N
Nurit Ballas
Researcher at Stony Brook University
Publications - 18
Citations - 3848
Nurit Ballas is an academic researcher from Stony Brook University. The author has contributed to research in topics: Rett syndrome & MECP2. The author has an hindex of 15, co-authored 17 publications receiving 3608 citations. Previous affiliations of Nurit Ballas include State University of New York System.
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Journal ArticleDOI
REST and Its Corepressors Mediate Plasticity of Neuronal Gene Chromatin throughout Neurogenesis
TL;DR: It is shown that REST regulates the transitions from pluripotent to neural stem/progenitor cell and from progenitor to mature neuron, indicating that REST defines a gene set subject to plasticity in mature neurons.
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CoREST: A functional corepressor required for regulation of neural-specific gene expression
María Estela Andrés,Corinna Burger,Maria J. Peral-Rubio,Elena Battaglioli,Mary E. Anderson,Julia A. Grimes,Julia E. Dallman,Nurit Ballas,Gail Mandel +8 more
TL;DR: It is shown that CoREST, a newly identified human protein, functions as a corepressor for REST, a structural feature of the nuclear receptor and silencing mediator for retinoid and thyroid human receptors (SMRT)-extended corepressors that mediate inducible repression by steroid hormone receptors.
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A role for glia in the progression of Rett's syndrome.
Daniel T. Lioy,Saurabh K. Garg,Saurabh K. Garg,Caitlin E. Monaghan,Caitlin E. Monaghan,Jacob Raber,Jacob Raber,Kevin D. Foust,Brian K. Kaspar,Petra G. Hirrlinger,Frank Kirchhoff,John M. Bissonnette,Nurit Ballas,Gail Mandel,Gail Mandel +14 more
TL;DR: It is shown that glia, like neurons, are integral components of the neuropathology of RTT, and supports the targeting of glia as a strategy for improving the associated symptoms.
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Non-cell autonomous influence of MeCP2-deficient glia on neuronal dendritic morphology
TL;DR: These studies suggest that astrocytes in the RTT brain carrying MeCP2 mutations have a non–cell autonomous effect on neuronal properties, probably as a result of aberrant secretion of soluble factor(s).
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Regulation of neuronal traits by a novel transcriptional complex.
Nurit Ballas,Elena Battaglioli,Fouad Atouf,María Estela Andrés,Josh Chenoweth,Mary E. Anderson,Corinna Burger,Mariko Moniwa,James R. Davie,William J. Bowers,Howard J. Federoff,David W. Rose,Michael G. Rosenfeld,Paul Brehm,Gail Mandel +14 more
TL;DR: A novel HDAC complex is defined that is recruited by the C-terminal repressor domain of REST to actively repress genes essential to the neuronal phenotype.