GERARDO ANDRES MORFINI

Summary

Affiliation: University of Illinois at Chicago
Country: USA

Publications

  1. pmc ALS-linked FUS exerts a gain of toxic function involving aberrant p38 MAPK activation.
    Reddy Ranjith K Sama
    Sci Rep 7:115. 2017
  2. doi request reprint Conventional kinesin: Biochemical heterogeneity and functional implications in health and disease
    Gerardo Morfini
    Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, USA Electronic address
    Brain Res Bull 126:347-353. 2016
  3. pmc Inhibition of fast axonal transport by pathogenic SOD1 involves activation of p38 MAP kinase
    Gerardo A Morfini
    Depart of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, Illinois, United States of America
    PLoS ONE 8:e65235. 2013
  4. pmc 1-Methyl-4-phenylpyridinium affects fast axonal transport by activation of caspase and protein kinase C
    G Morfini
    Department of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612, USA
    Proc Natl Acad Sci U S A 104:2442-7. 2007
  5. pmc Pathogenic huntingtin inhibits fast axonal transport by activating JNK3 and phosphorylating kinesin
    Gerardo A Morfini
    Department of Anatomy and Cell Biology, University of Illinois at Chicago, USA
    Nat Neurosci 12:864-71. 2009
  6. pmc Axonal transport defects in neurodegenerative diseases
    Gerardo A Morfini
    Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, Illinois 60612, USA
    J Neurosci 29:12776-86. 2009
  7. pmc Disruption of fast axonal transport is a pathogenic mechanism for intraneuronal amyloid beta
    G Pigino
    Department of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612, USA
    Proc Natl Acad Sci U S A 106:5907-12. 2009
  8. ncbi request reprint Regulation of kinesin: implications for neuronal development
    G Morfini
    Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9039, USA
    Dev Neurosci 23:364-76. 2001

Collaborators

Detail Information

Publications8

  1. pmc ALS-linked FUS exerts a gain of toxic function involving aberrant p38 MAPK activation.
    Reddy Ranjith K Sama
    Sci Rep 7:115. 2017
    ..Accordingly, increased levels of active p38 MAPK were detected in post-mortem human ALS-FUS brain tissues. These data provide evidence for a novel gain-of-toxic function for ALS-linked FUS involving p38 MAPK activation...
  2. doi request reprint Conventional kinesin: Biochemical heterogeneity and functional implications in health and disease
    Gerardo Morfini
    Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, USA Electronic address
    Brain Res Bull 126:347-353. 2016
    ....
  3. pmc Inhibition of fast axonal transport by pathogenic SOD1 involves activation of p38 MAP kinase
    Gerardo A Morfini
    Depart of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, Illinois, United States of America
    PLoS ONE 8:e65235. 2013
    ..Axon-autonomous activation of the p38 pathway represents a novel gain of toxic function for FALS-linked SOD1 proteins consistent with the dying-back pattern of neurodegeneration characteristic of ALS...
  4. pmc 1-Methyl-4-phenylpyridinium affects fast axonal transport by activation of caspase and protein kinase C
    G Morfini
    Department of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612, USA
    Proc Natl Acad Sci U S A 104:2442-7. 2007
    ....
  5. pmc Pathogenic huntingtin inhibits fast axonal transport by activating JNK3 and phosphorylating kinesin
    Gerardo A Morfini
    Department of Anatomy and Cell Biology, University of Illinois at Chicago, USA
    Nat Neurosci 12:864-71. 2009
    ..These data identify JNK3 as a critical mediator of polyQ-Htt toxicity and provide a molecular basis for polyQ-Htt-induced inhibition of FAT...
  6. pmc Axonal transport defects in neurodegenerative diseases
    Gerardo A Morfini
    Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, Illinois 60612, USA
    J Neurosci 29:12776-86. 2009
    ..Illumination of such mechanisms provides a framework for the development of novel therapeutic strategies aimed to prevent axonal and synaptic dysfunction in several major AONDs...
  7. pmc Disruption of fast axonal transport is a pathogenic mechanism for intraneuronal amyloid beta
    G Pigino
    Department of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612, USA
    Proc Natl Acad Sci U S A 106:5907-12. 2009
    ..Therefore pharmacological modulation of CK2 activity may represent a promising target for therapeutic intervention in AD...
  8. ncbi request reprint Regulation of kinesin: implications for neuronal development
    G Morfini
    Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9039, USA
    Dev Neurosci 23:364-76. 2001
    ..Since kinesin is a phosphoprotein in vivo, we evaluated the correlation between kinesin phosphorylation and its membrane association and identified a number of kinases which phosphorylate kinesin and alter its function...