ReviewGenes & development2021
Time is of the essence: the molecular mechanisms of primary microcephaly.
Review in Genes & development, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 92 citations in OpenAlex.
- MCM3 Safeguards Neural Progenitor Maintenance and Cortical Development Against Replication-Associated Stress.Molecular neurobiology · 2026Article
- CDK1 and CEP97 cooperatively control centriole length to orchestrate ciliogenesis and developmental patterning.Genes & development · 2026Article
- Expanding the genetic spectrum of autosomal recessive microcephaly in Pakistani families.BMC neurology · 2026Article
- Microcephaly-associated genes asp and Sas4 influence chromatin organization and nuclear lamina structure in Drosophila melanogaster.Development (Cambridge, England) · 2026Article
- Mutation of Tubgcp6 induces hematopoietic stem and progenitor cell exhaustion in zebrafish.Communications biology · 2026Article
- Enhanced P-TEFb activity compromises dentate gyrus neurogenesis in mice.The EMBO journal · 2026Article
- Bi-allelic variants in FSD1L cause a neurodevelopmental disorder overlapping with L1 syndrome.American journal of human genetics · 2026Article
- ALIX and ITCH localize to the base of primary cilia and negatively regulate ciliary Polycystin-2 levels.BMC molecular and cell biology · 2026Article
- Mitotic errors as triggers of cell death and inflammation.Nature cell biology · 2026Review
- Ttc21b is required for proper proliferation of neural progenitor cells.Disease models & mechanisms · 2026Article
- SARS-CoV-2 pseudoparticles preferentially infect ectoderm in human embryonic tissues.Frontiers in cell and developmental biology · 2026Article
- Cancer-associated USP28 missense mutations disrupt 53BP1 interaction and p53 stabilization.Nature communications · 2025Article
- Review
- Mitotic dynamics of the nuclear lamina in the backstage of chromosome separation.Communications biology · 2025Review
- Metabolic functions for molecular chaperones and stress proteins in microcephaly.Cellular and molecular life sciences : CMLS · 2025Review
- PLK4: Master Regulator of Centriole Duplication and Its Therapeutic Potential.Cytoskeleton (Hoboken, N.J.) · 2025Review
- Mesoscale regulation of microtubule-organizing centers by the E3 ligase TRIM37.Nature structural & molecular biology · 2025Article
- Identification of mutation in ASPM gene in microcephaly families from Khyber Pakhtunkhwa.Molecular biology reports · 2025Article
- Contribution of rare coding variants to microcephaly in individuals with neurodevelopmental disorders.Genome medicine · 2025Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Primary microcephaly is a brain growth disorder characterized by a severe reduction of brain size and thinning of the cerebral cortex. Many primary microcephaly mutations occur in genes that encode centrosome proteins, highlighting an important role for centrosomes in cortical development. Centrosomes are microtubule organizing centers that participate in several processes, including controlling polarity, catalyzing spindle assembly in mitosis, and building primary cilia. Understanding which of these processes are altered and how these disruptions contribute to microcephaly pathogenesis is a central unresolved question. In this review, we revisit the different models that have been proposed to explain how centrosome dysfunction impairs cortical development. We review the evidence supporting a unified model in which centrosome defects reduce cell proliferation in the developing cortex by prolonging mitosis and activating a mitotic surveillance pathway. Finally, we also extend our discussion to centrosome-independent microcephaly mutations, such as those involved in DNA replication and repair.
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Identifiers
What OpenQuestion holds
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.