ArticleNeuroscience2023
Ribosomal S6 Kinase Regulates the Timing and Entrainment of the Mammalian Circadian Clock Located in the Suprachiasmatic Nucleus.
Article in Neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- β-arrestin1 orchestrates endosomal signaling to regulate translational control of circadian light entrainment.Communications biology · 2026Article
- Circadian timing and entrainment properties of the SCN pacemaker in the PS19 mouse model of tau pathology.Experimental neurology · 2025Article
- RSK1 and RSK2 as therapeutic targets: an up-to-date snapshot of emerging data.Expert opinion on therapeutic targets · 2024Review
- Ribosomal S6 kinase signaling regulates neuronal viability during development and confers resistance to excitotoxic cell death in mature neurons.Neuroscience · 2024Article
- Therapeutic targeting of p90 ribosomal S6 kinase.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Previous work in the suprachiasmatic nucleus (SCN), the locus of the principal circadian clock, has shown that the activation state of the ERK/MAPK effector p90 ribosomal S6 kinase (RSK) is responsive to photic stimulation and is modulated across the circadian cycle. These data raise the prospect that RSK signaling contributes to both SCN clock timing and entrainment. Here, we found marked expression of the three main RSK isoforms (RSK1/2/3) within the SCN of C57/Bl6 mice. Further, using a combination of immunolabeling and proximity ligation assays, we show that photic stimulation led to the dissociation of RSK from ERK and the translocation of RSK from the cytoplasm to the nucleus. To test for RSK functionality following light treatment, animals received an intraventricular infusion of the selective RSK inhibitor, SL0101, 30 min prior to light (100 lux) exposure during the early circadian night (circadian time 15). Notably, the disruption of RSK signaling led to a significant reduction (∼45 min) in the phase delaying effects of light, relative to vehicle-infused mice. To test the potential contribution of RSK signaling to SCN pacemaker activity, slice cultures from a per1-Venus circadian reporter mouse line were chronically treated with SL0101. Suppression of RSK signaling led to a significant lengthening of the circadian period (∼40 min), relative to vehicle-treated slices. Together, these data reveal that RSK functions as a signaling intermediate that regulates light-evoked clock entrainment and the inherent time keeping properties of the SCN.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.