ArticleNucleic acids research2020
Necdin regulates BMAL1 stability and circadian clock through SGT1-HSP90 chaperone machinery.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- BMAL1 in cardiovascular diseases: Molecular mechanisms, circadian regulation and translational perspectives (Review).Molecular medicine reports · 2026Review
- Tanycyte BMAL1 regulates high-fat diet weight gain and shapes arcuate neurogenesis in female mice.Cell reports · 2026Article
- Loss of Necdin causes social deficit and aberrant synaptic function through destabilization of SynGAP.Molecular psychiatry · 2026Article
- Review
- UBE3A reinstatement restores behaviorand proteome in an Angelman syndrome mouse model of imprinting defects.Molecular autism · 2025Article
- Mechanism by which SUGT1 downregulates FH to promote proliferation and migration in serous ovarian cancer.Journal of ovarian research · 2025Article
- Selective changes in vasopressin neurons and astrocytes in the suprachiasmatic nucleus of Prader-Willi syndrome subjects.Journal of neuroendocrinology · 2025Article
- Investigation of a mouse model of Prader-Willi Syndrome with combined disruption of Necdin and Magel2.JCI insight · 2025Article
- Prader-Willi syndrome protein necdin regulates the nucleocytoplasmic distribution and dopaminergic neuron development.Scientific reports · 2024Article
- Deficiency in Prader-Willi syndrome geneiScience · 2024Article
- Neuronal and glial vulnerability of the suprachiasmatic nucleus in tauopathies: evidence from human studies and animal models.Molecular neurodegeneration · 2024Review
- Hormonal Imbalances in Prader-Willi and Schaaf-Yang Syndromes Imply the Evolution of Specific Regulation of Hypothalamic Neuroendocrine Function in Mammals.International journal of molecular sciences · 2023Review
- CNTNAP2 intracellular domain (CICD) generated by γ-secretase cleavage improves autism-related behaviors.Signal transduction and targeted therapy · 2023Article
- Diurnal Changes in Capecitabine Clock-Controlled Metabolism Enzymes Are Responsible for Its Pharmacokinetics in Male Mice.Journal of biological rhythms · 2023Article
- TRITHORAX-dependent arginine methylation of HSP68 mediates circadian repression by PERIOD in the monarch butterfly.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Do the diverse phenotypes of Prader-Willi syndrome reflect extremes of covariation in typical populations?Frontiers in genetics · 2022Article
- Necdin: A purposive integrator of molecular interaction networks for mammalian neuron vitality.Genes to cells : devoted to molecular & cellular mechanisms · 2021Review
- Hypothalamic neuropeptides and neurocircuitries in Prader Willi syndrome.Journal of neuroendocrinology · 2021Review
- A Comprehensive Review of Genetically Engineered Mouse Models for Prader-Willi Syndrome Research.International journal of molecular sciences · 2021Review
- Translational Regulation of Clock Genes BMAL1 and REV-ERBα by Polyamines.International journal of molecular sciences · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Circadian clocks are endogenous oscillators that control ∼24-hour physiology and behaviors in virtually all organisms. The circadian oscillator comprises interconnected transcriptional and translational feedback loops, but also requires finely coordinated protein homeostasis including protein degradation and maturation. However, the mechanisms underlying the mammalian clock protein maturation is largely unknown. In this study, we demonstrate that necdin, one of the Prader-Willi syndrome (PWS)-causative genes, is highly expressed in the suprachiasmatic nuclei (SCN), the pacemaker of circadian clocks in mammals. Mice deficient in necdin show abnormal behaviors during an 8-hour advance jet-lag paradigm and disrupted clock gene expression in the liver. By using yeast two hybrid screening, we identified BMAL1, the core component of the circadian clock, and co-chaperone SGT1 as two necdin-interactive proteins. BMAL1 and SGT1 associated with the N-terminal and C-terminal fragments of necdin, respectively. Mechanistically, necdin enables SGT1-HSP90 chaperone machinery to stabilize BMAL1. Depletion of necdin or SGT1/HSP90 leads to degradation of BMAL1 through the ubiquitin-proteasome system, resulting in alterations in both clock gene expression and circadian rhythms. Taken together, our data identify the PWS-associated protein necdin as a novel regulator of the circadian clock, and further emphasize the critical roles of chaperone machinery in circadian clock regulation.
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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.