Bibliographies thématiques / Human corticogenesi

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Littérature scientifique sur le sujet « Human corticogenesi »

Auteur : Grafiati
Publié le 9 mars 2023
Mis à jour le 10 mars 2023

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Articles de revues sur le sujet "Human corticogenesi"

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Wang, Yanling, et Ricardo Dolmetsch. « In Vitro Human Corticogenesis ». Neuron 77, no 3 (février 2013) : 379–81. http://dx.doi.org/10.1016/j.neuron.2013.01.023.

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Trevino, Alexandro E., Nasa Sinnott-Armstrong, Jimena Andersen, Se-Jin Yoon, Nina Huber, Jonathan K. Pritchard, Howard Y. Chang, William J. Greenleaf et Sergiu P. Pașca. « Chromatin accessibility dynamics in a model of human forebrain development ». Science 367, no 6476 (23 janvier 2020) : eaay1645. http://dx.doi.org/10.1126/science.aay1645.

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Forebrain development is characterized by highly synchronized cellular processes, which, if perturbed, can cause disease. To chart the regulatory activity underlying these events, we generated a map of accessible chromatin in human three-dimensional forebrain organoids. To capture corticogenesis, we sampled glial and neuronal lineages from dorsal or ventral forebrain organoids over 20 months in vitro. Active chromatin regions identified in human primary brain tissue were observed in organoids at different developmental stages. We used this resource to map genetic risk for disease and to explore evolutionary conservation. Moreover, we integrated chromatin accessibility with transcriptomics to identify putative enhancer-gene linkages and transcription factors that regulate human corticogenesis. Overall, this platform brings insights into gene-regulatory dynamics at previously inaccessible stages of human forebrain development, including signatures of neuropsychiatric disorders.
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Gantner, Carlos W., Cameron P. J. Hunt, Jonathan C. Niclis, Vanessa Penna, Stuart J. McDougall, Lachlan H. Thompson et Clare L. Parish. « FGF-MAPK signaling regulates human deep-layer corticogenesis ». Stem Cell Reports 16, no 5 (mai 2021) : 1262–75. http://dx.doi.org/10.1016/j.stemcr.2021.03.014.

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Reilly, S. K., J. Yin, A. E. Ayoub, D. Emera, J. Leng, J. Cotney, R. Sarro, P. Rakic et J. P. Noonan. « Evolutionary changes in promoter and enhancer activity during human corticogenesis ». Science 347, no 6226 (5 mars 2015) : 1155–59. http://dx.doi.org/10.1126/science.1260943.

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Alshawaf, Abdullah J., Ana Antonic, Efstratios Skafidas, Dominic Chi-Hung Ng et Mirella Dottori. « WDR62 Regulates Early Neural and Glial Progenitor Specification of Human Pluripotent Stem Cells ». Stem Cells International 2017 (2017) : 1–9. http://dx.doi.org/10.1155/2017/7848932.

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Mutations in WD40-repeat protein 62 (WDR62) are commonly associated with primary microcephaly and other developmental cortical malformations. We used human pluripotent stem cells (hPSC) to examine WDR62 function during human neural differentiation and model early stages of human corticogenesis. Neurospheres lacking WDR62 expression showed decreased expression of intermediate progenitor marker, TBR2, and also glial marker, S100β. In contrast, inhibition of c-Jun N-terminal kinase (JNK) signalling during hPSC neural differentiation induced upregulation of WDR62 with a corresponding increase in neural and glial progenitor markers, PAX6 and EAAT1, respectively. These findings may signify a role of WDR62 in specifying intermediate neural and glial progenitors during human pluripotent stem cell differentiation.
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Begum, Aynun N., Jose S. Aguilar et Yiling Hong. « Aqueous cigarette tar extracts disrupt corticogenesis from human embryonic stem cells in vitro ». Environmental Research 158 (octobre 2017) : 194–202. http://dx.doi.org/10.1016/j.envres.2017.06.012.

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Furuta, Akiko, Sachio Takashima, Hideaki Yokoo, Jeffrey D. Rothstein, Keiji Wada et Toru Iwaki. « Expression of glutamate transporter subtypes during normal human corticogenesis and type II lissencephaly ». Developmental Brain Research 155, no 2 (mars 2005) : 155–64. http://dx.doi.org/10.1016/j.devbrainres.2005.01.005.

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Simonati, Alessandro, Cinzia Tosati, Tiziana Rosso, Elena Piazzola et Nicolo Rizzuto. « Cell proliferation and death : Morphological evidence during corticogenesis in the developing human brain ». Microscopy Research and Technique 45, no 6 (15 juin 1999) : 341–52. http://dx.doi.org/10.1002/(sici)1097-0029(19990615)45:6<341 ::aid-jemt2>3.0.co;2-u.

