DNA Methylation-Related Chromatin Remodeling in Activity-Dependent Bdnf Gene Regulation
By Keri Martinowich, Daisuke Hattori, Hao Wu, S. Fouse, Fei He, Yan Hu, G. Fan, Y. Sun. Science, 2003
1,473 citations recorded by the source corpus.
Subfields: Cognitive Neuroscience, Genetics, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/a3bc3b8faed3e861195fa8af0fade790a39b5823
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cognitive Neuroscience
- H. Zoghbi
- Maria H. Chahrour
- Mark F. Bear
- Michael E. Greenberg
- O. Marín
- J. Sweatt
- Hongjun Song
- Guo-li Ming
In Genetics
- H. Zoghbi
- Yi Zhang
- Mark F. Bear
- Maria H. Chahrour
- Michael E. Greenberg
- Hao Wu
- Peter A. Jones
- Michael Joseph Meaney
In Molecular Biology
- Yi Zhang
- Hao Wu
- Peter A. Jones
- Manel Esteller
- H. Zoghbi
- Michael Joseph Meaney
- Richard A. Young
- Michael E. Greenberg
Citations in the corpus
- Potential therapeutic uses of BDNF in neurological and psychiatric disorders (2011, background): “Studies in rodents suggest that long-term changes in BDNF expression may be achievable via epigenetic mechanism”
- Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders (2012, background): “Because exon IV seems to respond to activity and is a target for activity- and calcium-sensitive transcription factors, including cAMP response-element binding protein (CREB), upstreamstimulatory factors, calcium-responsive transcription factor, and methylated CpG binding protein (MeCP2), it is call”
- Synaptic dysfunction in neurodevelopmental disorders associated with autism and intellectual disabilities. (2012, background): “Indeed, MeCP2 binds to the promoter regions of several genes that are repressed upon loss of MeCP2 and are activated by its presence, including brain-derived neurotrophic factor (BDNF) and several other neuronal genes (Chen et al. 2003; Martinowich et al. 2003; Yasui et al. 2007; Chahrour et al. 200”
- 5-hmC–mediated epigenetic dynamics during postnatal neurodevelopment and aging (2011, background): “Epigenetic plasticity in DNA methylation–related regulatory processes influences activity-dependent gene regulatio”
- Mild overexpression of MeCP2 causes a progressive neurological disorder in mice. (2004, background): “Recently, analysis of neuronal cultures from MeCP2 null mice revealed that MeCP2 binds to regulatory elements of the brain-derived neurotrophic factor promoter and affects its expression (28,32).”
- Mouse and rat BDNF gene structure and expression revisited (2006, background): “…also plays an important role in cell-specific and activity-dependent regulation of BDNF gene by recruiting global repressors such as REST/NRSF to promoter II (Palm et al., 1998; Timmusk et al., 1999; Zuccato et al., 2003) and MeCP2 to promoter III (Chen et al., 2003a; Martinowich et al., 2003).”
- Is folic acid good for everyone? (2008, background): “A cell culture study has shown that depolarization of neurons, which leads to increased synthesis of brain-derived neurotrophic factor, is accompanied by a reduction in the level of CpG methylation in the regulatory region of the Bdnf gene (167).”
- Post-synaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity and Disease (2010, neutral): “In cultured neurons, MeCP2 binds the promoter region of a Bdnf gene and suppresses its transcription (Chen et al., 2003; Martinowich et al., 2003).”
- The story of Rett syndrome: from clinic to neurobiology. (2007, positive): “MeCP2 Regulates Gene Expression in an Activity-Dependent Manner Brain-derived neurotrophic factor (BDNF) was identified as a target of MeCP2 through a candidate gene approach (Chen et al., 2003; Martinowich et al., 2003).”
- DNA binding selectivity of MeCP2 due to a requirement for A/T sequences adjacent to methyl-CpG. (2005, neutral): “[A/T]R4 was found to be essential for high-affinity binding at selected sites and at known MeCP2 target regions in the Bdnf and Dlx6 genes.”
- Current research trends in early life stress and depression: review of human studies on sensitive periods, gene-environment interactions, and epigenetics. (2012, neutral): “All of these brain regions are generally modified by early life stress and have been implicated in depression risk (Mayberg, 2003) and control of neuroendocrine reactivity (Lupien et al., 2009).”
- Epigenetics and the biological definition of gene x environment interactions. (2010, background): “These effects are consistent with previous reports of activity-dependent alterations in the methylation of the same bdnf promoter (Martinowich et al., 2003) and suggest that epigenetic states might be altered by a wide range of biologically relevant events that result in synaptic remodeling (Meaney ”