Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.

By Dieter Edbauer, J. Neilson, K. Foster, Chi-Fong Wang, Daniel P. Seeburg, Matthew N. Batterton, T. Tada, Bridget M. Dolan, Phillip A. Sharp, Morgan Sheng. Neuron, 2010

1,405 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b5627d9ffedeb79d55c90ebc91e722789affd7f4

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Citations in the corpus

Removing brakes on adult brain plasticity: from molecular to behavioral interventions (2010, background): “Recovery from stroke is enhanced by factors hypothesized to promote brain plasticity (Moskowitz et al., 2010), and could therefore potentially benefit from such a pharmacological approach.”
Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions (2022, background): “cellular dysfunctions are termed excitotoxicity and involve NMDARs, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, and kainite receptors.(1,46) Despite their involvement in ischemic stroke-related excitotoxicity, NMDARs act as a double-edged sword.”
Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States (2018, background): “Cerebral ischemia results in the development of a core region of brain damage wherein cells die rapidly by necrosis and a surrounding penumbra inwhich cells experience partial ischemia and neurons may undergo delayed apoptotic cell death (Moskowitz et al., 2010).”
BDNF-induced local protein synthesis and synaptic plasticity. (2014, positive): “Recent evidences indicate that FMRP can also repress the translation of cognate mRNAs through the associationwithmiRNAs (Edbauer et al., 2010; Muddashetty et al., 2011) and through the reversible stalling of the ribosomes on polyribosomes containing FMRP-target mRNAs (Darnell et al., 2011).”
Neuroinflammation and M2 microglia: the good, the bad, and the inflamed (2014, background): “Inflammation generated by stroke and ischemic reperfusion injury is regarded as a major factor contributing to tissue damage [60] and, like spinal cord injury, the damaged tissue environment favors an M1 phenotype [78].”
Fragile X Mental Retardation Protein: A Paradigm for Translational Control by RNA-Binding Proteins (2015, positive): “Furthermore, FMRP was shown to promote the formation of an Argonaute 2-microRNA-125a inhibitory complex on postsynaptic density protein 95 (PSD-95) mRNA (Edbauer et al., 2010; Muddashetty et al., 2011).”
MicroRNA sponges: progress and possibilities. (2010, positive): “Sponges were transfected or transduced into human, mouse, and rat cell lines such as nonsmall cell lung cancer (Kumar et al. 2008), B cell lymphoma (Bolisetty et al. 2009), embryonic neural stem cells (Rybak et al. 2008), and dissociated hippocampal neurons (Edbauer et al. 2010).”
Non-coding RNAs in human disease (2011, neutral): “; fragile X syndrome (FXS) can be caused by mutations in the RISC complex component fragile X mental retardation 1 protein (FMRP”
The Vascular Endothelium and Human Diseases (2013, background): “This is a critical question for targeting preventive strategies in patients with specific risk factors (49).”
microRNA as Biomarkers and Diagnostics (2016, positive): “…mutations in the components of the Drosha microprocessor complexes, such as, Fus and TDP-43 caused familiar amyotrophic lateral sclerosis (Ling et al., 2010); fragile X syndrome was associated with mutations in the RISC component fragile X mental retardation 1 protein (Edbauer et al., 2010).”