Research Topics
Genomes and Genes | CHARLES LEE HOWESummaryAffiliation: Mayo Clinic Country: USA Publications
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Publications
Disrupted spatial memory is a consequence of picornavirus infectionEric J Buenz
Molecular Neuroscience Program, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
Neurobiol Dis 24:266-73. 2006..An important implication of such subclinical virus-induced neurologic deficit is that the injury may accumulate over the lifetime of the individual, eventually leading to the manifestation of clinical cognitive or memory deficits...
Induction of a gene expression program in dendritic cells with a cross-linking IgM antibody to the co-stimulatory molecule B7-DCFrank A Blocki
Department of Immunology, Mayo Clinic, College of Medicine, 200 First St. S.W, Rochester, MN 55905, USA
FASEB J 20:2408-10. 2006....
NGF signaling from clathrin-coated vesicles: evidence that signaling endosomes serve as a platform for the Ras-MAPK pathwayC L Howe
Department of Neurology, Stanford University Medical Center, 1201 Welch Road, MSLS P211, Stanford, CA 94305, USA
Neuron 32:801-14. 2001..Our results point to the existence of a population of signaling endosomes derived from clathrin-coated membranes in NGF-treated cells...
Activated microglia stimulate transcriptional changes in primary oligodendrocytes via IL-1betaCharles L Howe
Department of Neuroscience, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
Neurobiol Dis 23:731-9. 2006..We hypothesize that Fcmu-stimulated IL-1beta-induced upregulation of immediate early and late response genes in oligodendrocytes may promote CNS repair...
Antiapoptotic signaling by a remyelination-promoting human antimyelin antibodyCharles L Howe
Department of Neurology, Mayo Clinic and Foundation, Rochester, MN 55905, USA
Neurobiol Dis 15:120-31. 2004....
Signaling endosome hypothesis: A cellular mechanism for long distance communicationCharles L Howe
Mechanisms of Neural Repair Lab, Department of Neurology, Mayo Medical and Graduate Schools, Guggenheim 442C, 200 First Street SW, Rochester, Minnesota 55905, USA
J Neurobiol 58:207-16. 2004..Finally, a saltatory, regenerating inositol 1,4,5-trisphosphate wave model is offered to reconcile current discrepancies in the literature regarding endosomal-based retrograde signaling...
Absence of perforin expression confers axonal protection despite demyelinationCharles L Howe
Department of Neuroscience, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905, USA
Neurobiol Dis 25:354-9. 2007..We conclude that perforin-dependent effector cells such as cytotoxic T cells, gammadelta T cells, and natural killer cells may play a role in axon damage that is dependent upon but separable from demyelination...
Coated glass and vicryl microfibers as artificial axonsCharles L Howe
Department of Neuroscience and Neurology, Mayo Clinic College of Medicine, Rochester, Minn, USA
Cells Tissues Organs 183:180-94. 2006....
Depolarization of PC12 cells induces neurite outgrowth and enhances nerve growth factor-induced neurite outgrowth in ratsCharles L Howe
Department of Neurology, Mayo Medical and Graduate Schools, Guggenheim 442C, 200 First Street SW, Rochester, MN 55905, USA
Neurosci Lett 351:41-5. 2003..We conclude that normal synaptic function may depend upon the integration of synaptic activity and activity-dependent neurotrophin release and signaling, and that these findings have potential relevance to neural repair...
CD8+ T cells directed against a viral peptide contribute to loss of motor function by disrupting axonal transport in a viral model of fulminant demyelinationCharles L Howe
Department of Neuroscience, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
J Neuroimmunol 188:13-21. 2007..We conclude that cytotoxic T cells may be responsible for the initiation of axon injury following demyelination...
