The University of Chicago Header Logo

Search Result Details

This page shows the details of why an item matched the keywords from your search.
One or more keywords matched the following properties of Nelson, Deborah
PropertyValue
keywords ion channels and disease
overview The Nelson lab is interested in the role of ion channels in disease processes. Most recently, this has lead us to the study of the involvement of anion channels in innate immune processes, in neural secretion, in bone formation and in pancreatic hormone processing. Characterization of channel function has utilized a spectrum of tools including super-resolution microscopy, microfluidics, optogenetics, patch clamp electrophysiology, live cell fluorescence microscopy and basic biochemical techniques. We have created mouse models of channel mutations using CRISPER-Cas gene editing to examine loss of channel function in a variety of organ contexts. Anion channels drive a diversity of intracellular function and vesicle content at the molecular level and neuronal inhibition and microbicidal function at the cellular level. At the organellar level, they build new bone and process hormones for release. Anion channel loss of function results in fatal pulmonary infections in Cystic Fibrosis, osteoporosis in bone and contributes to the complex disease of diabetes. Recently, we have used microfluidic devices to visualize and quantify release of extracellular vesicles from cells in the immune system. These devices will allow us to examine fusion of individual vesicles or nanoparticles with target cells as they deliver diverse cargo including nucleic acids coding for signaling proteins and ion channels to restore function to cells lacking their expression. The extracellular vesicles are released by all cells and can be engineered to carry small therapeutic molecules and contribute to restoration of cell function. The microfluidic platform will allow us to visualize function in 3 dimensional arrays using organoids exposed to engineered extracellular vesicles. In summary, the laboratory seeks to examine cellular processes from the nanoparticle to the organellar level visualizing function from molecule to mouse model.
One or more keywords matched the following items that are connected to Nelson, Deborah
Item TypeName
Concept Potassium Channels
Concept Chloride Channels
Concept Potassium Channels, Inwardly Rectifying
Concept TRPC Cation Channels
Concept G Protein-Coupled Inwardly-Rectifying Potassium Channels
Academic Article Platelet-activating factor-induced chloride channel activation is associated with intracellular acidosis and apoptosis of intestinal epithelial cells.
Academic Article Presynaptic CLC-3 determines quantal size of inhibitory transmission in the hippocampus.
Academic Article Mutation of critical GIRK subunit residues disrupts N- and C-termini association and channel function.
Academic Article The granular chloride channel ClC-3 is permissive for insulin secretion.
Academic Article CLC-3 channels modulate excitatory synaptic transmission in hippocampal neurons.
Academic Article 5-amino-imidazole carboxamide riboside acutely potentiates glucose-stimulated insulin secretion from mouse pancreatic islets by KATP channel-dependent and -independent pathways.
Academic Article CLC-3 chloride channels moderate long-term potentiation at Schaffer collateral-CA1 synapses.
Academic Article TRPC6 channel translocation into phagosomal membrane augments phagosomal function.
Academic Article Claudin-2-dependent paracellular channels are dynamically gated.
Grant Role of Ion Channel in Mononuclear Phagocyte Activation
Grant MUSCARINIC GATED ATRIAL K+ CHANNEL
Grant Chloride Channel Involvement in Diabetes
Grant Alternate CI-secretory pathways in cystic fibrosis
Grant Chloride Channel Involvement in Diabetes
Search Criteria
  • Hyperpolarization Activated Cyclic Nucleotide Gated Channels