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- W2014454255 abstract "Mutations in genes encoding chromatin-remodeling proteins, such as the ATRX gene, underlie a number of genetic disorders including several X-linked mental retardation syndromes; however, the role of these proteins in normal CNS development is unknown. Here, we used a conditional gene-targeting approach to inactivate Atrx, specifically in the forebrain of mice. Loss of ATRX protein caused widespread hypocellularity in the neocortex and hippocampus and a pronounced reduction in forebrain size. Neuronal birthdating confirmed that fewer neurons reached the superficial cortical layers, despite normal progenitor cell proliferation. The loss of cortical mass resulted from a 12-fold increase in neuronal apoptosis during early stages of corticogenesis in the mutant animals. Moreover, cortical progenitors isolated from Atrx-null mice undergo enhanced apoptosis upon differentiation. Taken together, our results indicate that ATRX is a critical mediator of cell survival during early neuronal differentiation. Thus, increased neuronal loss may contribute to the severe mental retardation observed in human patients." @default.
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- W2014454255 date "2005-01-20" @default.
- W2014454255 modified "2023-09-25" @default.
- W2014454255 title "The chromatin-remodeling protein ATRX is critical for neuronal survival during corticogenesis" @default.
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- W2014454255 doi "https://doi.org/10.1172/jci22329" @default.
- W2014454255 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/544602" @default.
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