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BDNF — MYLIP
Text-mined interactions from Literome
Klein et al., Nat Neurosci 2007
:
Block of
miR132 mediated repression increased MeCP2 and brain derived neurotrophic factor (BDNF) levels in cultured rat neurons and the loss of MeCP2
reduced BDNF and miR132 levels in vivo
Dreyer et al., Genome medicine 2010
:
Recent studies have identified changes of several specific miRNA expression profiles and polymorphisms affecting the interactions between miRNAs and their targets in various brain disorders, including addiction : miR-16 causes adaptive changes in production of the serotonin transporter ; miR-133b is specifically expressed in midbrain dopaminergic neurons, and regulates the production of tyrosine hydroxylase and the dopamine transporter ;
miR-212 affects production of striatal
brain derived neurotrophic factor and synaptic plasticity upon cocaine
Miura et al., J Neurochem 2012
:
We thus examined whether
miR-206 mediated suppression is
responsible for the expression pattern of
BDNF during myogenic differentiation ... Conversely, suppression of
miR-206 levels resulted in de-repression of BDNF 3'UTR reporter activity and
increased endogenous
BDNF-L mRNA levels
Caputo et al., PloS one 2011
:
Brain derived neurotrophic factor (BDNF) expression is
regulated by microRNAs
miR-26a and miR-26b allele-specific binding
Lee et al., Ann Neurol 2012
(Alzheimer Disease...) :
miR-206 regulates
brain derived neurotrophic factor in Alzheimer disease model
Li et al., PloS one 2013
:
First, we identified that miR-182 may be a putative miRNA that regulates BDNF levels by bioinformatic studies, and characterized the
effects of
miR-182 on the
BDNF levels using cell based studies, side by side with miR-132 ( a known miRNA that regulates BDNF expression ) ... We showed that treatment of miR-132 and miR-182 respectively decreased the BDNF protein levels in a human neuronal cell model, supporting the regulatory
roles of
miR-132 and miR-182 on the
BDNF expression ... Furthermore, we explored the
roles of
miR-132 and miR-182 on the
BDNF levels in depression using human subjects by assessing their serum levels