of Per1, Per2, Per3, Cry1, Cry2, Npas2 (Clock paralogue), and Bmal1 and of the clock-controlled genes, Rev-erb [alpha]/[beta] and Dbp to GCs [47].
These cycles are controlled by a number of genes, including Bmal1 and Clock.
The experiment was repeated in mice lacking the gene Bmal1, which helps control the body clock, and they found high levels of virus replication regardless of the time of infection.