Immunological aspects of axon injury in multiple sclerosisC L Howe
Department of Neuroscience, Translational Immunovirology and Biodefense Program, Molecular Neuroscience Program, Mayo Clinic College of Medicine, Guggenheim 442 C, 200 First Street SW, Rochester, MN 55905, USA
Curr Top Microbiol Immunol 318:93-131. 2008..Finally, a unifying hypothesis that links neuronal stress associated with demyelination-induced axonal dysfunction to immune recognition and immunopathology is provided in an effort to shape future experimentation...
Modeling the signaling endosome hypothesis: why a drive to the nucleus is better than a (random) walkCharles L Howe
Departments of Neuroscience and Neurology, Mayo Clinic College of Medicine, Guggenheim 442 C, Rochester, MN 55905, USA
Theor Biol Med Model 2:43. 2005..We explore the relative efficiencies of signal diffusion versus retrograde transport of signaling endosomes...
CD8+ T cells cause disability and axon loss in a mouse model of multiple sclerosisChandra Deb
Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota, United States of America
PLoS ONE 5:e12478. 2010..We have previously observed that genetic deletion of the CD8+ T cell effector molecule perforin leads to preservation of motor function and preservation of spinal axons in chronically demyelinated mice...
Trafficking the NGF signal: implications for normal and degenerating neuronsJean-Dominique Delcroix
Department of Neurology and Neurological Sciences and of Pediatrics, Program in Neuroscience, Stanford University, Stanford, CA 94305, USA
Prog Brain Res 146:3-23. 2004..It is important to define further the significance of signaling endosomes in the biology of both normal and degenerating neurons...
Functional characterization of mouse spinal cord infiltrating CD8+ lymphocytesChandra Deb
Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
J Neuroimmunol 214:33-42. 2009..We conclude that target-derived lymphocytes in a mouse model of chronic spinal cord demyelination may have unique functional specificities...
Interleukin-6 protects anterior horn neurons from lethal virus-induced injuryKevin D Pavelko
Department of Immunology, Mayo Clinic, Rochester, Minnesota 55905, USA
J Neurosci 23:481-92. 2003..These data support the hypothesis that IL-6 plays a critical role in protecting specific populations of neurons from irreversible injury...
Human monoclonal IgM antibody promotes CNS myelin repair independent of Fc functionBogoljub Ciric
Department of Immunology, Mayo Medical and Graduate Schools, Mayo Clinic Rochester, Minn 55905, USA
Brain Pathol 13:608-16. 2003....
TREM-2 mediated signaling induces antigen uptake and retention in mature myeloid dendritic cellsSuresh Radhakrishnan
Department of Immunology, College of Medicine, Mayo Clinic, Rochester, MN 55905, USA
J Immunol 181:7863-72. 2008..The parallel signaling events observed in both human and mouse mDC support the hypothesis that B7-DC cross-linking may be useful as a therapeutic immune modulator in human patients...
Gamma interferon is critical for neuronal viral clearance and protection in a susceptible mouse strain following early intracranial Theiler's murine encephalomyelitis virus infectionMoses Rodriguez
Department of Immunology, Mayo Clinic, Rochester, Minnesota 55905, USA
J Virol 77:12252-65. 2003..These data support the hypothesis that IFN-gamma plays a critical role in protecting spinal cord neurons from persistent infection and death...
Human HLA-DR transgenes protect mice from fatal virus-induced encephalomyelitis and chronic demyelinationMoses Rodriguez
Department of Neurology, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA
J Virol 82:3369-80. 2008..The mechanism of protection appears to be the result of cytokines released by CD4(+) T cells...
NKG2D contributes to efficient clearance of picornavirus from the acutely infected murine brainChandra Deb
Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
J Neurovirol 14:261-6. 2008....
TRAIL mediates liver injury by the innate immune system in the bile duct-ligated mouseAlisan Kahraman
Miles and Shirley Fitterman Center for Digestive Diseases, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, USA
Hepatology 47:1317-30. 2008..Conclusion: These observations support a pivotal role for TRAIL in cholestatic liver injury mediated by NK 1.1-positive NK/NKT cells...
