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Example sentences for: bmal
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Recently, the search for components of the vertebrate circadian system has led to the identification of homologues of period [ 6, 7, 8, 9, 10, 11, 12] and timeless [ 13, 14, 15, 16], originally characterized as central clock genes in Drosophila , as well as Clock and Bmal1 ( Cycle ), identified initially in the mouse [ 17, 18, 19, 20, 21].
A recent study in Drosophila melanogaster implicates transcriptional regulation by the circadian gene cycle , a homolog of the mammalian bmal1 gene, in the homeostatic regulation of rest [ 16 ] . While rest in flies shares several features with sleep in mammals [ 17 18 ] , it remains to be determined whether a similar role for BMAL1 or related transcriptional regulators is necessary for the homeostatic regulation of sleep.
We assume that the effects on sleep we observed in cry1 , 2 -/-mice are a result of a lack of cryptochrome -dependent inhibition of the transcriptional activation provided by the bHLH-PAS heterodimers CLOCK:BMAL1 and NPAS2:BMAL1 [ 19 20 37 ] , although cryptochromes also play a role in stabilizing and nuclear sequestration of PER proteins [ 38 ] , and in photoreception [ 39 ] . Lack of cryptochromes results in increased mRNA levels of CLOCK/NPAS2:BMAL1 target genes, including the circadian genes per1 and per2 [ 20 23 ] . The expression of these two genes is viewed as a state variable of the molecular circadian clock or a marker of CLOCK/NPAS2:BMAL1-induced transcription, although at least per1 transcription can also be (rapidly) induced by light [ 40 41 ] , through a CREB-dependent signaling pathway [ 42 43 44 ] . The observation of high brain levels of per1,2 transcripts under baseline conditions in cry1,2 -/-mice raises the possibility that these or other CLOCK/NPAS2:BMAL1 target genes are involved in the homeostatic regulation of sleep.
Upon release into constant darkness cry1,2 -/-mice immediately become arrhythmic at the behavioral level [ 22 23 ] , at the level of SCN electrophysiology [ 28 ] , and at the cellular/molecular level [ 23 ] . Of the available mouse models for circadian dysfunction, only per1,2 double mutant mice [ 29 ] , bmal1 knockout mice [ 30 ] , and mice with an ablation of the SCN [ 31 ] show a similarly dramatic phenotype.
In mammals, the positive elements are two basic helix-loop-helix (bHLH) PAS-domain-containing transcription factors, CLOCK and BMAL1, that form heterodimers that can drive the transcription of three period ( per ) genes per1-3 and two cryptochromes ( cry1,2 ). PER1,2 and CRY1,2 proteins suppress CLOCK:BMAL1-mediated transcription thereby forming the negative elements in the feedback loop.
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