Bruce L Kagan

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint Electrophysiologic properties of channels induced by Abeta25-35 in planar lipid bilayers
    Meng chin Allison Lin
    Neuroscience Interdepartmental Program, Brain Research Institute of UCLA, Los Angeles, CA, USA
    Peptides 23:1215-28. 2002
  2. pmc Antimicrobial properties of amyloid peptides
    Bruce L Kagan
    Department of Psychiatry, David Geffen School of Medicine, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, California 90024, USA
    Mol Pharm 9:708-17. 2012
  3. ncbi request reprint The channel hypothesis of Huntington's disease
    B L Kagan
    Department of Psychiatry, Neuropsychiatric Institute and Brain Research Institute, UCLA School of Medicine, Los Angeles, CA 90024 1759, USA
    Brain Res Bull 56:281-4. 2001
  4. ncbi request reprint The channel hypothesis of Alzheimer's disease: current status
    Bruce L Kagan
    Department of Psychiatry, Neuropsychiatric Institute and Brain Research Institute, UCLA School of Medicine, 760 Westwood Plaza, Los Angeles, CA 90024 1759, USA
    Peptides 23:1311-5. 2002
  5. ncbi request reprint Amyloid peptide pores and the beta sheet conformation
    Bruce L Kagan
    Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
    Adv Exp Med Biol 677:150-67. 2010
  6. ncbi request reprint Amyloid peptide channels
    B L Kagan
    Department of Psychiatry, Neuropsychiatric Institute, David Geffen School of Medicine, UCLA, Los Angeles, California 90024 1759, USA
    J Membr Biol 202:1-10. 2004
  7. doi request reprint Effects of point substitutions on the structure of toxic Alzheimer's β-amyloid channels: atomic force microscopy and molecular dynamics simulations
    Laura Connelly
    Department of Bioengineering, University of California, San Diego, La Jolla, California 92093, USA
    Biochemistry 51:3031-8. 2012
  8. doi request reprint Atomic force microscopy and MD simulations reveal pore-like structures of all-D-enantiomer of Alzheimer's β-amyloid peptide: relevance to the ion channel mechanism of AD pathology
    Laura Connelly
    Department of Bioengineering, University of California, San Diego, La Jolla, California 92093, USA
    J Phys Chem B 116:1728-35. 2012
  9. doi request reprint Membrane pores in the pathogenesis of neurodegenerative disease
    Bruce L Kagan
    Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Semel Institute for Neuroscience and Human Behavior, Los Angeles, California, USA
    Prog Mol Biol Transl Sci 107:295-325. 2012
  10. pmc Isolation and characterization of the outer membrane of Borrelia hermsii
    E S Shang
    Department of Microbiology and Immunology, UCLA School of Medicine, Los Angeles, California 90095, USA
    Infect Immun 66:1082-91. 1998

