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Elizabeth J. Hong

Researcher at Harvard University

Publications -  15
Citations -  2530

Elizabeth J. Hong is an academic researcher from Harvard University. The author has contributed to research in topics: Brain-derived neurotrophic factor & Olfactory system. The author has an hindex of 10, co-authored 10 publications receiving 2292 citations. Previous affiliations of Elizabeth J. Hong include Boston Children's Hospital.

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Brain-Specific Phosphorylation of MeCP2 Regulates Activity-Dependent Bdnf Transcription, Dendritic Growth, and Spine Maturation

TL;DR: It is shown that neuronal activity and subsequent calcium influx trigger the de novo phosphorylation of MeCP2 at serine 421 (S421) by a CaMKII-dependent mechanism, which controls the ability of Me CP2 to regulate dendritic patterning, spine morphogenesis, and the activity-dependent induction of Bdnf transcription.
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Genome-Wide Analysis of MEF2 Transcriptional Program Reveals Synaptic Target Genes and Neuronal Activity-Dependent Polyadenylation Site Selection

TL;DR: The characterized genetic program that is activated by MEF2, a key regulator of activity-dependent synapse development, is characterized and it is suggested that the ubiquitously expressed transcription factor MEf2 regulates an intricate transcriptional program in neurons that controls synapses development.
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A Biological Function for the Neuronal Activity-Dependent Component of Bdnf Transcription in the Development of Cortical Inhibition

TL;DR: A specific requirement for activity-dependent Bdnf expression in the development of inhibition in the cortex is indicated and it is demonstrated that the activation of gene expression in response to experience-driven neuronal activity has important biological consequences in the nervous system.
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Brain-derived neurotrophic factor expression and respiratory function improve after ampakine treatment in a mouse model of Rett syndrome

TL;DR: It is found that mutant neurons express significantly lower levels of BDNF than wild-type cells in vitro, as in vivo, under both depolarizing and nondepolarizing conditions, and raise the possibility that ampakine compounds could be of therapeutic value in the treatment of RTT.
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Developmental axon pruning mediated by BDNF-p75NTR-dependent axon degeneration.

TL;DR: A mechanism by which, during developmental sympathetic axon competition, winning axons secrete brain-derived neurotrophic factor in an activity-dependent fashion, which binds to the p75 neurotrophin receptor (p75NTR) on losing axons to cause their degeneration and, ultimately, axon pruning is described.