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propose that the dCLK/CYC (Montrer COX6C Kits ELISA)-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 (Montrer COX6C Kits ELISA) E-box binding, thus enhancing the removal of CLK-CYC (Montrer COX6C Kits ELISA) 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 Kits ELISA) 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 Kits ELISA) 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 Kits ELISA) context-specific binding sites reveals sequence motifs for putative partner factors, which are predictive for individual binding sites
usp8 (Montrer USP8 Kits ELISA) loss of function (RNAi) or expression of a dominant-negative form of the protein (USP8 (Montrer USP8 Kits ELISA)-DN) enhances CLK/CYC (Montrer COX6C Kits ELISA) 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 (Montrer SMAD3 Kits ELISA) 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 Kits ELISA) promoter via its E-box1 element. (Clock1a = clock circadian regulator a; Nodal = nodal modulator 1 (Montrer NOMO1 Kits ELISA); Smad3a (Montrer SMAD3 Kits ELISA) = SMAD (Montrer SMAD1 Kits ELISA) family member 3a)
effect of CRY (Montrer CRY2 Kits ELISA) in repressing transcription mediated by CLOCK-BMAL heterodimer
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 (Montrer ARNTL Kits ELISA)
ASS1 (Montrer ASS1 Kits ELISA) acetylation by CLOCK exhibits circadian oscillation in human cells and mouse liver, possibly caused by rhythmic interaction between CLOCK and ASS1 (Montrer ASS1 Kits ELISA), leading to the circadian regulation of ASS1 (Montrer ASS1 Kits ELISA) and ureagenesis.
Disruption of CLOCK protein (Montrer ARNTL Kits ELISA) alters cortical circuits and leads to generation of focal epilepsy.
Development of Mineralocorticoid receptor (Montrer NR3C2 Kits ELISA)-mediated cardiac inflammation and fibrosis is dependent on intact signaling by the circadian protein CLOCK.
Clock protein (Montrer ARNTL Kits ELISA) role in proteasomal and autophagic BMAL1 (Montrer ARNTL Kits ELISA) degradation and glucose homeostasis
CLOCK transcription control of Wnt (Montrer WNT2 Kits ELISA) 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 Kits ELISA)
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 Kits ELISA) expression in osteoblasts.
Abundance of CDH1 (Montrer CDH1 Kits ELISA) and TP63 (Montrer TP63 Kits ELISA) 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.
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 (Montrer PER2 Kits ELISA) 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 Kits ELISA) 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 Kits ELISA) 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 Kits ELISA) 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
the second half of the photolyase homology region (PHR) of CRY (Montrer CRY2 Kits ELISA) 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