Research Topics
| CHRISTOPHER LINKSummaryAffiliation: University of Colorado Country: USA Publications
Research Grants
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Detail Information
Publications
C. elegans models of age-associated neurodegenerative diseases: lessons from transgenic worm models of Alzheimer's diseaseChristopher D Link
Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA
Exp Gerontol 41:1007-13. 2006..In particular, I consider the potential these models have for uncovering common and unique fundamental toxic mechanisms underlying human neurodegenerative diseases...- Direct observation of stress response in Caenorhabditis elegans using a reporter transgeneC D Link
Institute for Behavioral Genetics, University of Colorado Boulder 80309 0447, USA
Cell Stress Chaperones 4:235-42. 1999..The ability to directly observe the stress response in living animals significantly simplifies the identification of both exogenous treatments and genetic alterations that modulate stress response, and possibly life span, in C. elegans... - What have worm models told us about the mechanisms of neuronal dysfunction in human neurodegenerative diseases?Dawn Teschendorf
Institute for Behavioral Genetics, University of Colorado, Boulder, CO, 80309, USA
Mol Neurodegener 4:38. 2009..These studies have given us a variety of insights into the specific disruptions of cellular processes that may underlie human neurodegenerative diseases... - The beta amyloid peptide can act as a modular aggregation domainChristopher D Link
Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309, USA
Neurobiol Dis 32:420-5. 2008.... - Conversion of green fluorescent protein into a toxic, aggregation-prone protein by C-terminal addition of a short peptideChristopher D Link
Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA
J Biol Chem 281:1808-16. 2006..GFP::degron may serve as an instructive "generic" aggregating control protein for studies of disease-associated aggregating proteins, such as huntingtin, alpha-synuclein, and the beta-amyloid peptide... - A glycine zipper motif mediates the formation of toxic β-amyloid oligomers in vitro and in vivoVirginia Fonte
Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309, USA
Mol Neurodegener 6:61. 2011..abstract:.. - Invertebrate models of Alzheimer's diseaseC D Link
Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309, USA
Genes Brain Behav 4:147-56. 2005..This review describes the rationale for AD-relevant studies in worms and flies and discusses both what has been learned from these studies and what may be discovered in the future... - Gene expression analysis in a transgenic Caenorhabditis elegans Alzheimer's disease modelChristopher D Link
Institute for Behavioral Genetics, University of Colorado, Campus Box 447, Boulder, CO 80309, USA
Neurobiol Aging 24:397-413. 2003..elegans model. Both CRYAB and TNFAIP1 show increased transcript levels in AD brains, supporting the validity of this approach... - Visualization of fibrillar amyloid deposits in living, transgenic Caenorhabditis elegans animals using the sensitive amyloid dye, X-34C D Link
Institute for Behavioral Genetics, University of Colorado, Campus Box 447, Boulder, CO 80309, USA
Neurobiol Aging 22:217-26. 2001..In vivo amyloid staining with X-34 may be a useful tool for monitoring anti-amyloidic treatments in real time or screening for genetic alterations that affect amyloid formation... - Transgenic invertebrate models of age-associated neurodegenerative diseasesC D Link
Institute for Behavioral Genetics, University of Colorado, Campus Box 447, Boulder, CO 80309, USA
Mech Ageing Dev 122:1639-49. 2001..This review considers what has been learned from these invertebrate models, and speculates what further insight may be gained from them... - AIP-1 ameliorates beta-amyloid peptide toxicity in a Caenorhabditis elegans Alzheimer's disease modelWail M Hassan
Institute for Behavioral Genetics, University of Colorado at Boulder, Boulder, CO 80303, USA
Hum Mol Genet 18:2739-47. 2009..Our results implicate AIP-1 in the regulation of protein turnover and protection against Abeta toxicity and point at AIRAPL as the functional mammalian homologue of AIP-1... - Suppression of in vivo beta-amyloid peptide toxicity by overexpression of the HSP-16.2 small chaperone proteinVirginia Fonte
Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA
J Biol Chem 283:784-91. 2008.... - Interaction of intracellular beta amyloid peptide with chaperone proteinsVirginia Fonte
Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309, USA
Proc Natl Acad Sci U S A 99:9439-44. 2002..These results suggest that chaperone function can play a role in modulating intracellular A beta metabolism and toxicity... - Compensatory regulation among ER chaperones in C. elegansWadim J Kapulkin
Institute for Behavioral Genetics, Campus Box 447, University of Colorado, Boulder, CO 80309, USA
FEBS Lett 579:3063-8. 2005..We show that this compensatory regulation is specific for ER chaperones, not dependent on RNA interference, and required for maintaining viability in worms containing a deletion of the hsp-3 gene... - Life-span extension by dietary restriction is mediated by NLP-7 signaling and coelomocyte endocytosis in C. elegansSang Kyu Park
Institute for Behavioral Genetics, University of Colorado at Boulder, Box 447, Boulder, CO 80303, USA
FASEB J 24:383-92. 2010..We conclude that two novel pathways, NLP-7 signaling and endocytosis by coelomocytes, are required for life extension under dietary restriction in C. elegans... - Decreased insulin-receptor signaling promotes the autophagic degradation of beta-amyloid peptide in C. elegansMaria L Florez-McClure
Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA
