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Monika A. Davare

Researcher at Oregon Health & Science University

Publications -  78
Citations -  5415

Monika A. Davare is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: ROS1 & Crizotinib. The author has an hindex of 29, co-authored 68 publications receiving 4645 citations. Previous affiliations of Monika A. Davare include University of Wisconsin-Madison & Roy J. and Lucille A. Carver College of Medicine.

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An activity-regulated microRNA controls dendritic plasticity by down-regulating p250GAP

TL;DR: It is shown that microRNA 132 (miR132) is an activity-dependent rapid response gene regulated by the cAMP response element-binding (CREB) protein pathway and proposed that the miR132–p250GAP pathway plays a key role in activity- dependent structural and functional plasticity.
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A β2 Adrenergic Receptor Signaling Complex Assembled with the Ca2+ Channel Cav1.2

TL;DR: Electrophysiological recordings from hippocampal neurons demonstrate highly localized signal transduction from the receptor to the channel, providing insight into how a particular receptor selectively regulates specific targets by identifying a prototypical macromolecular signaling complex.
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SAP97 Is Associated with the α-Amino-3-hydroxy-5-methylisoxazole-4-propionic Acid Receptor GluR1 Subunit

TL;DR: The findings suggest that SAP97 may be involved in localizing AMPA receptors at postsynaptic sites through its interaction with the GluR1 subunit.
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An activity-induced microRNA controls dendritic spine formation by regulating Rac1-PAK signaling.

TL;DR: It is shown that the CREB- and activity-regulated microRNA, miR132, is induced during periods of active synaptogenesis, and it is suggested that neuronal activity regulates spine formation, in part, by increasing miR 132 transcription, which in turn activates a Rac1-Pak actin remodeling pathway.
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Activity-dependent Synaptogenesis: Regulation by a CaM-kinase kinase/CaM-kinase I/βPIX Signaling Complex

TL;DR: A Ca(2+)-signaling pathway downstream of the NMDA receptor that stimulates calmodulin-dependent kinase kinase (CaMKK) and CaMKI to promote formation of spines and synapses in hippocampal neurons can promote synapse formation during neuronal development and in structural plasticity.