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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 (zeige COX6C Proteine), and cry expression is sufficient to drive clock expression in naive cells
propose that the dCLK/CYC (zeige COX6C Proteine)-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 (zeige COX6C Proteine) E-box binding, thus enhancing the removal of CLK-CYC (zeige COX6C Proteine) 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 (zeige COX6C Proteine) 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 (zeige ARNTL Proteine) 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 (zeige COX6C Proteine) context-specific binding sites reveals sequence motifs for putative partner factors, which are predictive for individual binding sites
usp8 (zeige USP8 Proteine) loss of function (RNAi) or expression of a dominant-negative form of the protein (USP8 (zeige USP8 Proteine)-DN) enhances CLK/CYC (zeige COX6C Proteine) 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 (zeige SMAD3 Proteine) signaling; Clock1a alterations produce embryonic defects with shortened body length, lack of ventral tail fin, or partial defect of the eyes; Clock1a activates Smad3a (zeige SMAD3 Proteine) promoter via its E-box1 element. (Clock1a = clock circadian regulator a; Nodal = nodal modulator 1 (zeige NOMO1 Proteine); Smad3a (zeige SMAD3 Proteine) = SMAD (zeige SMAD1 Proteine) family member 3a)
effect of CRY (zeige CRY2 Proteine) in repressing transcription mediated by CLOCK-BMAL heterodimer
PML (zeige PML Proteine) mediates the binding of PER2 (zeige PER2 Proteine) to BMAL1 (zeige ARNTL Proteine) in the BMAL1 (zeige ARNTL Proteine)/CLOCK heterodimer and is an important component in the organization of a functional clock complex in the nucleus.
Data show that CRY1 (zeige CRY1 Proteine) binds directly to the PAS (zeige PASK Proteine) domain core of CLOCK:BMAL1, driven primarily by interaction with the CLOCK PAS (zeige PASK Proteine)-B domain.
CLOCK temporally gates mast cell responses to IL-33 (zeige IL33 Proteine) via regulation of ST2 (zeige SULT2A1 Proteine) expression. Our findings provide novel insights into IL-33 (zeige IL33 Proteine)/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 (zeige TFEB Proteine) regulates PER3 expression via glucose-dependent effects on CLOCK/BMAL1 (zeige ARNTL Proteine)
ASS1 (zeige ASS1 Proteine) acetylation by CLOCK exhibits circadian oscillation in human cells and mouse liver, possibly caused by rhythmic interaction between CLOCK and ASS1 (zeige ASS1 Proteine), leading to the circadian regulation of ASS1 (zeige ASS1 Proteine) and ureagenesis.
Disruption of CLOCK protein (zeige ARNTL Proteine) alters cortical circuits and leads to generation of focal epilepsy.
Development of Mineralocorticoid receptor (zeige NR3C2 Proteine)-mediated cardiac inflammation and fibrosis is dependent on intact signaling by the circadian protein CLOCK.
Clock protein (zeige ARNTL Proteine) role in proteasomal and autophagic BMAL1 (zeige ARNTL Proteine) degradation and glucose homeostasis
CLOCK transcription control of Wnt (zeige WNT2 Proteine) signaling promotes cell cycle progression in 3T3-L1 preadipocytes.
Study found three gene variants (CLOCK-rs4864548, PEMT (zeige PEMT Proteine)-rs936108, and GHRELIN (zeige GHRL Proteine)-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 (zeige ARNTL Proteine) 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 (zeige PER2 Proteine) gene with Late Onset Depression and Alzheimer's Disease in a Sample of a Brazilian Population
found that overexpression of both Clock and Bmal1 (zeige ARNTL Proteine) 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 (zeige CRY2 Proteine) 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