ArticleDevelopment (Cambridge, England)2015
Aspm sustains postnatal cerebellar neurogenesis and medulloblastoma growth in mice.
Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 65 citations in OpenAlex.
- The microcephaly protein Abnormal Spindle has an essential role in symmetrically dividing neural precursors to promote brain growth and development.Developmental biology · 2026Article
- Microcephaly-associated genes asp and Sas4 influence chromatin organization and nuclear lamina structure in Drosophila melanogaster.Development (Cambridge, England) · 2026Article
- Primate abnormal spindle-like microcephaly-associated knockout causes severe microcephaly and oligodendrocyte loss in the brain.Protein & cell · 2026Article
- Comparative transcriptomics and computational drug discovery identify ASPM as a key oncogenic driver and therapeutic target in hepatocellular carcinoma.Frontiers in bioinformatics · 2026Article
- Recessive variants in WSB2 encoding a substrate receptor of E3 ubiquitin ligase underlie a neurodevelopmental syndrome.European journal of human genetics : EJHG · 2026Article
- A human-specific, concerted repression of microcephaly genes contributes to radiation-induced growth defects in cortical organoids.iScience · 2025Article
- Mcph1, mutated in primary microcephaly, is also crucial for erythropoiesis.EMBO reports · 2024Article
- Review
- DNA damage and repair: underlying mechanisms leading to microcephaly.Frontiers in cell and developmental biology · 2023Review
- Loss of Aspm causes increased apoptosis of developing neural cells during mouse cerebral corticogenesis.PloS one · 2023Article
- The neurological and non-neurological roles of the primary microcephaly-associated protein ASPM.Frontiers in neuroscience · 2023Review
- The impact of TP53 activation and apoptosis in primary hereditary microcephaly.Frontiers in neuroscience · 2023Review
- Automated Immunofluorescence Staining for Analysis of Mitotic Stages and Division Orientation in Brain Sections.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Processing Neonatal Mouse Brains for Immunohistochemical Analysis: As Required for Including Spindle Orientation Analysis and Analysis of DNA Damage and Apoptosis.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Chromosomal Instability Characterizes Pediatric Medulloblastoma but Is Not Tolerated in the Developing Cerebellum.International journal of molecular sciences · 2022Article
- Article
- Oligodendrocytes depend on MCL-1 to prevent spontaneous apoptosis and white matter degeneration.Cell death & disease · 2021Article
- Inhibiting microcephaly genes as alternative to microtubule targeting agents to treat brain tumors.Cell death & disease · 2021Review
- METTL3-mediated m6A methylation of ASPM drives hepatocellular carcinoma cells growth and metastasis.Journal of clinical laboratory analysis · 2021Article
- p53 Activation in Genetic Disorders: Different Routes to the Same Destination.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Alterations in genes that regulate brain size may contribute to both microcephaly and brain tumor formation. Here, we report that Aspm, a gene that is mutated in familial microcephaly, regulates postnatal neurogenesis in the cerebellum and supports the growth of medulloblastoma, the most common malignant pediatric brain tumor. Cerebellar granule neuron progenitors (CGNPs) express Aspm when maintained in a proliferative state by sonic hedgehog (Shh) signaling, and Aspm is expressed in Shh-driven medulloblastoma in mice. Genetic deletion of Aspm reduces cerebellar growth, while paradoxically increasing the mitotic rate of CGNPs. Aspm-deficient CGNPs show impaired mitotic progression, altered patterns of division orientation and differentiation, and increased DNA damage, which causes progenitor attrition through apoptosis. Deletion of Aspm in mice with Smo-induced medulloblastoma reduces tumor growth and increases DNA damage. Co-deletion of Aspm and either of the apoptosis regulators Bax or Trp53 (also known as p53) rescues the survival of neural progenitors and reduces the growth restriction imposed by Aspm deletion. Our data show that Aspm functions to regulate mitosis and to mitigate DNA damage during CGNP cell division, causes microcephaly through progenitor apoptosis when mutated, and sustains tumor growth in medulloblastoma.
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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.