Paul J Muchowski

Summary

Affiliation: University of Washington
Country: USA

Publications

  1. ncbi request reprint Protein misfolding, amyloid formation, and neurodegeneration: a critical role for molecular chaperones?
    Paul J Muchowski
    Department of Pharmacology, University of Washington, Seattle 98195, USA
    Neuron 35:9-12. 2002
  2. pmc Connecting the dots in Huntington's disease with protein interaction networks
    Flaviano Giorgini
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    Genome Biol 6:210. 2005
  3. ncbi request reprint Modulation of neurodegeneration by molecular chaperones
    Paul J Muchowski
    Department of Pharmacology, The Center for Neurogenetics and Neurotherapeutics, University of Washington, Seattle, Washington 98195 7280, USA
    Nat Rev Neurosci 6:11-22. 2005
  4. pmc Loss of Hsp70 exacerbates pathogenesis but not levels of fibrillar aggregates in a mouse model of Huntington's disease
    Jennifer L Wacker
    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA
    J Neurosci 29:9104-14. 2009
  5. pmc Noninvasive measurement of protein aggregation by mutant huntingtin fragments or alpha-synuclein in the lens
    Paul J Muchowski
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    J Biol Chem 283:6330-6. 2008
  6. ncbi request reprint Histone deacetylase inhibition modulates kynurenine pathway activation in yeast, microglia, and mice expressing a mutant huntingtin fragment
    Flaviano Giorgini
    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA
    J Biol Chem 283:7390-400. 2008
  7. ncbi request reprint Hsp70 and Hsp40 attenuate formation of spherical and annular polyglutamine oligomers by partitioning monomer
    Jennifer L Wacker
    Department of Pharmacology, University of Washington, Seattle, Washington, 98195 2120, USA
    Nat Struct Mol Biol 11:1215-22. 2004
  8. ncbi request reprint Yeast genes that enhance the toxicity of a mutant huntingtin fragment or alpha-synuclein
    Stephen Willingham
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Science 302:1769-72. 2003
  9. doi request reprint Induction of the phase II detoxification pathway suppresses neuron loss in Drosophila models of Parkinson's disease
    Kien Trinh
    Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA
    J Neurosci 28:465-72. 2008
  10. pmc Genetic manipulation of palmitoylethanolamide production and inactivation in Saccharomyces cerevisiae
    Giulio G Muccioli
    Department of Pharmacology, University of Washington, Seattle, Washington, United States of America
    PLoS ONE 4:e5942. 2009