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Gao, Xue-Ling, Wen-Jia Tian, Bofeng Liu, Jingyi Wu, Wei Xie et Qin Shen. « High-mobility group nucleosomal binding domain 2 protects against microcephaly by maintaining global chromatin accessibility during corticogenesis ». Journal of Biological Chemistry 295, no 2 (7 novembre 2019) : 468–80. http://dx.doi.org/10.1074/jbc.ra119.010616.

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The surface area of the human cerebral cortex undergoes dramatic expansion during late fetal development, leading to cortical folding, an evolutionary feature not present in rodents. Microcephaly is a neurodevelopmental disorder defined by an abnormally small brain, and many gene mutations have been found to be associated with primary microcephaly. However, mouse models generated by ablating primary microcephaly-associated genes often fail to recapitulate the severe loss of cortical surface area observed in individuals with this pathology. Here, we show that a mouse model with deficient expression of high-mobility group nucleosomal binding domain 2 (HMGN2) manifests microcephaly with reduced cortical surface area and almost normal radial corticogenesis, with a pattern of incomplete penetrance. We revealed that altered cleavage plane and mitotic delay of ventricular radial glia may explain the rising ratio of intermediate progenitor cells to radial glia and the displacement of neural progenitor cells in microcephalic mutant mice. These led to decreased self-renewal of the radial glia and reduction in lateral expansion. Furthermore, we found that HMGN2 protected corticogenesis by maintaining global chromatin accessibility mainly at promoter regions, thereby ensuring the correct regulation of the transcriptome. Our findings underscore the importance of the regulation of chromatin structure in cortical development and highlight a mouse model with critical insights into the etiology of microcephaly.
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Orlova, Ksenia A., Whitney E. Parker, Gregory G. Heuer, Victoria Tsai, Jason Yoon, Marianna Baybis, Robert S. Fenning, Kevin Strauss et Peter B. Crino. « STRADα deficiency results in aberrant mTORC1 signaling during corticogenesis in humans and mice ». Journal of Clinical Investigation 120, no 5 (3 mai 2010) : 1591–602. http://dx.doi.org/10.1172/jci41592.

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Thèses sur le sujet "Human corticogenesi"

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TRATTARO, SEBASTIANO. « BRAIN ORGANOID MODELLING OF HUMAN CORTICOGENESIS:THE PARADIGM OF WEAVER SYNDROME ». Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/875973.

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Multiple strategies of brain organoidogenesis have enabled the investigation of human cerebral corticogenesis in-vitro with increasing accuracy. However, little is yet known about how closely the gene co-expression patterns seen in brain organoids (BO) match those of fetal cortex. Here we benchmarked BO against fetal corticogenesis by integrating transcriptomes from in-house differentiated cortical BO (CBO), other BO systems, human fetal brain samples processed in-house, and pre-natal cortices from the BrainSpan Atlas. We identified and ranked co-expression patterns and hubs of corticogenesis and CBO differentiation, highlighting well-preserved and variable trends across BO protocols, and we found heterochronicity of differentiation across BO models compared to fetal cortex. Once performed this benchmarking, we used CBO for disease-modelling of Weaver syndrome (WS), a rare disease characterized by intellectual disability. WS is associated with mutations in Polycomb repressive complex 2, a repressor of gene expression through H3K27me3. We differentiated patient-derived CBO and profiled their transcriptome and epigenome at different time-points, revealing upregulation of genes involved in neuronal maturation and migration as well as alteration of glucose metabolism in WS. Intersection of differentially expressed genes between WS- and control-CBO across stages with H3K27me3 ChIP-seq peaks, DNA-methylation profiles and dysregulated genes in CBO from a CRISPR/Cas9-engineered EZH2 KO revealed a set of PRC2 targets possibly mediating the WS intellectual disability phenotype. Our approach identified commonalities and divergences between state-of-the-art BO systems, providing a resource to query when modelling human corticogenesis, and identified molecular phenotypes and targets relevant for WS, generating the framework for future potential therapeutic intervention.
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Kadoshima, Taisuke. « Self-organization of axial polarity, inside-out layer pattern and species-specific progenitor dynamics in human ES cell-derived neocortex ». Kyoto University, 2014. http://hdl.handle.net/2433/188695.

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Chapitres de livres sur le sujet "Human corticogenesi"

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DEHAY, COLETTE, et HENRY KENNEDY. « Control Mechanisms of Primate Corticogenesis ». Dans Functional Organisation of the Human Visual Cortex, 13–27. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-08-042004-2.50006-x.

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