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anti-Mouse (Murine) CLOCK Antibodies:
anti-Rat (Rattus) CLOCK Antibodies:
anti-Human CLOCK Antibodies:
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Human Polyclonal CLOCK Primary Antibody for ChIP, WB - ABIN151057
Jin, Shearman, Weaver, Zylka, de Vries, Reppert: A molecular mechanism regulating rhythmic output from the suprachiasmatic circadian clock. in Cell 1999
Show all 6 Pubmed References
Human Polyclonal CLOCK Primary Antibody for IHC (p), ELISA - ABIN543943
Marino, Holt, Chen, Davis: Shift work, hCLOCK T3111C polymorphism, and endometriosis risk. in Epidemiology (Cambridge, Mass.) 2008
Show all 3 Pubmed References
Human Monoclonal CLOCK Primary Antibody for ICC, ELISA - ABIN969059
Lee, Paik, Kang, Lim, Kim: Allelic variants interaction of CLOCK gene and G-protein beta3 subunit gene with diurnal preference. in Chronobiology international 2007
Show all 2 Pubmed References
Human Polyclonal CLOCK Primary Antibody for IHC - ABIN965906
Steeves, King, Zhao, Sangoram, Du, Bowcock, Moore, Takahashi: Molecular cloning and characterization of the human CLOCK gene: expression in the suprachiasmatic nuclei. in Genomics 1999
Show all 9 Pubmed References
Human Polyclonal CLOCK Primary Antibody for ELISA, WB - ABIN564129
Kalamvoki, Roizman: Circadian CLOCK histone acetyl transferase localizes at ND10 nuclear bodies and enables herpes simplex virus gene expression. in Proceedings of the National Academy of Sciences of the United States of America 2010
Polyclonal CLOCK Primary Antibody for ChIP, IP - ABIN540419
Shearman, Weaver: Photic induction of Period gene expression is reduced in Clock mutant mice. in Neuroreport 1999
Show all 5 Pubmed References
experiments define the genetic architecture required to initiate circadian clock function in Drosophila, reveal mechanisms governing circadian activator stability that are conserved in perhaps all eukaryotes, and suggest that Clk, cyc, and cry expression is sufficient to drive clock expression in naive cells
propose that the dCLK/CYC-controlled TTFL operates differently in subsets of pacemaker neurons, which may contribute to their specific functions
ClkAR mutants showed significantly faster age-related locomotor deficits. Accelerated locomotor decline of the ClkAR mutant required expression of the PDF receptor and correlated to an apparent loss of dopaminergic neurons in the brain
Here we demonstrate that the transcription factor CLOCKWORK ORANGE (CWO) antagonizes CLK-CYC E-box binding, thus enhancing the removal of CLK-CYC from E-boxes to maintain transcriptional repression. This process requires PER, which suggests that PER-TIM and CWO cooperate to maintain a transcriptionally repressed state by removing CLK-CYC from E-boxes
these results demonstrate a key role of Clk post-transcriptional control in stabilizing circadian transcription.
Our findings suggest a novel role for clock protein phosphorylation in governing the relative strengths of entraining modalities by adjusting the dynamics of circadian gene expression.
These results demonstrate that CLK phosphorylation influences the circadian period by regulating CLK activity and progression through the feedback loop.
Computational dissection of CLK/CYC context-specific binding sites reveals sequence motifs for putative partner factors, which are predictive for individual binding sites
usp8 loss of function (RNAi) or expression of a dominant-negative form of the protein (USP8-DN) enhances CLK/CYC transcriptional activity and alters fly locomotor activity rhythms
CLK has specific targets in different tissues, implying that important CLK partner proteins and/or mechanisms contribute to gene-specific and tissue-specific regulation
CTRIP destabilizes CLK protein in a PER-independent manner and helps degradation of phosphorylated PER and TIM in the morning
dPER(DeltaCBD) does not provoke the daily hyperphosphorylation of dCLOCK, indicating that direct interactions between dPER and dCLOCK are necessary for the dCLOCK phosphorylation
findings show that Clk and cyc act during starvation to modulate the conflict of whether flies sleep or search for food
Here we examined the consequences of loss of clock function on reproductive fitness in Drosophila melanogaster with mutated period (per(0)), timeless (tim(0)), cycle (cyc(0)), and Clock (Clk(Jrk)) genes
dCLK levels are critical in mediating the direct photostimulation of locomotor activity in Drosophila.
