Cynthia M J Higgins

Summary

Affiliation: University of Massachusetts Medical School
Country: USA

Publications

  1. pmc ALS-associated mutant SOD1G93A causes mitochondrial vacuolation by expansion of the intermembrane space and by involvement of SOD1 aggregation and peroxisomes
    Cynthia M J Higgins
    Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, 364 Plantation St, Worcester, MA 01655, USA
    BMC Neurosci 4:16. 2003
  2. ncbi request reprint Mitochondrial electron transport chain complex dysfunction in a transgenic mouse model for amyotrophic lateral sclerosis
    Cheolwha Jung
    Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
    J Neurochem 83:535-45. 2002
  3. ncbi request reprint Mutant Cu, Zn superoxide dismutase that causes motoneuron degeneration is present in mitochondria in the CNS
    Cynthia M J Higgins
    Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA
    J Neurosci 22:RC215. 2002
  4. ncbi request reprint Inhibition of chaperone activity is a shared property of several Cu,Zn-superoxide dismutase mutants that cause amyotrophic lateral sclerosis
    Hemachand Tummala
    Department of Biochemistry and Molecular Pharmacology, Neurology, and Cell Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    J Biol Chem 280:17725-31. 2005
  5. ncbi request reprint A quantitative histochemical assay for activities of mitochondrial electron transport chain complexes in mouse spinal cord sections
    Cheolwha Jung
    Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
    J Neurosci Methods 114:165-72. 2002

Collaborators

Detail Information

Publications5

  1. pmc ALS-associated mutant SOD1G93A causes mitochondrial vacuolation by expansion of the intermembrane space and by involvement of SOD1 aggregation and peroxisomes
    Cynthia M J Higgins
    Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, 364 Plantation St, Worcester, MA 01655, USA
    BMC Neurosci 4:16. 2003
    ..To determine which of these possibilities are true, we examined the vacuolar patterns in detail in transgenic mice expressing mutant SOD1G93A...
  2. ncbi request reprint Mitochondrial electron transport chain complex dysfunction in a transgenic mouse model for amyotrophic lateral sclerosis
    Cheolwha Jung
    Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
    J Neurochem 83:535-45. 2002
    ..These results demonstrate a functional defect in mitochondria in the ventral horn region and support the view that mitochondrial damage plays a role in mutant SOD1-induced motoneuron degeneration pathway...
  3. ncbi request reprint Mutant Cu, Zn superoxide dismutase that causes motoneuron degeneration is present in mitochondria in the CNS
    Cynthia M J Higgins
    Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA
    J Neurosci 22:RC215. 2002
    ..By immunoelectron microscopy, we show that SOD1 is present within mitochondria at similar concentrations as in the cytoplasm. Thus SOD1, in addition to being a cytosolic enzyme, is present inside mitochondria in the CNS...
  4. ncbi request reprint Inhibition of chaperone activity is a shared property of several Cu,Zn-superoxide dismutase mutants that cause amyotrophic lateral sclerosis
    Hemachand Tummala
    Department of Biochemistry and Molecular Pharmacology, Neurology, and Cell Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    J Biol Chem 280:17725-31. 2005
    ..Thus, mutant SOD1 proteins may impair chaperone function independent of gene expression in vivo, and this inhibition may be a shared property of ALS-linked mutant SOD1 proteins...
  5. ncbi request reprint A quantitative histochemical assay for activities of mitochondrial electron transport chain complexes in mouse spinal cord sections
    Cheolwha Jung
    Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
    J Neurosci Methods 114:165-72. 2002
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