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Relevant bibliographies by topics / Basal radial glia cell

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Journal articles

Academic literature on the topic 'Basal radial glia cell'

Author: Grafiati

Published: 25 May 2024

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Journal articles on the topic "Basal radial glia cell"

1

Pereida-Jaramillo, Elizabeth, Gabriela B. Gómez-González, Angeles Edith Espino-Saldaña, and Ataúlfo Martínez-Torres. "Calcium Signaling in the Cerebellar Radial Glia and Its Association with Morphological Changes during Zebrafish Development." International Journal of Molecular Sciences 22, no. 24 (2021): 13509. http://dx.doi.org/10.3390/ijms222413509.

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Radial glial cells are a distinct non-neuronal cell type that, during development, span the entire width of the brain walls of the ventricular system. They play a central role in the origin and placement of neurons, since their processes form structural scaffolds that guide and facilitate neuronal migration. Furthermore, glutamatergic signaling in the radial glia of the adult cerebellum (i.e., Bergmann glia), is crucial for precise motor coordination. Radial glial cells exhibit spontaneous calcium activity and functional coupling spread calcium waves. However, the origin of calcium activity in

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2

Li, Zhen, William A. Tyler, Ella Zeldich, et al. "Transcriptional priming as a conserved mechanism of lineage diversification in the developing mouse and human neocortex." Science Advances 6, no. 45 (2020): eabd2068. http://dx.doi.org/10.1126/sciadv.abd2068.

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How the rich variety of neurons in the nervous system arises from neural stem cells is not well understood. Using single-cell RNA-sequencing and in vivo confirmation, we uncover previously unrecognized neural stem and progenitor cell diversity within the fetal mouse and human neocortex, including multiple types of radial glia and intermediate progenitors. We also observed that transcriptional priming underlies the diversification of a subset of ventricular radial glial cells in both species; genetic fate mapping confirms that the primed radial glial cells generate specific types of basal proge

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3

Moore, Rachel, and Paula Alexandre. "Delta-Notch Signaling: The Long and The Short of a Neuron’s Influence on Progenitor Fates." Journal of Developmental Biology 8, no. 2 (2020): 8. http://dx.doi.org/10.3390/jdb8020008.

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Maintenance of the neural progenitor pool during embryonic development is essential to promote growth of the central nervous system (CNS). The CNS is initially formed by tightly compacted proliferative neuroepithelial cells that later acquire radial glial characteristics and continue to divide at the ventricular (apical) and pial (basal) surface of the neuroepithelium to generate neurons. While neural progenitors such as neuroepithelial cells and apical radial glia form strong connections with their neighbours at the apical and basal surfaces of the neuroepithelium, neurons usually form the ma

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4

Kullmann, Jan A., Sophie Meyer, Fabrizia Pipicelli, et al. "Profilin1-Dependent F-Actin Assembly Controls Division of Apical Radial Glia and Neocortex Development." Cerebral Cortex 30, no. 6 (2019): 3467–82. http://dx.doi.org/10.1093/cercor/bhz321.

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Abstract Neocortex development depends on neural stem cell proliferation, cell differentiation, neurogenesis, and neuronal migration. Cytoskeletal regulation is critical for all these processes, but the underlying mechanisms are only poorly understood. We previously implicated the cytoskeletal regulator profilin1 in cerebellar granule neuron migration. Since we found profilin1 expressed throughout mouse neocortex development, we here tested the hypothesis that profilin1 is crucial for neocortex development. We found no evidence for impaired neuron migration or layering in the neocortex of prof

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5

Penisson, Maxime, Mingyue Jin, Shengming Wang, Shinji Hirotsune, Fiona Francis, and Richard Belvindrah. "Lis1 mutation prevents basal radial glia-like cell production in the mouse." Human Molecular Genetics 31, no. 6 (2021): 942–57. http://dx.doi.org/10.1093/hmg/ddab295.