Stress response genes protect against lethal effects of sleep deprivation in Drosophila
role for VRI in the rhythmic repression of output genes that cycle in phase with Clk
Clk, vri, and Pdp-1 have roles in controlling Drosophila circadian oscillations, as shown in a simulation
PER-dependent rhythms in CLK phosphorylation control rhythms in E-box-dependent transcription and CLK stability, thus linking PER and CLK function during the circadian cycle
constitutive levels of nuclear CLK regulate rhythmic transcription in circadian oscillator cells and CLK contributes to other behavioral processes by regulating gene expression in non-oscillator cells
Data suggest that Clock1a coordinates mesoderm development and primitive hematopoiesis in embryos by up-regulating Nodal-Smad3 signaling; Clock1a alterations produce embryonic defects with shortened body length, lack of ventral tail fin, or partial defect of the eyes; Clock1a activates Smad3a promoter via its E-box1 element. (Clock1a = clock circadian regulator a; Nodal = nodal modulator 1; Smad3a = SMAD family member 3a)
effect of CRY in repressing transcription mediated by CLOCK-BMAL heterodimer
zCRY and zPER2 regulate the sub-cellular distributions of zCLOCK.
Clock plays important roles in regulating the circadian rhythms in photoreceptor cells
endogenous CLOCK is essential for the transcriptional regulation of period1 in the embryo
Carcinogenic exposure decreased BMAL1 and CRYI- expression in the skin, CLOCK expression was upregulated and CRYl downregulated in tumor compared to normal skin. BMAL1 expression increased under disrupted light regimen; melatonin treatment affected CLOCK expression in tumors and CRYI in skin at the carcinogens application sites.
CLOCK phosphorylation by AKT on Ser-845 regulates its nuclear translocation and the expression levels of certain core circadian genes in insulin-sensitive tissues.
The expression of Epcam mRNA, which is a functional marker of potential hepatic stem-like cells, was controlled by LEF1, which was regulated by CLOCK.
Results indicate that circadian locomotor output cycles kaput protein (CLOCK) overexpression triggers the formation of atherosclerotic plaques by directly upregulating plasminogen activator inhibitor 1 (PAI-1) expression.
Low expression of CLOCK protein is associated with kidney tumor.
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.
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.
Data show that CRY1 binds directly to the PAS domain core of CLOCK:BMAL1, driven primarily by interaction with the CLOCK PAS-B domain.
CLOCK temporally gates mast cell responses to IL-33 via regulation of ST2 expression. Our findings provide novel insights into IL-33/mast cell-associated physiology and pathologies.
Study showed that CLOCK can interact with RANBP9 and bind with mRNAs, demonstrating that CLOCK is involved in alternative splicing in spermatogenesis. These results reveal a novel mechanism for CLOCK in spermatogenesis.
TFEB regulates PER3 expression via glucose-dependent effects on CLOCK/BMAL1
ASS1 acetylation by CLOCK exhibits circadian oscillation in human cells and mouse liver, possibly caused by rhythmic interaction between CLOCK and ASS1, leading to the circadian regulation of ASS1 and ureagenesis.
Disruption of CLOCK protein alters cortical circuits and leads to generation of focal epilepsy.
Development of Mineralocorticoid receptor-mediated cardiac inflammation and fibrosis is dependent on intact signaling by the circadian protein CLOCK.
Clock protein role in proteasomal and autophagic BMAL1 degradation and glucose homeostasis
CLOCK transcription control of Wnt signaling promotes cell cycle progression in 3T3-L1 preadipocytes.
results demonstrate that the core circadian gene Clock regulates bone formation via transcriptional control of 1,2,5(OH)2D3 receptor PDIA3
These results suggest that bone resorption and bone mass are regulated at a sophisticated level by osteoblastic Clock system through a mechanism relevant to the modulation of 1,25(OH)2 D3 -induced Rankl expression in osteoblasts.
