Use your antibodies-online credentials, if available.
抗Mouse (Murine) CLOCK 抗体:
抗Rat (Rattus) CLOCK 抗体:
抗Human CLOCK 抗体:
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 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
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
Here we demonstrate that the transcription factor CLOCKWORK ORANGE (CWO) antagonizes CLK-CYC (显示 COX6C 抗体) E-box binding, thus enhancing the removal of CLK-CYC (显示 COX6C 抗体) 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 (显示 COX6C 抗体) 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 (显示 ARNTL 抗体) 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 (显示 COX6C 抗体) context-specific binding sites reveals sequence motifs for putative partner factors, which are predictive for individual binding sites
usp8 (显示 USP8 抗体) loss of function (RNAi) or expression of a dominant-negative form of the protein (USP8 (显示 USP8 抗体)-DN) enhances CLK/CYC (显示 COX6C 抗体) 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 (显示 COX6C 抗体) act during starvation to modulate the conflict of whether flies sleep or search for food
Data suggest that Clock1a coordinates mesoderm development and primitive hematopoiesis in embryos by up-regulating Nodal-Smad3 (显示 SMAD3 抗体) signaling; Clock1a alterations produce embryonic defects with shortened body length, lack of ventral tail fin, or partial defect of the eyes; Clock1a activates Smad3a (显示 SMAD3 抗体) promoter via its E-box1 element. (Clock1a = clock circadian regulator a; Nodal = nodal modulator 1 (显示 NOMO1 抗体); Smad3a (显示 SMAD3 抗体) = SMAD (显示 SMAD1 抗体) family member 3a)
effect of CRY (显示 CRY2 抗体) in repressing transcription mediated by CLOCK-BMAL heterodimer
ASS1 (显示 ASS1 抗体) acetylation by CLOCK exhibits circadian oscillation in human cells and mouse liver, possibly caused by rhythmic interaction between CLOCK and ASS1 (显示 ASS1 抗体), leading to the circadian regulation of ASS1 (显示 ASS1 抗体) and ureagenesis.
Disruption of CLOCK protein (显示 ARNTL 抗体) alters cortical circuits and leads to generation of focal epilepsy.
Development of Mineralocorticoid receptor (显示 NR3C2 抗体)-mediated cardiac inflammation and fibrosis is dependent on intact signaling by the circadian protein CLOCK.
Clock protein (显示 ARNTL 抗体) role in proteasomal and autophagic BMAL1 (显示 ARNTL 抗体) degradation and glucose homeostasis
CLOCK transcription control of Wnt (显示 WNT2 抗体) 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 (显示 PDIA3 抗体)
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 (显示 TNFSF11 抗体) expression in osteoblasts.
Abundance of CDH1 (显示 CDH1 抗体) and TP63 (显示 TP63 抗体) 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 (显示 ARNTL 抗体) regulate muscle insulin (显示 INS 抗体) sensitivity via SIRT1 (显示 SIRT1 抗体), and activation of SIRT1 (显示 SIRT1 抗体) might be a potential valuable strategy to attenuate muscle insulin (显示 INS 抗体) resistance related to circadian misalignment.
These data establish the importance of circadian CLOCK-inhibin signaling in sepsis.
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 (显示 PER2 抗体) gene with Late Onset Depression and Alzheimer's Disease in a Sample of a Brazilian Population
found that overexpression of both Clock and Bmal1 (显示 ARNTL 抗体) 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).
Immunostaining of CLOCK and PER2 (显示 PER2 抗体) protein was detected in the granulosa cells of dominant antral follicles but was absent in the primordial, primary, or preantral follicles of human ovaries.Oscillating expression of the circadian gene PER2 (显示 PER2 抗体) can be induced by testosterone in human granulosa cells in vitro. Expression of STAR also displayed an oscillating pattern after testosterone stimulation
possible circadian rhythm in full-term placental expression
Findings indicate that CLOCK protein (显示 ARNTL 抗体) plays an important role in fertility and its knockdown leads to reduction in reproduction and increased miscarriage risk.
Upregulation of CLOCK is associated with the expression of HIF-1alpha and VEGF in varicose veins.
when overexpressed, c-MYC (显示 MYC 抗体) is able to repress Per1 (显示 PER1 抗体) transactivation by BMAL1 (显示 ARNTL 抗体)/CLOCK via targeting selective E-box sequences. Importantly, upon serum stimulation, MYC (显示 MYC 抗体) was detected in BMAL1 (显示 ARNTL 抗体) protein complexes
the second half of the photolyase homology region (PHR) of CRY (显示 CRY2 抗体) 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