Collaborators

Detail Information

Publications23

  1. ncbi request reprint Protein misfolding, amyloid formation, and neurodegeneration: a critical role for molecular chaperones?
    Paul J Muchowski
    Department of Pharmacology, University of Washington, Seattle 98195, USA
    Neuron 35:9-12. 2002
    ..Here we review recent studies that have revealed a critical role for molecular chaperones in several neurodegenerative disorders...
  2. pmc Connecting the dots in Huntington's disease with protein interaction networks
    Flaviano Giorgini
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    Genome Biol 6:210. 2005
    ....
  3. ncbi request reprint Modulation of neurodegeneration by molecular chaperones
    Paul J Muchowski
    Department of Pharmacology, The Center for Neurogenetics and Neurotherapeutics, University of Washington, Seattle, Washington 98195 7280, USA
    Nat Rev Neurosci 6:11-22. 2005
    ....
  4. pmc Loss of Hsp70 exacerbates pathogenesis but not levels of fibrillar aggregates in a mouse model of Huntington's disease
    Jennifer L Wacker
    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA
    J Neurosci 29:9104-14. 2009
    ..Thus, endogenous Hsp70s are a critical component of the cellular defense against the toxic effects of misfolded htt protein in neurons, but buffer toxicity by mechanisms independent of the deposition of fibrillar aggregates...
  5. pmc Noninvasive measurement of protein aggregation by mutant huntingtin fragments or alpha-synuclein in the lens
    Paul J Muchowski
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    J Biol Chem 283:6330-6. 2008
    ..These novel mouse models will facilitate the characterization of protein aggregation in vivo and are being used in efficient and economical screens for chemical and genetic modifiers of disease-relevant protein aggregation...
  6. ncbi request reprint Histone deacetylase inhibition modulates kynurenine pathway activation in yeast, microglia, and mice expressing a mutant huntingtin fragment
    Flaviano Giorgini
    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA
    J Biol Chem 283:7390-400. 2008
    ....
  7. ncbi request reprint Hsp70 and Hsp40 attenuate formation of spherical and annular polyglutamine oligomers by partitioning monomer
    Jennifer L Wacker
    Department of Pharmacology, University of Washington, Seattle, Washington, 98195 2120, USA
    Nat Struct Mol Biol 11:1215-22. 2004
    ....
  8. ncbi request reprint Yeast genes that enhance the toxicity of a mutant huntingtin fragment or alpha-synuclein
    Stephen Willingham
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Science 302:1769-72. 2003
    ....
  9. doi request reprint Induction of the phase II detoxification pathway suppresses neuron loss in Drosophila models of Parkinson's disease
    Kien Trinh
    Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA
    J Neurosci 28:465-72. 2008
    ..Our results suggest that oxidative stress is a feature of alpha-synuclein toxicity and that induction of the phase II detoxification pathway represents a potential preventative therapy for PD...
  10. pmc Genetic manipulation of palmitoylethanolamide production and inactivation in Saccharomyces cerevisiae
    Giulio G Muccioli
    Department of Pharmacology, University of Washington, Seattle, Washington, United States of America
    PLoS ONE 4:e5942. 2009
    ....
  11. pmc A genomic screen in yeast implicates kynurenine 3-monooxygenase as a therapeutic target for Huntington disease
    Flaviano Giorgini
    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA
    Nat Genet 37:526-31. 2005
    ..This finding is suggestive of a conserved mechanism of polyglutamine toxicity from yeast to humans and identifies new candidate therapeutic targets for the treatment of Huntington disease...
  12. pmc Requirement of an intact microtubule cytoskeleton for aggregation and inclusion body formation by a mutant huntingtin fragment
    Paul J Muchowski
    Department of Genome Sciences University of Washington, Box 357730, Seattle, WA 98195, USA
    Proc Natl Acad Sci U S A 99:727-32. 2002
    ....
  13. ncbi request reprint Functional similarities between the small heat shock proteins Mycobacterium tuberculosis HSP 16.3 and human alphaB-crystallin
    Melissa M Valdez
    Department of Biological Structure, University of Washington, Seattle, WA 98195 7420, USA
    Eur J Biochem 269:1806-13. 2002
    ..While the sequence similarity between human alphaB-crystallin and MTB HSP 16.3 is only 18%, these results suggest that the functional similarities between these proteins containing the core 'alpha-crystallin' domain are much closer...
  14. ncbi request reprint Molecular genetics approaches in yeast to study amyloid diseases
    Tiago Fleming Outeiro
    Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA
    J Mol Neurosci 23:49-60. 2004
    ..A final advantage of using yeast to study amyloid formation and toxicity is the ease and rapidity with which large-scale drug-screening efforts can be conducted in this model organism...
  15. pmc Flanking sequences profoundly alter polyglutamine toxicity in yeast
    Martin L Duennwald
    Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA
    Proc Natl Acad Sci U S A 103:11045-50. 2006
    ..Very tight aggregates always are benign, whereas amorphous aggregates can be toxic. We thereby establish a previously undescribed systematic characterization of the influence of flanking amino acid sequences on polyQ toxicity...
  16. ncbi request reprint Making yeast tremble: yeast models as tools to study neurodegenerative disorders
    Michael Y Sherman
    Department of Biochemistry, Boston University School of Medicine, Boston, MA 02118, USA
    Neuromolecular Med 4:133-46. 2003
    ....
  17. ncbi request reprint Cysteine string protein (CSP) inhibition of N-type calcium channels is blocked by mutant huntingtin
    Linda C Miller
    Cellular and Molecular Neurobiology Research Group, Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta T2N 4N1, Canada
    J Biol Chem 278:53072-81. 2003
    ..These results indicate that CSP's modulation of G protein inhibition of calcium channel activity is blocked in the presence of a huntingtin fragment with expanded polyglutamine tracts...
  18. ncbi request reprint Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models
    Irene H Cheng
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Biol Chem 282:23818-28. 2007
    ..Thus, Abeta*56 is a likelier determinant of functional deficits in hAPP mice than fibrillar Abeta deposits. Therapeutic interventions that reduce Abeta fibrils at the cost of augmenting nonfibrillar Abeta assemblies could be harmful...
  19. ncbi request reprint Chaperone functions of the E3 ubiquitin ligase CHIP
    Meredith F N Rosser
    Department of Cell and Developmental Biology, University of North Carolina Chapel Hill School of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599, USA
    J Biol Chem 282:22267-77. 2007
    ..The ability of CHIP to recognize nonnative protein structure may aid in selection of slow folding or misfolded polypeptides for ubiquitination...
  20. ncbi request reprint Screening for genetic modifiers of amyloid toxicity in yeast
    Flaviano Giorgini
    Department of Genetics, Univeristy of Leicester, Leicester, United Kingdom LE1 7RH
    Methods Enzymol 412:201-22. 2006
    ..We suggest approaches for development of new yeast models of amyloid toxicity and provide an overview of screening protocols for genetic modifiers of amyloid toxicity by both random and systematic approaches...
  21. ncbi request reprint Disease-modifying pathways in neurodegeneration
    Steven Finkbeiner
    Gladstone Institute of Neurological Disease and Department of Physiology, University of California, San Francisco, San Francisco, California 94158, USA
    J Neurosci 26:10349-57. 2006
  22. ncbi request reprint Green tea (-)-epigallocatechin-gallate modulates early events in huntingtin misfolding and reduces toxicity in Huntington's disease models
    Dagmar E Ehrnhoefer
    Max Delbrueck Center for Molecular Medicine, Department of Neuroproteomics, Berlin, Germany
    Hum Mol Genet 15:2743-51. 2006
    ..Our studies may provide the basis for the development of a novel pharmacotherapy for HD and related polyQ disorders...
  23. pmc A network of protein interactions determines polyglutamine toxicity
    Martin L Duennwald
    Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA
    Proc Natl Acad Sci U S A 103:11051-6. 2006
    ....