Area of research
Molecular Biology · Cellular and Molecular Neuroscience
Research interest
Research interests include Neuroscience and Neuropharmacology Research, Ion channel regulation and function, Signaling Pathways in Disease, and Receptor Mechanisms and Signaling.
The clinical missense variant E282K in PPP3CA/calcineurin shifts substrate dephosphorylation by altering active site recruitment.
Synapse-to-Nucleus ERK→CREB Transcriptional Signaling Requires Dendrite-to-Soma Ca<sup>2+</sup> Propagation Mediated by L-Type Voltage-Gated Ca<sup>2+</sup> Channels.
Amyloid-β-induced dendritic spine elimination requires Ca<sup>2+</sup>-permeable AMPA receptors, AKAP-Calcineurin-NFAT signaling, and the NFAT target gene Mdm2.
AKAP150-anchored PKA regulates synaptic transmission and plasticity, neuronal excitability and CRF neuromodulation in the mouse lateral habenula.
Amyloid-β Causes NMDA Receptor Dysfunction and Dendritic Spine Loss through mGluR1 and AKAP150-Anchored Calcineurin Signaling.
miRNA-mediated control of gephyrin synthesis drives sustained inhibitory synaptic plasticity.
Increased KIF11/kinesin-5 expression offsets Alzheimer Aβ-mediated toxicity and cognitive dysfunction
Complementary Use of Super-Resolution Imaging Modalities to Study the Nanoscale Architecture of Inhibitory Synapses.
The Ca<sub>V</sub>1.2 G406R mutation decreases synaptic inhibition and alters L-type Ca<sup>2+</sup> channel-dependent LTP at hippocampal synapses in a mouse model of Timothy Syndrome.
Palmitoylation of A-kinase anchoring protein 79/150 modulates its nanoscale organization, trafficking, and mobility in postsynaptic spines.
Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels
Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.
β-Amyloid disruption of LTP/LTD balance is mediated by AKAP150-anchored PKA and Calcineurin regulation of Ca<sup>2+</sup>-permeable AMPA receptors.
Stepwise disassembly of GABAergic synapses during pathogenic excitotoxicity.
AKAP79/150 coordinates leptin-induced PKA signaling to regulate K<sub>ATP</sub> channel trafficking in pancreatic β-cells.
Precision Mapping of Amyloid-β Binding Reveals Perisynaptic Localization and Spatially Restricted Plasticity Deficits.
Kif11 overexpression rescues cognition, long-term potentiation, and spine defects in mouse and cell models of Alzheimer’s disease
Phosphorylation-Dependent Regulation of Ca<sup>2+</sup>-Permeable AMPA Receptors During Hippocampal Synaptic Plasticity.
Local miRNA-Dependent Translational Control of GABA<sub>A</sub>R Synthesis during Inhibitory Long-Term Potentiation.
AKAP79/150 coordinates leptin-induced PKA activation to regulate K <sub>ATP</sub> channel trafficking in pancreatic β-cells
Nanoscale Subsynaptic Domains Underlie the Organization of the Inhibitory Synapse.
Synapse-to-Nucleus Communication through NFAT Is Mediated by L-type Ca<sup>2+</sup> Channel Ca<sup>2+</sup> Spike Propagation to the Soma.
AKAP79/150 recruits the transcription factor NFAT to regulate signaling to the nucleus by neuronal L-type Ca<sup>2+</sup> channels.
Synaptic crosstalk conferred by a zone of differentially regulated Ca<sup>2+</sup> signaling in the dendritic shaft adjoining a potentiated spine.
Subcellular Localization and Activity of the Mitogen-Activated Protein Kinase Kinase 7 (MKK7) <i>γ</i> Isoform are Regulated through Binding to the Phosphatase Calcineurin.
Control of Homeostatic Synaptic Plasticity by AKAP-Anchored Kinase and Phosphatase Regulation of Ca <sup>2+</sup> -Permeable AMPA Receptors
Selective Down-regulation of KV2.1 Function Contributes to Enhanced Arterial Tone during Diabetes
AKAP150 participates in calcineurin/NFAT activation during the down-regulation of voltage-gated K+ currents in ventricular myocytes following myocardial infarction
A-kinase Anchoring Protein 79/150 Recruits Protein Kinase C to Phosphorylate Roundabout Receptors
AKAP-Anchored PKA Maintains Neuronal L-type Calcium Channel Activity and NFAT Transcriptional Signaling