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Abstract Human cerebral cortical malformations are associated with progenitor proliferation and neuronal migration abnormalities. Progenitor cells include apical radial glia, intermediate progenitors and basal (or outer) radial glia (bRGs or oRGs). bRGs are few in number in lissencephalic species (e.g. the mouse) but abundant in gyrencephalic brains. The LIS1 gene coding for a dynein regulator, is mutated in human lissencephaly, associated also in some cases with microcephaly. LIS1 was shown to be important during cell division and neuronal migration. Here, we generated bRG-like cells in the m

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6

Zhang, Sanguo, Huanhuan Joyce Wang, Jia Li, Xiao-Ling Hu, and Qin Shen. "Radial Glial Cell-Derived VCAM1 Regulates Cortical Angiogenesis Through Distinct Enrichments in the Proximal and Distal Radial Processes." Cerebral Cortex 30, no. 6 (2020): 3717–30. http://dx.doi.org/10.1093/cercor/bhz337.

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Abstract Angiogenesis in the developing cerebral cortex accompanies cortical neurogenesis. However, the precise mechanisms underlying cortical angiogenesis at the embryonic stage remain largely unknown. Here, we show that radial glia-derived vascular cell adhesion molecule 1 (VCAM1) coordinates cortical vascularization through different enrichments in the proximal and distal radial glial processes. We found that VCAM1 was highly enriched around the blood vessels in the inner ventricular zone (VZ), preventing the ingrowth of blood vessels into the mitotic cell layer along the ventricular surfac

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7

Shohayeb, Belal, Uda Ho, Yvonne Y. Yeap, et al. "The association of microcephaly protein WDR62 with CPAP/IFT88 is required for cilia formation and neocortical development." Human Molecular Genetics 29, no. 2 (2019): 248–63. http://dx.doi.org/10.1093/hmg/ddz281.

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Abstract WDR62 mutations that result in protein loss, truncation or single amino-acid substitutions are causative for human microcephaly, indicating critical roles in cell expansion required for brain development. WDR62 missense mutations that retain protein expression represent partial loss-of-function mutants that may therefore provide specific insights into radial glial cell processes critical for brain growth. Here we utilized CRISPR/Cas9 approaches to generate three strains of WDR62 mutant mice; WDR62 V66M/V66M and WDR62R439H/R439H mice recapitulate conserved missense mutations found in h

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8

Golden, J. A., J. C. Zitz, K. McFadden, and C. L. Cepko. "Cell migration in the developing chick diencephalon." Development 124, no. 18 (1997): 3525–33. http://dx.doi.org/10.1242/dev.124.18.3525.

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We previously reported that retrovirally marked clones in the mature chick diencephalon were widely dispersed in the mediolateral, dorsoventral and rostrocaudal planes. The current study was undertaken to define the migration routes that led to the dispersion. Embryos were infected between stages 10 and 14 with a retroviral stock encoding alkaline phosphatase and a library of molecular tags. Embryos were harvested 2.5-5.5 days later and the brains were fixed and serially sectioned. Sibling relationships were determined following PCR amplification and sequencing of the molecular tag. On embryon

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9

Li, Xiaosu, Guoping Liu, Lin Yang, et al. "Decoding Cortical Glial Cell Development." Neuroscience Bulletin 37, no. 4 (2021): 440–60. http://dx.doi.org/10.1007/s12264-021-00640-9.

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AbstractMouse cortical radial glial cells (RGCs) are primary neural stem cells that give rise to cortical oligodendrocytes, astrocytes, and olfactory bulb (OB) GABAergic interneurons in late embryogenesis. There are fundamental gaps in understanding how these diverse cell subtypes are generated. Here, by combining single-cell RNA-Seq with intersectional lineage analyses, we show that beginning at around E16.5, neocortical RGCs start to generate ASCL1+EGFR+ apical multipotent intermediate progenitors (MIPCs), which then differentiate into basal MIPCs that express ASCL1, EGFR, OLIG2, and MKI67.

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10

Sawada, Kazuhiko. "Tracking of neurons derived from basal radial glia experiencing multiple cell division in the developing neocortex of ferrets." IBRO Reports 6 (September 2019): S84. http://dx.doi.org/10.1016/j.ibror.2019.07.272.

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