A5003155578- Neuroscience and Neuropharmacology Research
- Receptor Mechanisms and Signaling
- Genetics and Neurodevelopmental Disorders
- Neuropeptides and Animal Physiology
- RNA Research and Splicing
- Pharmacological Receptor Mechanisms and Effects
- Cellular transport and secretion
- Alzheimer's disease research and treatments
- Photoreceptor and optogenetics research
- RNA regulation and disease
- Ion channel regulation and function
- Herpesvirus Infections and Treatments
- Autism Spectrum Disorder Research
- Tryptophan and brain disorders
- Cannabis and Cannabinoid Research
- Neurogenesis and neuroplasticity mechanisms
- Cytomegalovirus and herpesvirus research
- Adipose Tissue and Metabolism
- Congenital heart defects research
- Neurological disorders and treatments
- Genomics and Rare Diseases
- Nicotinic Acetylcholine Receptors Study
- Photochromic and Fluorescence Chemistry
- Genetic Mapping and Diversity in Plants and Animals
- Immune cells in cancer
Albert Einstein College of Medicine
2013-2024
New York University
1998-2010
John F. Kennedy Center for the Performing Arts
2009
Icahn School of Medicine at Mount Sinai
2003
Johns Hopkins Medicine
2000
Johns Hopkins University
2000
G-protein-coupled receptors (GPCRs) have recently joined the list of cell surface that dimerize.Dimerization has been shown to alter ligand-binding, signaling, and trafficking properties these receptors.Recent studies GPCRs heterodimerize with closely related members, resulting in modulation their function.In this study, we attempted determine whether members GPCR superfamilies couple different families G-proteins can associate form oligomers.We chose 2 adrenergic receptor couples...
Adrenergic and opioid receptors belong to the rhodopsin family of G-protein coupled receptors, couple analogous signal transduction pathways, affect nociceptive system. Although a number previous studies have reported functional interactions between these two basis for this has not been well explored. We propose that direct receptor-receptor could account, in part, opioid-adrenergic cross-talk. In report, we addressed using biophysical, biochemical, pharmacological studies. show mu alpha2A...
Matrix metalloproteinases (MMPs) have been proposed to remodel the extracellular environment of neurons. Here, we report that metalloproteinase membrane-type 5 MMP (MT5-MMP) binds AMPA receptor binding protein (ABP) and GRIP (glutamate interaction protein), two related postsynaptic density (PSD) PDZ (postsynaptic density-95/Discs large/zona occludens-1) domain proteins target receptors synapses. The MT5-MMP C terminus ABP PDZ5 coimmunoprecipitated colocalized in heterologous cells localized...
Neuronal activity elicits changes in synaptic composition that play an important role experience-dependent plasticity (Choquet and Triller, 2003; Lisman Raghavachari, 2006; Bourne Harris, 2008; Holtmaat Svoboda, 2009). We used a modified version of stable isotope labeling by amino acids cell culture to identify activity-dependent modifications the postsynaptic densities (PSDs) isolated from rat primary neuronal cultures. found altered ∼2% PSD proteome, which included increase diverse RNA...
Women are at increased risk for Alzheimer's disease (AD), but the reason why remains unknown. One hypothesis is that low estrogen levels menopause increases vulnerability to AD, this unproven.We compared neuronal genes upregulated by in ovariectomized female rhesus macaques with a database of >17,000 diverse gene sets and applied rare variant burden test exome sequencing data from 1208 AD patients age onset < 75 years 2162 controls.We found striking overlap between downregulated human...
Proper synaptic function requires the spatial and temporal compartmentalization of RNA metabolism via transacting RNA-binding proteins (RBPs). Loss RBP activity leads to abnormal posttranscriptional regulation results in diverse neurological disorders with underlying deficits morphology transmission. Functional loss 68-kDa Src associated mitosis (Sam68) is pathogenesis disorder fragile X tremor/ataxia syndrome. Sam68 binds mRNA β-actin (actb), an integral cytoskeletal component dendritic...
Dendritic protein homeostasis is crucial for most forms of long-term synaptic plasticity, and its dysregulation linked to a wide range brain disorders. Current models metabotropic glutamate receptor mediated depression (mGluR-LTD) suggest that rapid, local synthesis key proteins necessary the induction expression LTD. Here, we find mGluR-LTD can be induced in absence translation if proteasome concurrently inhibited. We report enhanced proteasomal degradation during depletes dendritic...
NMDA receptors (NMDARs) are key mediators of glutamatergic transmission and synaptic plasticity, their dysregulation has been linked to diverse neuropsychiatric neurodegenerative disorders. While normal NMDAR function requires regulated expression trafficking its different subunits, the molecular mechanisms underlying these processes not fully understood. Here we report that amyloid precursor protein intracellular domain associated-1 (AIDA-1), which associates with NMDARs is encoded by...
G-protein-coupled receptors (GPCRs) have recently joined the list of cell surface that dimerize. Dimerization has been shown to alter ligand-binding, signaling, and trafficking properties these receptors. Recent studies GPCRs heterodimerize with closely related members, resulting in modulation their function. In this study, we attempted determine whether members GPCR superfamilies couple different families G-proteins can associate form oligomers. We chose beta2 adrenergic receptor couples...
Long-lasting forms of postsynaptic plasticity commonly involve protein synthesis-dependent structural changes dendritic spines. However, the relationship between synthesis and presynaptic remains unclear. Here, we investigated in cannabinoid-receptor 1 (CB )-mediated long-term depression inhibitory transmission (iLTD), a form that involves protein-synthesis-dependent long-lasting reduction GABA release. We found CB -iLTD acute rat hippocampal slices was associated with changes. Using...
Stress is the most common trigger among episodic neurologic disorders. In ataxia type 2 (EA2), physical or emotional stress causes episodes of severe motor dysfunction that manifest as and dystonia. We used