Aquaporin-4-binding autoantibodies in patients with neuromyelitis optica impair glutamate transport by down-regulating EAAT2Shannon R Hinson
Department of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
J Exp Med 205:2473-81. 2008..Thus, binding of NMO-IgG to astrocytic AQP4 initiates several potentially neuropathogenic mechanisms: complement activation, AQP4 and EAAT2 down-regulation, and disruption of glutamate homeostasis...
Apoptosis of hippocampal pyramidal neurons is virus independent in a mouse model of acute neurovirulent picornavirus infectionEric J Buenz
Department of Neurology, Mayo Clinic College of Medicine, Guggenheim 442 D, 200 First St SW, Rochester, MN 55905, USA
Am J Pathol 175:668-84. 2009..These observations suggest that therapeutic strategies other than antiviral interventions may be useful for neuroprotection during acute CNS picornavirus infection...
Long-distance retrograde neurotrophic signalingCharles L Howe
Departments of Neuroscience and Neurology, Mayo Clinic College of Medicine, Guggenheim 442 C, 200 First Street SW, Rochester, MN 55905, USA
Curr Opin Neurobiol 15:40-8. 2005....
Preparation of biologically active subcellular fractions using the Balch homogenizerChristopher L German
Program in Molecular Neuroscience, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905, USA
Anal Biochem 394:117-24. 2009..Importantly, these fractions maintain their biologic activity following isolation and may be used for both localization and biochemical analyses...
Beta-methylamino-alanine (BMAA) injures hippocampal neurons in vivoEric J Buenz
BioSciential, LLC, Rochester, MN, USA
Neurotoxicology 28:702-4. 2007..We provide evidence that introduction of BMAA into the CNS of mice leads to sporadic death of hippocampal neurons, supporting a direct causal link between BMAA and neuronal injury...
A high-throughput 3-parameter flow cytometry-based cell death assayEric J Buenz
Complementary and Integrative Medicine Program, Mayo Clinic College of Medicine, Rochester, Minnesota, USA
Cytometry A 71:170-3. 2007..This system is particularly well-suited for toxicologic evaluation of novel compounds and profiling of new apoptosis-inducing agents...
Growth factor treatment of demyelinating disease: at last, a leap into the lightRichard M Ransohoff
Depts of Neurosciences and Nerology, The Cleveland Clinic Foundation, 9500 Euclid Avenue, OH 44195, USA
Trends Immunol 23:512-6. 2002....
Differences in the surface binding and endocytosis of neurotrophins by p75NTRSmita Saxena
Division of Neuropathology, Institute of Pathology, University of Bern, CH-3010 Bern, Switzerland
Mol Cell Neurosci 26:292-307. 2004..Our results suggest that p75NTR may have multiple roles in different subcellular locations, functioning both at the cell surface and also within endocytic compartments...
Differential endocytic sorting of p75NTR and TrkA in response to NGF: a role for late endosomes in TrkA traffickingSmita Saxena
Division of Neuropathology, Institute of Pathology, University of Bern, CH 3010 Bern, Switzerland
Mol Cell Neurosci 28:571-87. 2005..Disrupting p75NTR recycling diminished TrkA activation in response to low concentrations of NGF, demonstrating a functional role for the recycling of p75NTR...
Research Grants
- Mechanisms of neuronal injury during virus infection of the CNSCharles Howe; Fiscal Year: 2009..Importantly, we have found that treatment with an FDA-approved drug protects neurons and cognitive function without altering the ability of the immune system to clear the virus from the brain. ..
- Mechanisms of neuronal injury during virus infection of the CNSCHARLES LEE HOWE; Fiscal Year: 2010..Importantly, we have found that treatment with an FDA-approved drug protects neurons and cognitive function without altering the ability of the immune system to clear the virus from the brain. ..
- Mechanisms of neuronal injury during virus infection of the CNSCHARLES LEE HOWE; Fiscal Year: 2010..abstract_text> ..
