ArticleCell cycle (Georgetown, Tex.)2015
Loss of CDK5RAP2 affects neural but not non-neural mESC differentiation into cardiomyocytes.
Article in Cell cycle (Georgetown, Tex.), 2015. 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, 14 citations in OpenAlex.
- Expanding the genetic spectrum of autosomal recessive microcephaly in Pakistani families.BMC neurology · 2026Article
- Pathogenic LRRK2 regulates centrosome cohesion via Rab10/RILPL1-mediated CDK5RAP2 displacement.iScience · 2022Article
- Homozygous mutation inJournal of medical genetics · 2022Article
- Characterization of the Synergistic Inhibition ofInternational journal of molecular sciences · 2020Article
- Whole-exome sequencing identifies homozygous mutation in TTI2 in a child with primary microcephaly: a case report.BMC neurology · 2020Article
- Endoplasmic reticulum and Golgi stress in microcephaly.Cell stress · 2019Review
- Arrayed mutant haploid embryonic stem cell libraries facilitate phenotype-driven genetic screens.Nucleic acids research · 2017Article
- CDK5RAP2 Is Required to Maintain the Germ Cell Pool during Embryonic Development.Stem cell reports · 2017Article
- Novel Alternative Splice Variants of Mouse Cdk5rap2.PloS one · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Biallelic mutations in the gene encoding centrosomal CDK5RAP2 lead to autosomal recessive primary microcephaly (MCPH), a disorder characterized by pronounced reduction in volume of otherwise architectonical normal brains and intellectual deficit. The current model for the microcephaly phenotype in MCPH invokes a premature shift from symmetric to asymmetric neural progenitor-cell divisions with a subsequent depletion of the progenitor pool. The isolated neural phenotype, despite the ubiquitous expression of CDK5RAP2, and reports of progressive microcephaly in individual MCPH cases prompted us to investigate neural and non-neural differentiation of Cdk5rap2-depleted and control murine embryonic stem cells (mESC). We demonstrate an accumulating proliferation defect of neurally differentiating Cdk5rap2-depleted mESC and cell death of proliferative and early postmitotic cells. A similar effect does not occur in non-neural differentiation into beating cardiomyocytes, which is in line with the lack of non-central nervous system features in MCPH patients. Our data suggest that MCPH is not only caused by premature differentiation of progenitors, but also by reduced propagation and survival of neural progenitors.
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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.