ArticleMolecular and cellular biology2011
Deregulation of the p57-E2F1-p53 axis results in nonobstructive hydrocephalus and cerebellar malformation in mice.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Role of the imprinted allele of the Cdkn1c gene in mouse neocortical development.Scientific reports · 2020Article
- Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development.Nature communications · 2020Article
- Role of genomic imprinting in mammalian development.Journal of biosciences · 2020Review
- Functional Versatility of the CDK Inhibitor p57Frontiers in cell and developmental biology · 2020Review
- New Perspectives on Genomic Imprinting, an Essential and Multifaceted Mode of Epigenetic Control in the Developing and Adult Brain.Annual review of neuroscience · 2016Review
- Stem cells: slow and steady wins the race.Nature neuroscience · 2015Article
- Slowly dividing neural progenitors are an embryonic origin of adult neural stem cells.Nature neuroscience · 2015Article
- GABAergic neurons regulate lateral ventricular development via transcription factor Pax5.Genesis (New York, N.Y. : 2000) · 2013Article
- Morinda citrifolia L. (noni) and memantine attenuate periventricular tissue injury of the fourth ventricle in hydrocephalic rabbits.Neural regeneration research · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cyclin-dependent kinase inhibitor (CKI) p57(Kip2) plays a pivotal role in cell cycle arrest during development, in particular, in the regulation of the entry of proliferating progenitors into quiescence. The gene encoding p57 undergoes genomic imprinting, and impairment of the regulation of p57 expression results in various developmental anomalies in humans and mice. We now show that p57 is expressed predominantly in the subcommissural organ and cerebellar interneurons in the mouse brain and that mice with brain-specific deletion of the p57 gene (Kip2) manifest prominent nonobstructive hydrocephalus as well as cerebellar malformation associated with the loss of Pax2-positive interneuron precursors and their descendants, including Golgi cells and γ-aminobutyric acid-containing neurons of the deep cerebellar nuclei. These abnormalities were found to be attributable to massive apoptosis of precursor cells in the developing brain. The morphological defects of the p57-deficient mice were corrected by knock-in of the gene for the related CKI p27(Kip1) at the Kip2 locus. The abnormalities were also prevented by additional genetic ablation of p53 or E2F1. Our results thus implicate p57 in cell cycle arrest in the subcommissural organ and Pax2-positive interneuron precursors, with the lack of p57 resulting in induction of p53-dependent apoptosis due to hyperactivation of E2F1.
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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.