ArticleProceedings of the National Academy of Sciences of the United States of America2019
Loss of postnatal quiescence of neural stem cells through mTOR activation upon genetic removal of cysteine string protein-α.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Metabolic functions for molecular chaperones and stress proteins in microcephaly.Cellular and molecular life sciences : CMLS · 2025Review
- Neuronal lipofuscinosis caused by Kufs disease/CLN4 DNAJC5 mutations but not by a CSPα/DNAJC5 deficiency.Science advances · 2025Article
- DNAJC5 facilitates the proliferation and migration of lung adenocarcinoma cells by augmenting EGFR trafficking.Communications biology · 2025Article
- Cysteine string protein α and a link between rare and common neurodegenerative dementias.NPJ dementia · 2025Review
- Unifying biology of neurodegeneration in lysosomal storage diseases.Journal of inherited metabolic disease · 2025Review
- MFGE8 promotes adult hippocampal neurogenesis in rats following experimental subarachnoid hemorrhage via modifying the integrin β3/Akt signaling pathway.Cell death discovery · 2024Article
- mTOR pathway occupies a central role in the emergence of latent cancer cells.Cell death & disease · 2024Review
- FOXO1-mediated lipid metabolism maintains mammalian embryos in dormancy.Nature cell biology · 2024Article
- Kidins220 sets the threshold for survival of neural stem cells and progenitors to sustain adult neurogenesis.Cell death & disease · 2023Article
- Dephosphorylation of 4EBP1/2 Induces Prenatal Neural Stem Cell Quiescence.bioRxiv : the preprint server for biology · 2023Article
- Single-cell profiling of human subventricular zone progenitors identifies SFRP1 as a target to re-activate progenitors.Nature communications · 2022Article
- Lysosomes at the Crossroads of Cell Metabolism, Cell Cycle, and Stemness.International journal of molecular sciences · 2022Review
- CSPα in neurodegenerative diseases.Frontiers in aging neuroscience · 2022Review
- Adult-Onset Neuronal Ceroid Lipofuscinosis With a NovelFrontiers in aging neuroscience · 2022Article
- Sestrins regulate muscle stem cell metabolic homeostasis.Stem cell reports · 2021Article
- Mechanisms of enhanced quiescence in neural stem cell aging.Mechanisms of ageing and development · 2020Review
- Stem Cells of the Aging Brain.Frontiers in aging neuroscience · 2020Review
- The Autophagy Status of Cancer Stem Cells in Gliobastoma Multiforme: From Cancer Promotion to Therapeutic Strategies.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neural stem cells continuously generate newborn neurons that integrate into and modify neural circuitry in the adult hippocampus. The molecular mechanisms that regulate or perturb neural stem cell proliferation and differentiation, however, remain poorly understood. Here, we have found that mouse hippocampal radial glia-like (RGL) neural stem cells express the synaptic cochaperone cysteine string protein-α (CSP-α). Remarkably, in CSP-α knockout mice, RGL stem cells lose quiescence postnatally and enter into a high-proliferation regime that increases the production of neural intermediate progenitor cells, thereby exhausting the hippocampal neural stem cell pool. In cell culture, stem cells in hippocampal neurospheres display alterations in proliferation for which hyperactivation of the mechanistic target of rapamycin (mTOR) signaling pathway is the primary cause of neurogenesis deregulation in the absence of CSP-α. In addition, RGL cells lose quiescence upon specific conditional targeting of CSP-α in adult neural stem cells. Our findings demonstrate an unanticipated cell-autonomic and circuit-independent disruption of postnatal neurogenesis in the absence of CSP-α and highlight a direct or indirect CSP-α/mTOR signaling interaction that may underlie molecular mechanisms of brain dysfunction and neurodegeneration.
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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.