Autophagy 3:569-80. 2007..Also, Abeta; daf-2(e1370) nematodes contain more lysosomes than either Abeta or control strains. Finally, we demonstrate that decreased insulin-receptor signaling promotes the autophagic degradation of Abeta... - Reporter transgenes for study of oxidant stress in Caenorhabditis elegansChristopher D Link
Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA
Methods Enzymol 353:497-505. 2002 - Amyloid-beta-induced pathological behaviors are suppressed by Ginkgo biloba extract EGb 761 and ginkgolides in transgenic Caenorhabditis elegansYanjue Wu
Department of Pharmaceutical Sciences, School of Pharmacy, University of Maryland, Baltimore, Maryland 21201, USA
J Neurosci 26:13102-13. 2006.... - Identification of a novel cis-regulatory element involved in the heat shock response in Caenorhabditis elegans using microarray gene expression and computational methodsDebraj GuhaThakurta
Department of Genetics, Washington University School of Medicine, St. Louis, Missouri 63114, USA
Genome Res 12:701-12. 2002..The contributions of individual sites toward induction of transcription on HS are nonadditive, which indicates interaction and cross-talk between the sites, possibly through the transcription factors (TFs) binding to these sites... - A global analysis of Caenorhabditis elegans operonsThomas Blumenthal
Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Box B121, 4200 E 9th Avenue, Denver, Colorado 80262, USA
Nature 417:851-4. 2002..elegans genes. Numerous examples of co-transcription of genes encoding functionally related proteins are evident. Inspection of the operon list should reveal previously unknown functional relationships... - Soy isoflavone glycitein protects against beta amyloid-induced toxicity and oxidative stress in transgenic Caenorhabditis elegansAstrid Gutierrez-Zepeda
Department of Biological Sciences, University of Southern Mississippi, Hattiesburg, MS 39406, USA
BMC Neurosci 6:54. 2005..elegans, that express human beta amyloid (Abeta), were fed with soy derived isoflavones genistein, daidzein and glycitein (100 microg/ml) and then examined for Abeta-induced paralysis and the levels of reactive oxygen species... - Proteomic identification of proteins specifically oxidized in Caenorhabditis elegans expressing human Abeta(1-42): implications for Alzheimer's diseaseDebra Boyd-Kimball
Department of Chemistry, Center of Membrane Sciences, and Sanders-Brown Center on Aging, 121 Chemistry-Physics Building, University of Kentucky, Lexington, KY 40506-0055, USA
Neurobiol Aging 27:1239-49. 2006..We identified 16 oxidized proteins involved in energy metabolism, proteasome function, and scavenging of oxidants that are more oxidized compared to control lines. These results are discussed with reference to Alzheimer's disease... - Expression of the small heat-shock protein Hsp16-2 in Caenorhabditis elegans is suppressed by Ginkgo biloba extract EGb 761Amy Strayer
Department of Biological Sciences, The University of Southern Mississippi, Hattiesburg 39406-5018, USA
FASEB J 17:2305-7. 2003..These results support the hypothesis that EGb 761 augments the natural antistress system of C. elegans, thus increasing stress resistance and life span... - A stress-responsive glutathione S-transferase confers resistance to oxidative stress in Caenorhabditis elegansBritta Leiers
Institute for Genetics and Biological Medical Research Center, Heinrich Heine University, Dusseldorf, Germany
Free Radic Biol Med 34:1405-15. 2003..The Ce-GST-p24 was also localized in BL1 C. elegans by confocal laser-scanning microscopy, revealing a wide-spread distribution profile... - Oxidative stress precedes fibrillar deposition of Alzheimer's disease amyloid beta-peptide (1-42) in a transgenic Caenorhabditis elegans modelJennifer Drake
Department of Chemistry and Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA
Neurobiol Aging 24:415-20. 2003..These results are discussed with reference to Alzheimer's disease... - 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 elegansAndreas Kampkotter
Institut fur Genetik, Heinrich Heine Universitat, Universitatsstrasse 1, 40225 Dusseldorf, Germany
J Mol Biol 325:25-37. 2003..This study also shows the applicability of C.elegans as a model organism for the functional characterization of genes from (parasitic) nematode species which are not accessible to genetic manipulations... - A pilot proteomic study of amyloid precursor interactors in Alzheimer's diseaseBarbara A Cottrell
Buck Institute for Age Research, Novato, CA 94945, USA
Ann Neurol 58:277-89. 2005..In agreement with previous studies, our results are compatible with an involvement of APP in axonal transport and vesicular trafficking, and with a potential association of APP with cellular protein folding/protein degradation systems...
Research Grants
- Transgenic C.elegans as Amyloid Disease ModelCHRISTOPHER LINK; Fiscal Year: 2006..The role of specific genes and gene products in Abeta toxicity will be investigated using double-stranded RNA inhibition (RNAi) and Green Fluorescent Protein (GFP)-based transgenic reporter constructs. ..
- Comparative Modeling of Neurodegenerative DiseasesCHRISTOPHER LINK; Fiscal Year: 2006..elegans to manipulate these molecular responses to determine their role in disease protein toxicity. These studies will directly test whether there is a common underlying toxic mechanism for these neurodegenerative diseases. ..
- Investigation of TDP-43 Function and Toxicity in C. elegansChristopher D Link; Fiscal Year: 2010..In this project we will use model systems to determine the functions of TDP-43 and how its deposition may cause neurodegeneration. ..
- TRANSGENIC C. ELEGANS AS AMYLOID DISEASE MODELCHRISTOPHER LINK; Fiscal Year: 2001..abstract_text> ..
- TRANSGENIC C. ELEGANS AS AMYLOID DISEASE MODELChristopher D Link; Fiscal Year: 2010..The proposed study seeks to determine the cellular and molecular basis of -amyloid peptide toxicity. Understanding the toxic mechanism of this protein make be critical for developing therapeutics for Alzheimer's disease. ..