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anti-Mouse (Murine) CLOCK Anticorps:
anti-Rat (Rattus) CLOCK Anticorps:
anti-Human CLOCK Anticorps:
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Human Polyclonal CLOCK Primary Antibody pour ChIP, WB - ABIN151057
Jin, Shearman, Weaver, Zylka, de Vries, Reppert: A molecular mechanism regulating rhythmic output from the suprachiasmatic circadian clock. dans Cell 1999
Show all 6 Pubmed References
Human Monoclonal CLOCK Primary Antibody pour ICC, ELISA - ABIN969059
Lee, Paik, Kang, Lim, Kim: Allelic variants interaction of CLOCK gene and G-protein beta3 subunit gene with diurnal preference. dans Chronobiology international 2007
Show all 2 Pubmed References
Human Polyclonal CLOCK Primary Antibody pour ELISA, WB - ABIN564129
Kalamvoki, Roizman: Circadian CLOCK histone acetyl transferase localizes at ND10 nuclear bodies and enables herpes simplex virus gene expression. dans Proceedings of the National Academy of Sciences of the United States of America 2010
Polyclonal CLOCK Primary Antibody pour ChIP, IP - ABIN540419
Shearman, Weaver: Photic induction of Period gene expression is reduced in Clock mutant mice. dans Neuroreport 1999
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Human Polyclonal CLOCK Primary Antibody pour IHC - ABIN965906
Steeves, King, Zhao, Sangoram, Du, Bowcock, Moore, Takahashi: Molecular cloning and characterization of the human CLOCK gene: expression in the suprachiasmatic nuclei. dans Genomics 1999
Show all 9 Pubmed References
Here we demonstrate that the transcription factor CLOCKWORK ORANGE (CWO) antagonizes CLK-CYC (Montrer COX6C Anticorps) E-box binding, thus enhancing the removal of CLK-CYC (Montrer COX6C Anticorps) 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 (Montrer COX6C Anticorps) 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 (Montrer ARNTL Anticorps) 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 (Montrer COX6C Anticorps) context-specific binding sites reveals sequence motifs for putative partner factors, which are predictive for individual binding sites
usp8 (Montrer USP8 Anticorps) loss of function (RNAi) or expression of a dominant-negative form of the protein (USP8 (Montrer USP8 Anticorps)-DN) enhances CLK/CYC (Montrer COX6C Anticorps) 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 (Montrer COX6C Anticorps) 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 (Montrer SMAD3 Anticorps) signaling; Clock1a alterations produce embryonic defects with shortened body length, lack of ventral tail fin, or partial defect of the eyes; Clock1a activates Smad3a (Montrer SMAD3 Anticorps) promoter via its E-box1 element. (Clock1a = clock circadian regulator a; Nodal = nodal modulator 1 (Montrer NOMO1 Anticorps); Smad3a (Montrer SMAD3 Anticorps) = SMAD (Montrer SMAD1 Anticorps) family member 3a)
effect of CRY (Montrer CRY2 Anticorps) in repressing transcription mediated by CLOCK-BMAL heterodimer
ASS1 (Montrer ASS1 Anticorps) acetylation by CLOCK exhibits circadian oscillation in human cells and mouse liver, possibly caused by rhythmic interaction between CLOCK and ASS1 (Montrer ASS1 Anticorps), leading to the circadian regulation of ASS1 (Montrer ASS1 Anticorps) and ureagenesis.
Disruption of CLOCK protein (Montrer ARNTL Anticorps) alters cortical circuits and leads to generation of focal epilepsy.
Development of Mineralocorticoid receptor (Montrer NR3C2 Anticorps)-mediated cardiac inflammation and fibrosis is dependent on intact signaling by the circadian protein CLOCK.
Clock protein (Montrer ARNTL Anticorps) role in proteasomal and autophagic BMAL1 (Montrer ARNTL Anticorps) degradation and glucose homeostasis
CLOCK transcription control of Wnt (Montrer WNT2 Anticorps) 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 (Montrer PDIA3 Anticorps)
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 (Montrer TNFSF11 Anticorps) expression in osteoblasts.
Abundance of CDH1 (Montrer CDH1 Anticorps) and TP63 (Montrer TP63 Anticorps) 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 (Montrer ARNTL Anticorps) regulate muscle insulin (Montrer INS Anticorps) sensitivity via SIRT1 (Montrer SIRT1 Anticorps), and activation of SIRT1 (Montrer SIRT1 Anticorps) might be a potential valuable strategy to attenuate muscle insulin (Montrer INS Anticorps) resistance related to circadian misalignment.
These data establish the importance of circadian CLOCK-inhibin signaling in sepsis.
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 (Montrer PER2 Anticorps) gene with Late Onset Depression and Alzheimer's Disease in a Sample of a Brazilian Population
found that overexpression of both Clock and Bmal1 (Montrer ARNTL Anticorps) 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 (Montrer PER2 Anticorps) 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 (Montrer PER2 Anticorps) 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 (Montrer ARNTL Anticorps) 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 (Montrer MYC Anticorps) is able to repress Per1 (Montrer PER1 Anticorps) transactivation by BMAL1 (Montrer ARNTL Anticorps)/CLOCK via targeting selective E-box sequences. Importantly, upon serum stimulation, MYC (Montrer MYC Anticorps) was detected in BMAL1 (Montrer ARNTL Anticorps) protein complexes
CLOCK, ARNTL (Montrer ARNTL Anticorps), and NPAS2 (Montrer NPAS2 Anticorps) gene polymorphisms may have a role in seasonal variations in mood and behavior
the second half of the photolyase homology region (PHR) of CRY (Montrer CRY2 Anticorps) 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