Below are a collection of excerpts from biomedical research articles. Excerpts are separated by newlines. Your task is to answer a question based these excerpts. Your response should be formatted as a `json` array.

For instance, given excerpts from articles studying breast cancer, and the question "what are some common genes associated with breast cancer?", an answer might be formatted like: ["BRCA1", "BRCA2", "TP53", ...]. Only include answers that are mentioned in the provided exerpts. The array should always have at least one answer; do not respond with an empty array []. Do not include any text in your response other than the answer array.

Context: Mammalian CLOCK and BMAL1 are two members of bHLH-PAS-containing family of transcription factors that represent the positive elements of circadian autoregulatory feedback loop.
We have examined abundance, posttranslational modifications, cellular localization of endogenous and ectopically expressed CLOCK and BMAL1 proteins. Nuclear/cytoplasm distribution of CLOCK was found to be under circadian regulation.
Formation of CLOCK/BMAL1 complex following ectopic coexpression of both proteins is followed by their codependent phosphorylation, which is tightly coupled to CLOCK nuclear translocation and degradation
Altogether, these results provide evidence for an additional level of circadian system control, which is based on regulation of transcriptional activity or/and availability of CLOCK/BMAL1 complex.
Two basic helix-loop-helix (bHLH) PAS (for Period-Arnt-Sim) domain-containing transcriptional activators, CLOCK and BMAL1, are known to regulate gene expression by interacting with a promoter element termed the E-box (CACGTG).
Circadian rhythms in mammals are generated by a transcriptional negative feedback loop that is driven primarily by oscillations of PER and CRY, which inhibit their own transcriptional activators, CLOCK and BMAL1.
Our biochemical evidence supports an elegant mechanism for the disparity: PER2 directly and rhythmically binds to CLOCK:BMAL1, while CRY only interacts indirectly; PER2 bridges CRY and CLOCK:BMAL1 to drive the circadian negative feedback loop.<br>
Two basic helix-loop-helix (bHLH) PAS (for Period-Arnt-Sim) domain-containing transcriptional activators, CLOCK and BMAL1, are known to regulate gene expression by interacting with a promoter element termed the E-box (CACGTG).
The CRY proteins in turn inhibit CLOCK:BMAL-mediated transcription closing the negative feedback loop.
In the vertebrate circadian feedback loop, CLOCK:BMAL heterodimers induce the expression of Cry genes.
Two basic helix-loop-helix (bHLH) PAS (for Period-Arnt-Sim) domain-containing transcriptional activators, CLOCK and BMAL1, are known to regulate gene expression by interacting with a promoter element termed the E-box (CACGTG).
In the present study, we demonstrate that Id2 is involved in stabilization of the amplitudes of the circadian oscillations by suppressing transcriptional activation of clock genes Clock and Bmal1.
bmal1 is an essential transcriptional activator within the mammalian circadian clock we report here that the suprachiasmatic nucleus scn of bmal1 null mutant mice unexpectedly generates stochastic oscillations with periods that overlap the circadian range dissociated scn neurons expressed fluctuating levels of per2 detected by bioluminescence imaging but could not generate circadian oscillations intrinsically inhibition of intercellular communication or cyclic amp signaling in scn slices which provide a positive feed forward signal to drive the intracellular negative feedback loop abolished the stochastic oscillations propagation of this feed forward signal between scn neurons then promotes quasi circadian oscillations that arise as an emergent property of the scn network experimental analysis and mathematical modeling argue that both intercellular coupling and molecular noise are required for the stochastic rhythms providing a novel biological example of noise induced oscillations the emergence of stochastic circadian oscillations from the scn network in the absence of cell autonomous circadian oscillatory function highlights a previously unrecognized level of circadian organization.
transcriptional regulation appears to be fundamental to circadian oscillations of clock gene expression these oscillations are believed to control output rhythms the transcriptional feedback loop and a model of interlocked loops have been proposed as the basis for these oscillations we characterized the genomic structure of the mouse bmal1 gene mbmal1 and defined the mbmal1 promoter region transcription of mbmal1 was activated by cry1 cry2 and per2 and was repressed by bmal1 clock dimers therefore cry per2 and bmal1 clock play bidirectional roles in transcription when they are at high levels by late day and midnight respectively this underlies the opposite phase of bmal1 compared to cry and per we propose that a bmal1 negative feedback loop interlocks with the cry and per2 negative feedback loop by inter activation forming a third positive forward loop this transcriptional model suggests a molecular basis for the maintenance of stability persistence and period of circadian rhythms the transcriptional potency of cry is predominant within the mammalian clock suggesting a clearance mechanism for cry in period maintenance c 2002 elsevier science usa.
the circadian expression of the mammalian clock genes is based on transcriptional feedback loops two basic helix loop helix bhlh pas for period arnt sim domain containing transcriptional activators clock and bmal1 are known to regulate gene expression by interacting with a promoter element termed the e box cacgtg the non canonical e boxes or e box like sequences have also been reported to be necessary for circadian oscillation we report a new cis element required for cell autonomous circadian transcription of clock genes this new element consists of a canonical e box or a non canonical e box and an e box like sequence in tandem with the latter with a short interval 6 base pairs between them we demonstrate that both e box or e box like sequences are needed to generate cell autonomous oscillation we also verify that the spacing nucleotides with constant length between these 2 e elements are crucial for robust oscillation furthermore by in silico analysis we conclude that several clock and clock controlled genes possess a direct repeat of the e box like elements in their promoter region we propose a novel possible mechanism regulated by double e box like elements not to a single e box for circadian transcriptional oscillation the direct repeat of the e box like elements identified in this study is the minimal required element for the generation of cell autonomous transcriptional oscillation of clock and clock controlled genes.
clock bmal independent circadian oscillation of zebrafish cryptochrome1a gene

Question:
Which are the main transcriptional activators of circadian oscillations?
["BMAL1", "CLOCK"]