Abundance of CDH1 and TP63 proteins were significantly reduced in cultures transfected with shClock These data support how CLOCK plays a role in regulation of epithelial cell growth and differentiation in the mammary gland.
Data demonstrate that CLOCK and BMAL1 regulate muscle insulin sensitivity via SIRT1, and activation of SIRT1 might be a potential valuable strategy to attenuate muscle insulin resistance related to circadian misalignment.
The CLOCK SNP may affect daytime gastric motility less than food stimulation.
Significant associations for polymorphisms in CLOCK, NPSR1 and SLC6A3 with traffic crash parameters in professional bus drivers were found.
As a novel CLOCK-dependent diurnal gene, TIMP3 inhibits the expression of inflammatory cytokines that are up-regulated by UV irradiation in human keratinocytes.
the CLOCK gene polymorphism is one of factors determining elastic properties of vascular wall
Rhythmic luciferase activity from clock gene luciferase reporter cells lines was used to test the effect of p38 MAPK inhibition on clock properties as determined using the damped sine fit and Levenberg-Marquardt algorithm.Glioma treatment with p38 MAPK inhibitors may be more effective and less toxic if administered at the appropriate time of the day.
data suggest that SNP variability in the CLOCK gene for rs6850524 and rs11932595 is associated with idiopathic recurrent spontaneous abortion in pregnancies from Slovenia and Serbia
Results indicated that inhibiting the circadian gene Clock expression can reverse the cisplatin resistance of ovarian cancer SKOV3/DDP cell lines by affecting the protein expression of drug resistance genes during which autophagy plays an important role.
Association between HCRTR2, ADH4,CLOCK gene polymorphisms and cluster headache was not significant in the present study.
No association between 3111T/C Clock gene polymorphism and complaints of patients with insomnia was detected.
Study found three gene variants (CLOCK-rs4864548, PEMT-rs936108, and GHRELIN-rs696217) that exhibited uncorrected gene-by-sleep duration interactions in relation to BMI z-scores in a cohort of New Zealand European children. However, no interactions were identified in percentage body fat differences. Notably, these interactions are evident without detectable effects on sleep duration.
These findings suggest that upregulation of the circadian gene hClock plays an important role in metastasis of colorectal cancer.
results of this study suggest that genetic variability in the ARNTL and CLOCK genes might be associated with risk for multiple sclerosis
CLOCK rs1801260*C and PER3(4/4) influence myelination processes by regulating sleep quality and quantity.
Evening chronotype is associated with higher obesity in severely obese subjects and with lower weight loss effectiveness after bariatric surgery. In addition, circadian preferences interact with CLOCK 3111T/C for obesity. The circadian and genetic assessment could provide tailored weight loss recommendations in subjects who underwent bariatric surgery.
CLOCK regulates the expression of genes involved in neuronal migration, and a functional assay showed that CLOCK knockdown increased neuronal migratory distance.
Our findings suggest that CLOCK and CRY1 polymorphisms might be involved in individual susceptibility to abdominal obesity in Chinese Han population.
Our results suggest that the circadian gene human Clock may play an important role in carcinogenesis by inhibiting apoptotic cell death via attenuating proapoptotic signaling
the second half of the photolyase homology region (PHR) of CRY is important for repression through facilitating interaction with CLOCK
This gene product regulates circadian rhythm and metabolism. The protein encodes a transcription factor of the basic helix-loop-helix (bHLH) family and a DNA binding histone acetyltransferase. Polymorphisms in this gene may be associated with behavioral changes in certain populations and with obesity and metabolic syndrome. Alternative splicing results in multiple transcript variants.
, clock homolog (mouse)
, clock homolog
, circadian locomoter output cycles protein kaput
, circadian locomoter output cycles protein kaput-like
, circadian locomoter output cycles kaput
, circadian locomoter output cycles kaput protein
, class E basic helix-loop-helix protein 8
, circadian rhythmicity protein CLOCK