Collaborators

Detail Information

Publications14

  1. ncbi request reprint Electrophysiologic properties of channels induced by Abeta25-35 in planar lipid bilayers
    Meng chin Allison Lin
    Neuroscience Interdepartmental Program, Brain Research Institute of UCLA, Los Angeles, CA, USA
    Peptides 23:1215-28. 2002
    ..The nonlinear function relating [Abeta25-35] and membrane activity suggests that aggregation of at least three monomers is required for channel formation...
  2. pmc Antimicrobial properties of amyloid peptides
    Bruce L Kagan
    Department of Psychiatry, David Geffen School of Medicine, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, California 90024, USA
    Mol Pharm 9:708-17. 2012
    ..In this paper, we will review the reported antimicrobial properties of amyloids and the implications of these discoveries for our understanding of amyloid structure and function...
  3. ncbi request reprint The channel hypothesis of Huntington's disease
    B L Kagan
    Department of Psychiatry, Neuropsychiatric Institute and Brain Research Institute, UCLA School of Medicine, Los Angeles, CA 90024 1759, USA
    Brain Res Bull 56:281-4. 2001
    ....
  4. ncbi request reprint The channel hypothesis of Alzheimer's disease: current status
    Bruce L Kagan
    Department of Psychiatry, Neuropsychiatric Institute and Brain Research Institute, UCLA School of Medicine, 760 Westwood Plaza, Los Angeles, CA 90024 1759, USA
    Peptides 23:1311-5. 2002
    ..Channel formation by several other amyloid peptides lends credence to the notion that this is a critical mechanism of cytotoxicity...
  5. ncbi request reprint Amyloid peptide pores and the beta sheet conformation
    Bruce L Kagan
    Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
    Adv Exp Med Biol 677:150-67. 2010
    ....
  6. ncbi request reprint Amyloid peptide channels
    B L Kagan
    Department of Psychiatry, Neuropsychiatric Institute, David Geffen School of Medicine, UCLA, Los Angeles, California 90024 1759, USA
    J Membr Biol 202:1-10. 2004
    ....
  7. doi request reprint Effects of point substitutions on the structure of toxic Alzheimer's β-amyloid channels: atomic force microscopy and molecular dynamics simulations
    Laura Connelly
    Department of Bioengineering, University of California, San Diego, La Jolla, California 92093, USA
    Biochemistry 51:3031-8. 2012
    ..MD simulations predict site 20 to face the solvated pore. Overall, the mutations support the previously predicted β-sheet-based channel structure...
  8. doi request reprint Atomic force microscopy and MD simulations reveal pore-like structures of all-D-enantiomer of Alzheimer's β-amyloid peptide: relevance to the ion channel mechanism of AD pathology
    Laura Connelly
    Department of Bioengineering, University of California, San Diego, La Jolla, California 92093, USA
    J Phys Chem B 116:1728-35. 2012
    ..Taken together, our results support the direct mechanism of Aβ ion channel-mediated destabilization of ionic homeostasis rather than the indirect mechanism through Aβ interaction with membrane receptors...
  9. doi request reprint Membrane pores in the pathogenesis of neurodegenerative disease
    Bruce L Kagan
    Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Semel Institute for Neuroscience and Human Behavior, Los Angeles, California, USA
    Prog Mol Biol Transl Sci 107:295-325. 2012
    ..The molecular structure of these pores may resemble the β-barrel structure of the toxics pore formed by bacterial toxins, such as staphylococcal α-hemolysin, anthrax toxin, and Clostridium perfringolysin...
  10. pmc Isolation and characterization of the outer membrane of Borrelia hermsii
    E S Shang
    Department of Microbiology and Immunology, UCLA School of Medicine, Los Angeles, California 90095, USA
    Infect Immun 66:1082-91. 1998
    ..This identification and characterization of the OMV proteins should aid in further studies of pathogenesis and immunity of tick-borne relapsing fever...
  11. ncbi request reprint Membrane perturbation by the neurotoxic Alzheimer amyloid fragment beta 25-35 requires aggregation and beta-sheet formation
    Y Hirakura
    School of Pharmaceutical Sciences, University of Tokyo, Japan
    Biochem Mol Biol Int 46:787-94. 1998
    ..These results suggest that membrane perturbation by aggregated beta 25-35 constitutes the molecular basis of the peptide's neurotoxicity...
  12. ncbi request reprint Channel formation by serum amyloid A: a potential mechanism for amyloid pathogenesis and host defense
    Yutaka Hirakura
    Department of Psychiatry, Neuropsychiatric Institute, UCLA School of Medicine, 90024, USA
    Amyloid 9:13-23. 2002
    ..Channel formation may thus be related to a host defense role of acute phase SAA isoforms and may also be the mechanism of end organ damage in AA and other amyloidoses...
  13. ncbi request reprint Pore formation by beta-2-microglobulin: a mechanism for the pathogenesis of dialysis associated amyloidosis
    Y Hirakura
    Department of Psychiatry, UCLA Neuropsychiatric Institute, Brain Research Institute and Mental Retardation Research Center, UCLA School of Medicine and West Los Angeles VA Medical Center, Los Angeles, CA, USA
    Amyloid 8:94-100. 2001
    ..We suggest that beta 2M channel formation may account for some of the pathophysiologic effects seen in dialysis associated amyloidosis. These findings lend further weight to the "channel hypothesis" of amyloid pathogenesis...
  14. ncbi request reprint Amyloidosis and protein folding
    Bruce L Kagan
    Science 307:42-3; author reply 42-3. 2005