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Validated All-in-One™ qPCR Primer for CLOCK(NM_001267843.2) Search again
Product ID:
HQP130499
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
KAT13D, bHLHe8
Gene Description:
clock circadian regulator
Target Gene Accession:
NM_001267843.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes a protein that belongs to the basic helix-loop-helix (bHLH) family of transcription factors.
Gene References into function
- essential regulator of circadian rhythms
- BMAL1 and CLOCK have roles in circadian system control
- a role for the CLOCK gene polymorphism in the regulation of long-term illness recurrence in bipolar disorder
- CLOCK was cloned & sequenced and its circadian expression studied.
- Findings suggest the significance of the association of the 3111C/C allele of hClock with evening preference in a Japanese population sample.
- RNA interference against beta-TRCP greatly decreases Clock-dependent gene expression in tissue culture cells, indicating that beta-TRCP controls endogenous Per1 activity and the circadian clock by directly targeting Per1 for degradation
- Findings may suggest that CLOCK genotype influences the time course of insomnia during antidepressant treatment.
- Single Nucleotide Polymorphism in the 3'-untranslated region of clock gene is associated with Sleep Disorders
- Single nucleotide polymorphism is not associated with narcolepsy.
- a molecular genetic screen in mammalian cells to identify mutants of the circadian transcriptional activators CLOCK and BMAL1.
- The results of this study suggests that the T3111C polymorphism of the CLOCK gene is associated with schizophrenia.
- compared to T/T homozygotes, bipolar depressed carriers of the C allele had a similar degree of severity of depression, but showed higher activity levels in the evening, a delayed sleep onset and a reduced amount of sleep during the night
- These results show that there is no association between either polymorphism T3111C or T257G in the Clock gene with diurnal preference or delayed sleep phase syndrome (DSPS).
- CLOCK 3111 T/C SNP was associated with activity levels in the second part of the day, neuropsychological performance and BOLD fMRI correlates (interaction of genotype and moral valence of the stimuli).
- The difference between the mean value for the lowest expression individual (DeltaCT 8.8) and the highest expression individual (DeltaCT 3.7) revealed an approximately 34-fold difference in relative clock gene expression levels.
- polymorphism of the CLOCK gene confers a predisposition to a lifetime lower body weight in patients with anorexia nervosa and bulimia nervosa
- Our study suggests a potential role of the CLOCK polymorphisms and their haplotypes in susceptibility to nonalcoholic fatty liver disease and disease severity.
- Allelic variants interaction of CLOCK gene and GNB3 subunit gene with diurnal preference.
- peripheral clock in vascular endothelial cells regulates TM gene expression and that the oscillation of TM expression may contribute to the circadian variation of cardiovascular events
- This is the first study suggesting that a polymorphism of a gene within the circadian "clock" mechanism is a direct or linked contributing factor in adult ADHD
- CLOCK/BMAL1-mediated activation of PER1 by AP1 and E-Box elements is distinct from peripheral transcriptional modulation via cAMP-induced CREB and C/EBP.
- the Clock gene CGC haplotype may be protective for the development of obesity and support the hypothesis that genetic variation in the Clock gene may play a role in the development of the metabolic syndrome, type 2 diabetes and cardiovascular disease.
- A multi-locus interaction between rs6442925 in the 5' upstream of BHLHB2, rs1534891 in CSNK1E, and rs534654 near the 3' end of the CLOCK gene, however, is significantly associated with bipolar disorder
- study does not support the hypothesis that the T3111C CLOCK polymorphism is associated with cluster headache
- Present findings show for the first time that the 3111T/C SNP of the CLOCK gene is not associated to human obesity and/or BED, but it seems to predispose obese individuals to a higher BMI.
- No relationship between hCLOCK T3111C polymorphism and endometriosis, nor any effect of the polymorphism on the relationship of shift work to endometriosis.
- DEC1, along with DEC2, plays a role in the finer regulation and robustness of the molecular clock CLOCK/BMAL1
- Evidence linking circadian rhythms, the Clock gene, and bipolar disorder is discussed, along with the possible biology that underlies this connection. Review.
- The regulators of clock-controlled transcription PER2, CRY1 and CRY2 differ in their capacity to interact with each single component of the BMAL1-CLOCK heterodimer and, in the case of BMAL1, also in their interaction sites.
- HAT gene expression is required for cisplatin resistance and Clock and Tip60 regulate not only transcription, but also DNA repair, through periodic histone acetylation
- Putative role of the CLOCK polymorphism and related haplotypes in susceptibility to obesity.
- The transcription of human nocturnin gene displayed circadian oscillations in Huh7 cells (a human hepatoma cell line) and was regulated by CLOCK/BMAL1 heterodimer via the E-box of nocturnin promoter.