A cAMP-response element binding protein-induced microRNA regulates neuronal morphogenesis.

By Ngan K. Vo, Matthew E. Klein, O. Varlamova, D. Keller, Tadashi Yamamoto, Richard H. Goodman, S. Impey. Proceedings of the National Academy of Sciences of the United States of America, 2005

880 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/bd103c40c73018b8ac6a2d1907d6cf91dace4d68

Citations in the corpus

• Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. (2007, neutral): “For instance, a number of well-studied mammalian transcription factors including c-Myc, cAMP-response element binding protein (CREB), and MyoD have been shown to control both mRNA and miRNA expression (O’Donnell et al., 2005;Rao et al., 2006;Vo et al., 2005;Zhao et al., 2005).”
• Identification of miRNA Changes in Alzheimer's Disease Brain and CSF Yields Putative Biomarkers and Insights into Disease Pathways (2008, neutral): “MiR-132 is an activator of neuronal process outgrowth which translationally inhibits the p250GAP protein and has an emerging role in regulating BDNF and MeCP2 expression [34,67].”
• Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132. (2010, neutral): “Although miR-132 has been implicated in regulating neuron morphology (Siegel et al., 2009; Vo et al., 2005; Wayman et al., 2008), here we show a role for miR-125b in spine morphogenesis.”
• An activity-regulated microRNA controls dendritic plasticity by down-regulating p250GAP (2008, neutral): “We showed (14) that BDNF treatment increased miR132 levels in immature neurons.”
• microRNA modulation of circadian-clock period and entrainment. (2007, neutral): “For these studies, we initially examined miR-132, a CREB-regulated miRNA that is induced by neurotrophins (Vo et al., 2005).”
• BDNF-induced local protein synthesis and synaptic plasticity. (2014, neutral): “These results, together with the previous reports showing the upregulation of miR-132 by BDNF (Kawashima et al., 2010; Remenyi et al., 2010; Vo et al., 2005), suggest a homeostatic mechanism for maintaining MeCP2 levels.”
• The Addicted Synapse: Mechanisms of Synaptic and Structural Plasticity in Nucleus Accumbens (2010, neutral): “induce neurite outgrowth of hippocampal neurons in culture, in part, by reducing levels of the GTPase p250GAP [66].”
• From synapse to nucleus: calcium-dependent gene transcription in the control of synapse development and function. (2008, neutral): “Overexpression of miRNA132 increases, while blocking miRNA132 function decreases, neurite growth (Vo et al., 2005). miRNA132 controls dendritic growth by regulating the translation of p250GAP, a protein that affects actin cytoskeletal dynamics (Wayman et al., 2008a).”
• The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease (2008, neutral): “REST interacts with CoREST and other transcriptional repressors to regulate neuronal gene expression and lineage commitment through its direct control of both mRNA and, as shown more recently, miRNA transcripts (Vo et al., 2005; Conaco et al., 2006; Mortazavi et al., 2006 ; Visvanathan et al., 2007)”