Kim A. Caldwell

Suppression of polyglutamine-induced protein aggregation in Caenorhabditis elegans by torsin proteins.

Role for NudC, a dynein-associated nuclear movement protein, in mitosis and cytokinesis.

An animal model to discern torsin function: suppression of protein aggregation in C. elegans.

Using Caenorhabditis elegans to probe toxicity of 1-alkyl-3-methylimidazolium chloride based ionic liquids.

Epileptic-like convulsions associated with LIS-1 in the cytoskeletal control of neurotransmitter signaling in Caenorhabditis elegans.

Torsin-mediated protection from cellular stress in the dopaminergic neurons of Caenorhabditis elegans.

Alpha-synuclein blocks ER-Golgi traffic and Rab1 rescues neuron loss in Parkinson's models.

Deletion of the ubiquitin ligase CHIP leads to the accumulation, but not the aggregation, of both endogenous phospho- and caspase-3-cleaved tau species.

Genetic interactions among cortical malformation genes that influence susceptibility to convulsions in C. elegans.

Ubiquitin conjugating enzymes participate in polyglutamine protein aggregation.

The Parkinson's disease protein alpha-synuclein disrupts cellular Rab homeostasis.

Hypothesis-based RNAi screening identifies neuroprotective genes in a Parkinson's disease model.

Acetaminophen attenuates dopamine neuron degeneration in animal models of Parkinson's disease.

The microtubule-associated protein, NUD-1, exhibits chaperone activity in vitro.

Lysosomal enzyme cathepsin D protects against alpha-synuclein aggregation and toxicity.

Traversing a wormhole to combat Parkinson's disease.

Alpha-synuclein is part of a diverse and highly conserved interaction network that includes PARK9 and manganese toxicity.

Rapid selection of cyclic peptides that reduce alpha-synuclein toxicity in yeast and animal models.

Pharmacogenetic analysis reveals a post-developmental role for Rac GTPases in Caenorhabditis elegans GABAergic neurotransmission.

Investigating bacterial sources of toxicity as an environmental contributor to dopaminergic neurodegeneration.

VPS41, a protein involved in lysosomal trafficking, is protective in Caenorhabditis elegans and mammalian cellular models of Parkinson's disease.

Compounds from an unbiased chemical screen reverse both ER-to-Golgi trafficking defects and mitochondrial dysfunction in Parkinson's disease models.

C. elegans as a model organism to investigate molecular pathways involved with Parkinson's disease.

The early-onset torsion dystonia-associated protein, torsinA, displays molecular chaperone activity in vitro.

Chemical enhancement of torsinA function in cell and animal models of torsion dystonia.

Low-dose bafilomycin attenuates neuronal cell death associated with autophagy-lysosome pathway dysfunction.

The early-onset torsion dystonia-associated protein, torsinA, is a homeostatic regulator of endoplasmic reticulum stress response.

Caenorhabditis elegans as a model system for identifying effectors of α-synuclein misfolding and dopaminergic cell death associated with Parkinson's disease.

Structural features and chaperone activity of the NudC protein family.

TorsinA participates in endoplasmic reticulum-associated degradation.

Inhibitors of LRRK2 kinase attenuate neurodegeneration and Parkinson-like phenotypes in Caenorhabditis elegans and Drosophila Parkinson's disease models.

Modeling dopamine neuron degeneration in Caenorhabditis elegans.

Functional links between Aβ toxicity, endocytic trafficking, and Alzheimer's disease risk factors in yeast.

Different 8-Hydroxyquinolines Protect Models of TDP-43 Protein, α-Synuclein, and Polyglutamine Proteotoxicity through Distinct Mechanisms.

Functional Analysis of VPS41-Mediated Neuroprotection in Caenorhabditis elegans and Mammalian Models of Parkinson's Disease.