CLOCK antibody - N-terminal region (ARP33730_P050)
- Known as:
- CLOCK (anti-) - N-terminal region (ARP33730_P050)
- Catalog number:
- arp33730_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CLOCK antibody - N-terminal region (ARP33730_P050)
Related genes to: CLOCK antibody - N-terminal region (ARP33730_P050)
- Gene:
- CLOCK NIH gene
- Name:
- clock circadian regulator
- Previous symbol:
- -
- Synonyms:
- KIAA0334, KAT13D, bHLHe8
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-19
- Date modifiied:
- 2015-09-11
Related products to: CLOCK antibody - N-terminal region (ARP33730_P050)
Related articles to: CLOCK antibody - N-terminal region (ARP33730_P050)
- - Source: PubMed
Publication date: 2026/09/04
- Bone remodeling is regulated by circadian rhythm, yet the molecular mechanisms linking circadian clock components to osteoclast function remain largely undefined. We previously showed that osteoclast-specific deletion of Per1, a core circadian regulator, increased osteoclastogenesis and reduced bone mass in male mice, whereas deletion of Per2 had little effect. Here, we investigated Per1;Per2 conditional double-knockout (dKO) mice and unexpectedly found the opposite phenotype. In contrast to Per1 deficiency, dKO suppressed osteoclastogenesis and increased bone mass specifically in male mice, revealing previously unrecognized functional interactions between PER1 and PER2 in osteoclasts. Transcriptomic analyses showed that dKO osteoclasts preferentially downregulated innate immunity genes, including both positive and negative regulators of osteoclastogenesis. Chromatin immunoprecipitation and reporter assays further identified innate immunity genes as downstream targets of PER-dependent circadian regulation. These findings indicate that PER1 and PER2 regulate osteoclastogenesis through coordinated control of a network of immune genes with opposing effects on osteoclast differentiation, rather than acting as simple promoters or inhibitors of bone resorption. More broadly, this study establishes innate immunity as a mechanistic interface between the circadian clock and osteoclast function, providing a framework for understanding how circadian disruption influences bone remodeling and inflammatory bone diseases. - Source: PubMed
Publication date: 2026/09/04
Katoku-Kikyo NobukoVu Elizabeth KMitchell SamuelKarkache Ismael YPatterson EmilyBradley Elizabeth WKikyo Nobuaki - Circadian rhythms are endogenous oscillations of approximately 24 h that regulate a wide range of cellular and physiological processes, including gene expression, metabolism, and behavior. These rhythms arise from interconnected transcriptional-translational feedback loops that respond to temporal and environmental cues. Because circadian regulation is highly dynamic, even minor experimental variations can influence phase, amplitude, and rhythmicity, making standardized experimental workflows essential for generating reliable and reproducible results. The goal of the present protocol is to provide a practical and reproducible workflow for synchronizing cultured cells, performing time-course sampling, and analyzing circadian clock gene expression under standard laboratory conditions. The protocol describes serum shock-based synchronization, staggered sample collection over 24-72 h to avoid overnight sampling, ribonucleic acid extraction, complementary deoxyribonucleic acid synthesis, quantitative real-time polymerase chain reaction, and circadian rhythm analysis using appropriate statistical approaches. The workflow also highlights critical experimental considerations, including synchronization conditions, sample quality assessment, reference gene selection, and data analysis, to improve reproducibility across experiments. This method provides an accessible approach for investigating molecular circadian mechanisms and evaluating rhythmic gene expression in cultured cells, facilitating studies of circadian regulation in physiological and disease-related experimental models. - Source: PubMed
Publication date: 2026/09/03
Ramalho BárbaraFernandes CristianaSantos BárbaraGaspar Laetitia SRibeiro Rodrigo F NCavadas CláudiaCapitão AnaÁlvaro Ana Rita - Caffeine, a widely consumed psychoactive substance, has known effects on physiological and behavioral processes. Recent studies report that caffeine can influence the circadian rhythm, which is linked to many aspects of physiology, energy metabolism, and homeostasis. Therefore, we examined the arousal effects of caffeine via behavioral tests and assessed its impact on the circadian rhythm by measuring clock gene and clock-controlled gene expression in the brains of mice and Neuro 2a (N2a) cells. - Source: PubMed
Park SookyoungKhan Zeeshan AhmadAnsari AbuZarShamali Urala Kalasi ApsaraKar Anik KumarLee YejinLee GwangbaeKim JaeyeongSon SeminHong Yonggeun - Previous research in time perception has predominantly focused on how cognitive and emotional factors influence subjective time perception. However, investigations into whether subjective time perception, in turn, affects emotional and cognitive outcomes remain limited. To address this, the current study systematically examined how external clocks, rigged to run faster or slower, impact cognitive performance and subjective experience across tasks varying in complexity and attentional demand. Our findings challenge previous findings of enhanced cognitive performance under accelerated clocks and suggest that task demands may have superseded clock speed effects. This study highlights the complexities of subjective time perception, suggesting that effective clock speed manipulations require a more active engagement with temporal cues and tasks of moderate cognitive load. Future research should explore the interaction of attention allocation, task difficulty, and subjective time in shaping cognitive and emotional outcomes. - Source: PubMed
Publication date: 2026/09/04
Utegaliyev Narimanvon Castell Christoph