ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Bmi1 loss produces an increase in astroglial cells and a decrease in neural stem cell population and proliferation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 120 citations in OpenAlex.
- Genetic Variants of BMI1 (rs1042059 and rs11591377) and Their Potential Role in Leukemia Susceptibility: A Narrative Review.Health science reports · 2026Article
- Widespread association of Polycomb complex-deposited histone H2A monoubiquitylation with enhancers and neuronal gene regulation.Science advances · 2025Article
- Canonical and non-canonical PRC1 differentially contribute to regulation of neural stem cell fate.Life science alliance · 2025Article
- The Crucial Roles of Bmi-1 in Cancer: Implications in Pathogenesis, Metastasis, Drug Resistance, and Targeted Therapies.International journal of molecular sciences · 2022Review
- Article
- The role of miR-128 in cancer development, prevention, drug resistance, and immunotherapy.Frontiers in oncology · 2022Review
- RYBP modulates embryonic neurogenesis involving the Notch signaling pathway in a PRC1-independent pattern.Stem cell reports · 2021Article
- Bmi1 regulate tooth and mandible development by inhibiting p16 signal pathway.Journal of cellular and molecular medicine · 2021Article
- MicroRNA-128 increases glioma cell radio-sensitivity by suppressing senescent evasion through oncogene Bmi-1.International journal of clinical and experimental pathology · 2018Article
- Epigenome profiling and editing of neocortical progenitor cells during development.The EMBO journal · 2017Article
- MiR-203 Interplays with Polycomb Repressive Complexes to Regulate the Proliferation of Neural Stem/Progenitor Cells.Stem cell reports · 2017Article
- Upregulation of the proto-oncogene Bmi-1 predicts a poor prognosis in pediatric acute lymphoblastic leukemia.BMC cancer · 2017Article
- miR128-1 inhibits the growth of glioblastoma multiforme and glioma stem-like cells via targeting BMI1 and E2F3.Oncotarget · 2016Article
- The putative tumor suppressor gene EphA7 is a novel BMI-1 target.Oncotarget · 2016Article
- Radioresistance of Brain Tumors.Cancers · 2016Review
- Regulation of gene transcription by Polycomb proteins.Science advances · 2015Article
- Bmi-1: At the crossroads of physiological and pathological biology.Genes & diseases · 2015Article
- Ezh2 maintains retinal progenitor proliferation, transcriptional integrity, and the timing of late differentiation.Developmental biology · 2015Article
- Radiosensitization of Primary Human Glioblastoma Stem-like Cells with Low-Dose AKT Inhibition.Molecular cancer therapeutics · 2015Article
- Nuclear-encoded cytochrome c oxidase subunit 4 regulates BMI1 expression and determines proliferative capacity of high-grade gliomas.Oncotarget · 2015Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The polycomb transcriptional repressor Bmi1 promotes cell cycle progression, controls cell senescence, and is implicated in brain development. Loss of Bmi1 leads to a decreased brain size and causes progressive ataxia and epilepsy. Recently, Bmi1 was shown to control neural stem cell (NSC) renewal. However, the effect of Bmi1 loss on neural cell fate in vivo and the question whether the action of Bmi1 was intrinsic to the NSCs remained to be investigated. Here, we show that Bmi1 is expressed in the germinal zone in vivo and in NSCs as well as in progenitors proliferating in vitro, but not in differentiated cells. Loss of Bmi1 led to a decrease in proliferation in zones known to contain progenitors: the newborn cortex and the newborn and adult subventricular zone. This decrease was accentuated in vitro, where we observed a drastic reduction in NSC proliferation and renewal because of NSC-intrinsic effects of Bmi1 as shown by the means of RNA interference. Bmi1(-/-) mice also presented more astrocytes at birth, and a generalized gliosis at postnatal day 30. At both stages, colocalization of bromodeoxyuridine and GFAP demonstrated that Bmi1 loss did not prevent astrocyte precursor proliferation. Supporting these observations, Bmi1(-/-) neurospheres generate preferentially astrocytes probably attributable to a different responsiveness to environmental factors. Bmi1 is therefore necessary for NSC renewal in a cell-intrinsic mode, whereas the altered cell pattern of the Bmi1(-/-) brain shows that in vivo astrocyte precursors can proliferate in the absence of Bmi1.
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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.