Christopher D. Link

Identification of a novel cis-regulatory element involved in the heat shock response in Caenorhabditis elegans using microarray gene expression and computational methods.

A global analysis of Caenorhabditis elegans operons.

Reporter transgenes for study of oxidant stress in Caenorhabditis elegans.

Interaction of intracellular beta amyloid peptide with chaperone proteins.

Functional analysis of the glutathione S-transferase 3 from Onchocerca volvulus (Ov-GST-3): a parasite GST confers increased resistance to oxidative stress in Caenorhabditis elegans.

Gene expression analysis in a transgenic Caenorhabditis elegans Alzheimer's disease model.

Oxidative stress precedes fibrillar deposition of Alzheimer's disease amyloid beta-peptide (1-42) in a transgenic Caenorhabditis elegans model.

A stress-responsive glutathione S-transferase confers resistance to oxidative stress in Caenorhabditis elegans.

Expression of the small heat-shock protein Hsp16-2 in Caenorhabditis elegans is suppressed by Ginkgo biloba extract EGb 761.

Compensatory regulation among ER chaperones in C. elegans.

A pilot proteomic study of amyloid precursor interactors in Alzheimer's disease.

Proteomic identification of proteins specifically oxidized in Caenorhabditis elegans expressing human Abeta(1-42): implications for Alzheimer's disease.

Soy isoflavone glycitein protects against beta amyloid-induced toxicity and oxidative stress in transgenic Caenorhabditis elegans.

Conversion of green fluorescent protein into a toxic, aggregation-prone protein by C-terminal addition of a short peptide.

C. elegans models of age-associated neurodegenerative diseases: lessons from transgenic worm models of Alzheimer's disease.

Amyloid-beta-induced pathological behaviors are suppressed by Ginkgo biloba extract EGb 761 and ginkgolides in transgenic Caenorhabditis elegans.

Decreased insulin-receptor signaling promotes the autophagic degradation of beta-amyloid peptide in C. elegans.

Suppression of in vivo beta-amyloid peptide toxicity by overexpression of the HSP-16.2 small chaperone protein.

The beta amyloid peptide can act as a modular aggregation domain.

Aberrant cleavage of TDP-43 enhances aggregation and cellular toxicity.

AIP-1 ameliorates beta-amyloid peptide toxicity in a Caenorhabditis elegans Alzheimer's disease model.

Life-span extension by dietary restriction is mediated by NLP-7 signaling and coelomocyte endocytosis in C. elegans.

What have worm models told us about the mechanisms of neuronal dysfunction in human neurodegenerative diseases?

Behavioral Phenotyping of a Transgenic C. Elegans Expressing Neuronal Amyloid-beta.

Behavioral phenotyping of a transgenic Caenorhabditis elegans expressing neuronal amyloid-beta.

Neurotoxic effects of TDP-43 overexpression in C. elegans.

Genetic mechanisms of coffee extract protection in a Caenorhabditis elegans model of β-amyloid peptide toxicity.

Insulin-like signaling determines survival during stress via posttranscriptional mechanisms in C. elegans.

Genetic dissection of late-life fertility in Caenorhabditis elegans.

A glycine zipper motif mediates the formation of toxic β-amyloid oligomers in vitro and in vivo.