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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 (show COX6C Proteins), and cry expression is sufficient to drive clock expression in naive cells
propose that the dCLK/CYC (show COX6C Proteins)-controlled TTFL operates differently in subsets of pacemaker neurons, which may contribute to their specific functions
Here we demonstrate that the transcription factor CLOCKWORK ORANGE (CWO) antagonizes CLK-CYC (show COX6C Proteins) E-box binding, thus enhancing the removal of CLK-CYC (show COX6C Proteins) 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 (show COX6C Proteins) 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 (show ARNTL Proteins) 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 (show COX6C Proteins) context-specific binding sites reveals sequence motifs for putative partner factors, which are predictive for individual binding sites
usp8 (show USP8 Proteins) loss of function (RNAi) or expression of a dominant-negative form of the protein (USP8 (show USP8 Proteins)-DN) enhances CLK/CYC (show COX6C Proteins) 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
Data suggest that Clock1a coordinates mesoderm development and primitive hematopoiesis in embryos by up-regulating Nodal-Smad3 (show SMAD3 Proteins) signaling; Clock1a alterations produce embryonic defects with shortened body length, lack of ventral tail fin, or partial defect of the eyes; Clock1a activates Smad3a (show SMAD3 Proteins) promoter via its E-box1 element. (Clock1a = clock circadian regulator a; Nodal = nodal modulator 1 (show NOMO1 Proteins); Smad3a (show SMAD3 Proteins) = SMAD (show SMAD1 Proteins) family member 3a)
effect of CRY (show CRY2 Proteins) in repressing transcription mediated by CLOCK-BMAL heterodimer
Low expression of CLOCK protein (show ARNTL Proteins) is associated with kidney tumor.
PML (show PML Proteins) mediates the binding of PER2 (show PER2 Proteins) to BMAL1 (show ARNTL Proteins) in the BMAL1 (show ARNTL Proteins)/CLOCK heterodimer and is an important component in the organization of a functional clock complex in the nucleus.
Data show that CRY1 (show CRY1 Proteins) binds directly to the PAS (show PASK Proteins) domain core of CLOCK:BMAL1, driven primarily by interaction with the CLOCK PAS (show PASK Proteins)-B domain.
CLOCK temporally gates mast cell responses to IL-33 (show IL33 Proteins) via regulation of ST2 (show SULT2A1 Proteins) expression. Our findings provide novel insights into IL-33 (show IL33 Proteins)/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 (show TFEB Proteins) regulates PER3 expression via glucose-dependent effects on CLOCK/BMAL1 (show ARNTL Proteins)
ASS1 (show ASS1 Proteins) acetylation by CLOCK exhibits circadian oscillation in human cells and mouse liver, possibly caused by rhythmic interaction between CLOCK and ASS1 (show ASS1 Proteins), leading to the circadian regulation of ASS1 (show ASS1 Proteins) and ureagenesis.
Disruption of CLOCK protein (show ARNTL Proteins) alters cortical circuits and leads to generation of focal epilepsy.
Development of Mineralocorticoid receptor (show NR3C2 Proteins)-mediated cardiac inflammation and fibrosis is dependent on intact signaling by the circadian protein CLOCK.
Clock protein (show ARNTL Proteins) role in proteasomal and autophagic BMAL1 (show ARNTL Proteins) degradation and glucose homeostasis
Rhythmic luciferase activity from clock gene luciferase reporter cells lines was used to test the effect of p38 MAPK (show MAPK14 Proteins) inhibition on clock properties as determined using the damped sine fit and Levenberg-Marquardt algorithm.Glioma treatment with p38 MAPK (show MAPK14 Proteins) inhibitors may be more effective and less toxic if administered at the appropriate time of the day.
Results indicated that inhibiting the circadian gene Clock expression can reverse the cisplatin resistance of ovarian cancer SKOV3/DDP (show TIMM8A Proteins) 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.
Study found three gene variants (CLOCK-rs4864548, PEMT (show PEMT Proteins)-rs936108, and GHRELIN (show GHRL Proteins)-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 (show ARNTL Proteins) 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.
Our findings suggest that CLOCK and CRY1 polymorphisms might be involved in individual susceptibility to abdominal obesity in Chinese Han population.
the second half of the photolyase homology region (PHR) of CRY (show CRY2 Proteins) 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