2012
DOI: 10.1038/nbt.2158
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Inhibition of natural antisense transcripts in vivo results in gene-specific transcriptional upregulation

Abstract: Here we demonstrate that natural antisense transcripts (NATs), which are abundant in mammalian genomes, can function as repressors of specific genomic loci and that their removal or inhibition by AntagoNAT oligonucleotides leads to transient and reversible upregulation of sense gene expression. As one example, we show that Brain-Derived Neurotrophic Factor (BDNF) is under the control of a conserved noncoding antisense RNA transcript, BDNF-AS, both in vitro and in vivo. BDNF-AS tonically represses BDNF sense RN… Show more

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Cited by 597 publications
(594 citation statements)
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“…EZH2 alters the chromatin structure by adding the repressive mark H3K27me3 and inducing transcriptional silencing. In the case of neurological disorders, the effectiveness of this approach has been recently validated in vivo [90]. This study by Modarresi et al [90] was the first demonstration of oligonucleotide-mediated transcriptional gene activation in brain.…”
Section: Gene-specific Epigenetic Therapymentioning
confidence: 99%
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“…EZH2 alters the chromatin structure by adding the repressive mark H3K27me3 and inducing transcriptional silencing. In the case of neurological disorders, the effectiveness of this approach has been recently validated in vivo [90]. This study by Modarresi et al [90] was the first demonstration of oligonucleotide-mediated transcriptional gene activation in brain.…”
Section: Gene-specific Epigenetic Therapymentioning
confidence: 99%
“…In the case of neurological disorders, the effectiveness of this approach has been recently validated in vivo [90]. This study by Modarresi et al [90] was the first demonstration of oligonucleotide-mediated transcriptional gene activation in brain. Delivery of locked nucleic acid (LNA) gapmer antisense oligonucleotides by intracerebroventricular delivery using an osmotic minipump was shown to upregulate expression of brain-derived neurotrophic factor (BDNF ), glial-derived neurotrophic factor (GDNF) and the Ephrin receptor B2 (EPHB2 ).…”
Section: Gene-specific Epigenetic Therapymentioning
confidence: 99%
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“…La plupart d'entre eux implique de petits ARN interférents (siRNA) ou des oligonucléotides antisens (ASO) qui mènent à la dégradation de leurs ARN cibles. Par exemple, l'utilisation in vivo chez la souris d'un ASO dirigé contre le lncRNA Bdnf-as (brain-derived neutrophic factor) lève la répression de Bdnf et permet la prolifération neuronale [36]. Alternativement, les ASO pourraient agir comme agents bloquants en pré-venant la liaison d'un lncRNA avec une protéine ou une séquence d'ADN ou d'ARN.…”
Section: Les Lncrna Comme Agents Thérapeutiques Et Biomarqueursunclassified