Tuoc, Tran

[["dc.bibliographiccitation.artnumber","226"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in Neuroscience"],["dc.bibliographiccitation.lastpage","25"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Castro-Hernandez, Ricardo"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2019-07-09T11:45:16Z"],["dc.date.available","2019-07-09T11:45:16Z"],["dc.date.issued","2018"],["dc.description.abstract","The generation of individual neurons (neurogenesis) during cortical development occurs in discrete steps that are subtly regulated and orchestrated to ensure normal histogenesis and function of the cortex. Notably, various gene expression programs are known to critically drive many facets of neurogenesis with a high level of specificity during brain development. Typically, precise regulation of gene expression patterns ensures that key events like proliferation and differentiation of neural progenitors, specification of neuronal subtypes, as well as migration and maturation of neurons in the developing cortex occur properly. ATP-dependent chromatin remodeling complexes regulate gene expression through utilization of energy fromATP hydrolysis to reorganize chromatin structure. These chromatin remodeling complexes are characteristically multimeric, with some capable of adopting functionally distinct conformations via subunit reconstitution to perform specific roles in major aspects of cortical neurogenesis. In this review, we highlight the functions of such chromatin remodelers during cortical development. We also bring together various proposed mechanisms by which ATP-dependent chromatin remodelers function individually or in concert, to specifically modulate vital steps in cortical neurogenesis."],["dc.identifier.doi","10.3389/fnins.2018.00226"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15084"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59196"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1662-453X"],["dc.relation.issn","1662-453X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","ATP-Dependent Chromatin Remodeling During Cortical Neurogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","655"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Annals of Clinical and Translational Neurology"],["dc.bibliographiccitation.lastpage","668"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Pringsheim, Milka"],["dc.contributor.author","Mitter, Diana"],["dc.contributor.author","Schröder, Simone"],["dc.contributor.author","Warthemann, Rita"],["dc.contributor.author","Plümacher, Kim"],["dc.contributor.author","Kluger, Gerhard"],["dc.contributor.author","Baethmann, Martina"],["dc.contributor.author","Bast, Thomas"],["dc.contributor.author","Braun, Sarah"],["dc.contributor.author","Büttel, Hans‐Martin"],["dc.contributor.author","Conover, Elizabeth"],["dc.contributor.author","Courage, Carolina"],["dc.contributor.author","Datta, Alexandre N."],["dc.contributor.author","Eger, Angelika"],["dc.contributor.author","Grebe, Theresa A."],["dc.contributor.author","Hasse‐Wittmer, Annette"],["dc.contributor.author","Heruth, Marion"],["dc.contributor.author","Höft, Karen"],["dc.contributor.author","Kaindl, Angela M."],["dc.contributor.author","Karch, Stephanie"],["dc.contributor.author","Kautzky, Torsten"],["dc.contributor.author","Korenke, Georg C."],["dc.contributor.author","Kruse, Bernd"],["dc.contributor.author","Lutz, Richard E."],["dc.contributor.author","Omran, Heymut"],["dc.contributor.author","Patzer, Steffi"],["dc.contributor.author","Philippi, Heike"],["dc.contributor.author","Ramsey, Keri"],["dc.contributor.author","Rating, Tina"],["dc.contributor.author","Rieß, Angelika"],["dc.contributor.author","Schimmel, Mareike"],["dc.contributor.author","Westman, Rachel"],["dc.contributor.author","Zech, Frank‐Martin"],["dc.contributor.author","Zirn, Birgit"],["dc.contributor.author","Ulmke, Pauline A."],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Tuoc, Tran"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Staudt, Martin"],["dc.contributor.author","Brockmann, Knut"],["dc.date.accessioned","2019-11-25T10:20:06Z"],["dc.date.accessioned","2021-10-27T13:21:31Z"],["dc.date.available","2019-11-25T10:20:06Z"],["dc.date.available","2021-10-27T13:21:31Z"],["dc.date.issued","2019"],["dc.description.abstract","Objective: FOXG1 syndrome is a rare neurodevelopmental disorder associated with heterozygous FOXG1 variants or chromosomal microaberrations in 14q12. The study aimed at assessing the scope of structural cerebral anomalies revealed by neuroimaging to delineate the genotype and neuroimaging phenotype associations. Methods: We compiled 34 patients with a heterozygous (likely) pathogenic FOXG1 variant. Qualitative assessment of cerebral anomalies was performed by standardized re-analysis of all 34 MRI data sets. Statistical analysis of genetic, clinical and neuroimaging data were performed. We quantified clinical and neuroimaging phenotypes using severity scores. Telencephalic phenotypes of adult Foxg1+/- mice were examined using immunohistological stainings followed by quantitative evaluation of structural anomalies. Results: Characteristic neuroimaging features included corpus callosum anomalies (82%), thickening of the fornix (74%), simplified gyral pattern (56%), enlargement of inner CSF spaces (44%), hypoplasia of basal ganglia (38%), and hypoplasia of frontal lobes (29%). We observed a marked, filiform thinning of the rostrum as recurrent highly typical pattern of corpus callosum anomaly in combination with distinct thickening of the fornix as a characteristic feature. Thickening of the fornices was not reported previously in FOXG1 syndrome. Simplified gyral pattern occurred significantly more frequently in patients with early truncating variants. Higher clinical severity scores were significantly associated with higher neuroimaging severity scores. Modeling of Foxg1 heterozygosity in mouse brain recapitulated the associated abnormal cerebral morphology phenotypes, including the striking enlargement of the fornix. Interpretation: Combination of specific corpus callosum anomalies with simplified gyral pattern and hyperplasia of the fornices is highly characteristic for FOXG1 syndrome."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2019"],["dc.identifier.doi","10.1002/acn3.735"],["dc.identifier.eissn","2328-9503"],["dc.identifier.issn","2328-9503"],["dc.identifier.pmid","31019990"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16705"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92029"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","2328-9503"],["dc.relation.issn","2328-9503"],["dc.relation.issn","2328-9503"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Structural brain anomalies in patients with FOXG 1 syndrome and in Foxg1+/− mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","243"],["dc.bibliographiccitation.journal","Frontiers in Molecular Neuroscience"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Xie, Yuanbin"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2019-07-09T11:43:37Z"],["dc.date.available","2019-07-09T11:43:37Z"],["dc.date.issued","2017"],["dc.description.abstract","The ATP-dependent BRG1/BRM associated factor (BAF) chromatin remodeling complexes are crucial in regulating gene expression by controlling chromatin dynamics. Over the last decade, it has become increasingly clear that during neural development in mammals, distinct ontogenetic stage-specific BAF complexes derived from combinatorial assembly of their subunits are formed in neural progenitors and post-mitotic neural cells. Proper functioning of the BAF complexes plays critical roles in neural development, including the establishment and maintenance of neural fates and functionality. Indeed, recent human exome sequencing and genome-wide association studies have revealed that mutations in BAF complex subunits are linked to neurodevelopmental disorders such as Coffin-Siris syndrome, Nicolaides-Baraitser syndrome, Kleefstra’s syndrome spectrum, Hirschsprung’s disease, autism spectrum disorder, and schizophrenia. In this review, we focus on the latest insights into the functions of BAF complexes during neural development and the plausible mechanistic basis of how mutations in known BAF subunits are associated with certain neurodevelopmental disorders."],["dc.identifier.doi","10.3389/fnmol.2017.00243"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14595"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58929"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1662-5099"],["dc.relation.issn","1662-5099"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Chromatin Remodeling BAF (SWI/SNF) Complexes in Neural Development and Disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]