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anti-Mouse (Murine) CLOCK Antibodies:
anti-Rat (Rattus) 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 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
propose that the dCLK/CYC (show COX6C Antibodies)-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 Antibodies) E-box binding, thus enhancing the removal of CLK-CYC (show COX6C Antibodies) 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 Antibodies) 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 Antibodies) 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 Antibodies) context-specific binding sites reveals sequence motifs for putative partner factors, which are predictive for individual binding sites
usp8 (show USP8 Antibodies) loss of function (RNAi) or expression of a dominant-negative form of the protein (USP8 (show USP8 Antibodies)-DN) enhances CLK/CYC (show COX6C Antibodies) 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
Data suggest that Clock1a coordinates mesoderm development and primitive hematopoiesis in embryos by up-regulating Nodal-Smad3 (show SMAD3 Antibodies) 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 Antibodies) promoter via its E-box1 element. (Clock1a = clock circadian regulator a; Nodal = nodal modulator 1 (show NOMO1 Antibodies); Smad3a (show SMAD3 Antibodies) = SMAD (show SMAD1 Antibodies) family member 3a)
effect of CRY (show CRY2 Antibodies) in repressing transcription mediated by CLOCK-BMAL heterodimer
CLOCK temporally gates mast cell responses to IL-33 (show IL33 Antibodies) via regulation of ST2 (show SULT2A1 Antibodies) expression. Our findings provide novel insights into IL-33 (show IL33 Antibodies)/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 Antibodies) regulates PER3 expression via glucose-dependent effects on CLOCK/BMAL1 (show ARNTL Antibodies)
ASS1 (show ASS1 Antibodies) acetylation by CLOCK exhibits circadian oscillation in human cells and mouse liver, possibly caused by rhythmic interaction between CLOCK and ASS1 (show ASS1 Antibodies), leading to the circadian regulation of ASS1 (show ASS1 Antibodies) and ureagenesis.
Disruption of CLOCK protein (show ARNTL Antibodies) alters cortical circuits and leads to generation of focal epilepsy.
Development of Mineralocorticoid receptor (show NR3C2 Antibodies)-mediated cardiac inflammation and fibrosis is dependent on intact signaling by the circadian protein CLOCK.
Clock protein (show ARNTL Antibodies) role in proteasomal and autophagic BMAL1 (show ARNTL Antibodies) degradation and glucose homeostasis
CLOCK transcription control of Wnt (show WNT2 Antibodies) 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 (show PDIA3 Antibodies)
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 (show TNFSF11 Antibodies) expression in osteoblasts.
Study found three gene variants (CLOCK-rs4864548, PEMT (show PEMT Antibodies)-rs936108, and GHRELIN (show GHRL Antibodies)-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 Antibodies) 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.
This study showed that Lack of Association between Genetic Polymorphism of clock gene with Late Onset Depression and Alzheimer's Disease in a Sample of a Brazilian Population This study showed that Lack of Association between Genetic Polymorphism of PER2 (show PER2 Antibodies) gene with Late Onset Depression and Alzheimer's Disease in a Sample of a Brazilian Population
found that overexpression of both Clock and Bmal1 (show ARNTL Antibodies) suppressed cell growth
Clock circadian regulator (CLOCK) gene single nucleotide polymorphism rs1801260 minor allele C showed a significantly higher association with the prevalence of diabetes in the Japanese population independent of body mass index (BMI).
the second half of the photolyase homology region (PHR) of CRY (show CRY2 Antibodies) 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