A5071397864- Neuroscience and Neuropharmacology Research
- Receptor Mechanisms and Signaling
- Ion channel regulation and function
- Cellular transport and secretion
- Photoreceptor and optogenetics research
- Genetics and Neurodevelopmental Disorders
- Neuroinflammation and Neurodegeneration Mechanisms
- Lipid Membrane Structure and Behavior
- Retinal Development and Disorders
- Mitochondrial Function and Pathology
- Memory and Neural Mechanisms
- Neurobiology and Insect Physiology Research
- Ubiquitin and proteasome pathways
- Glycosylation and Glycoproteins Research
- Autism Spectrum Disorder Research
- RNA and protein synthesis mechanisms
- Neurogenesis and neuroplasticity mechanisms
- Neural dynamics and brain function
- Photochromic and Fluorescence Chemistry
- Genomics and Rare Diseases
- Amino Acid Enzymes and Metabolism
- Hypothalamic control of reproductive hormones
- Protein Kinase Regulation and GTPase Signaling
- Protein Tyrosine Phosphatases
- Biochemical Analysis and Sensing Techniques
National Institute of Neurological Disorders and Stroke
2015-2025
National Institutes of Health
2015-2025
The University of Tokyo
2011
National Institute on Deafness and Other Communication Disorders
1999-2002
Howard Hughes Medical Institute
1994-1997
Johns Hopkins University
1993-1997
Eunice Kennedy Shriver National Institute of Child Health and Human Development
1997
Modulation of α-amino-3-hydroxy-5-methylisoxazole-4-propionic Acid (AMPA) receptors in the brain by protein phosphorylation may play a crucial role regulation synaptic plasticity. Previous studies have demonstrated that calmodulin (CaM) kinase II can phosphorylate and modulate AMPA receptors. However, sites CaM not been unequivocally identified. In current study, we generated two site-specific antibodies to analyze glutamate receptor GluR1 subunit. These recognize only when it is...
Traditionally, hippocampal long-term potentiation (LTP) of synaptic strength requires Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) and other kinases, whereas depression (LTD) phosphatases. Here, we found that LTD also CaMKII its phospho-T286-induced "autonomous" (Ca2+-independent) activity. However, LTP is known to induce phosphorylation the AMPA-type glutamate receptor (AMPAR) subunit GluA1 at S831, instead induced CaMKII-mediated S567, a site reduce localization. S831 by was...
At excitatory synapses, both NMDA and AMPA receptors are localized to the postsynaptic density (PSD). However, unlike receptors, synaptic stable components of PSD. Even so, surface-expressed undergo endocytosis, which is more robust early in development declines during development. We investigated subunit-specific contributions receptor specifically defining endocytic motifs pathways preferred by NR2A NR2B subunits. find that have distinct encoded their distal C termini these interact with...
The molecular basis for glutamate receptor trafficking to the plasma membrane is not understood. In present study, we demonstrate that Homer 1b (H1b), a constitutively expressed splice form of immediate early gene product (now termed 1a) regulates and surface expression group I metabotropic receptors. H1b inhibits mGluR5 in heterologous cells, causing be retained endoplasmic reticulum (ER). contrast, alone or coexpressed with 1a successfully travels through secretory pathway membrane....
Abstract CaMKII is one of the most studied synaptic proteins, but many critical issues regarding its role in function remain unresolved. Using a CRISPR-based system to delete and replace it with mutated forms single neurons, we have rigorously addressed various roles. In brief, basal AMPAR NMDAR transmission both require CaMKIIα, not CaMKIIβ, indicating that, even adult, determined by ongoing action CaMKIIα. While requires kinase activity, does not, implying scaffolding for protein instead....
<h3>Importance</h3>Schizophrenia is a complex genetic disorder demonstrating considerable heritability. Genetic studies have implicated many different genes and pathways, but much of the liability remains unaccounted for. Investigation forms schizophrenia will lead to better understanding underlying molecular which then enable targeted approaches for disease prevention treatment.<h3>Objective</h3>To identify new factors strongly predisposing in families with multiple affected individuals...