ArticleCerebral cortex (New York, N.Y. : 1991)2011
The cyclin-dependent kinase inhibitor p57Kip2 regulates cell cycle exit, differentiation, and migration of embryonic cerebral cortical precursors.
Article in Cerebral cortex (New York, N.Y. : 1991), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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.
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Who cites it
42 citing papers in PubMed, 77 citations in OpenAlex.
- A low-level Cdkn1c/p57EMBO reports · 2026Article
- p57International journal of molecular sciences · 2024Article
- Article
- IGF2 interacts with the imprinted gene Cdkn1c to promote terminal differentiation of neural stem cells.Development (Cambridge, England) · 2023Article
- p27International journal of molecular sciences · 2022Article
- Deep exploration of aJournal of medical genetics · 2022Article
- p57 Suppresses the Pluripotency and Proliferation of Mouse Embryonic Stem Cells by Positively Regulating p53 Activation.Stem cells international · 2021Article
- Case Report: Liraglutide for Weight Management in Beckwith-Wiedemann Syndromic Obesity.Frontiers in endocrinology · 2021Article
- Core cell cycle machinery is crucially involved in both life and death of post-mitotic neurons.Cellular and molecular life sciences : CMLS · 2020Review
- Visualizing Cell Cycle Phase Organization and Control During Neural Lineage Elaboration.Cells · 2020Article
- Cyclins, Cyclin-Dependent Kinases, and Cyclin-Dependent Kinase Inhibitors in the Mouse Nervous System.Molecular neurobiology · 2020Review
- Requirement of PP2A-B56iScience · 2020Article
- Role of the imprinted allele of the Cdkn1c gene in mouse neocortical development.Scientific reports · 2020Article
- Functional Versatility of the CDK Inhibitor p57Frontiers in cell and developmental biology · 2020Review
- Divide or Commit - Revisiting the Role of Cell Cycle Regulators in Adult Hippocampal Neurogenesis.Frontiers in cell and developmental biology · 2019Review
- Modulation of Nerve Cell Differentiation: Role of Polyphenols and of Contactin Family Components.Frontiers in cell and developmental biology · 2019Article
- Genetic and Epigenetic Control of CDKN1C Expression: Importance in Cell Commitment and Differentiation, Tissue Homeostasis and Human Diseases.International journal of molecular sciences · 2018Review
- Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells (NPCs).Journal of visualized experiments : JoVE · 2018Article
- Dopaminergic and behavioural changes in a loss-of-imprinting model of Cdkn1c.Genes, brain, and behavior · 2018Article
- Territorial Behavior and Social Stability in the Mouse Require Correct Expression of ImprintedFrontiers in behavioral neuroscience · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mounting evidence indicates cyclin-dependent kinase (CDK) inhibitors (CKIs) of the Cip/Kip family, including p57(Kip2) and p27(Kip1), control not only cell cycle exit but also corticogenesis. Nevertheless, distinct activities of p57(Kip2) remain poorly defined. Using in vivo and culture approaches, we show p57(Kip2) overexpression at E14.5-15.5 elicits precursor cell cycle exit, promotes transition from proliferation to neuronal differentiation, and enhances process outgrowth, while opposite effects occur in p57(Kip2)-deficient precursors. Studies at later ages indicate p57(Kip2) overexpression also induces precocious glial differentiation, suggesting stage-dependent effects. In embryonic cortex, p57(Kip2) overexpression advances cell radial migration and alters postnatal laminar positioning. While both CKIs induce differentiation, p57(Kip2) was twice as effective as p27(Kip1) in inducing neuronal differentiation and was not permissive to astrogliogenic effects of ciliary neurotrophic factor, suggesting that the CKIs differentially modulate cell fate decisions. At molecular levels, although highly conserved N-terminal regions of both CKIs elicit cycle withdrawal and differentiation, the C-terminal region of p57(Kip2) alone inhibits in vivo migration. Furthermore, p57(Kip2) effects on neurogenesis and gliogenesis require the N-terminal cyclin/CDK binding/inhibitory domains, while previous p27(Kip1) studies report cell cycle-independent functions. These observations suggest p57(Kip2) coordinates multiple stages of corticogenesis and exhibits distinct and common activities compared with related family member p27(Kip1).
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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.