Assistant Professor, Department of Anatomy & Cell Biology, College of Medicine
Office: 6051 COMRB
Phone: (312) 996-6869
Web Site: Gerardo Morfini Departmental Page
The exquisitely organized distribution of cellular components within discrete subcellular compartments underlies the unique ability of neurons to receive, process, and transmit information. Precise targeting and delivery of these components in mature neurons largely depends upon axonal transport (AT), a cellular process largely mediated by the molecular motor proteins conventional kinesin and cytoplasmic dynein (CDyn). An illumination of molecular mechanisms regulating AT is critical for a comprehensive understanding of neuronal function. Within this context, the goals of our research program are: 1) To elucidate regulatory mechanisms of AT ; and: 2) To determine how alterations in these mechanisms contribute to the pathogenesis of human neurodegenerative conditions.
Morfini, G., et al. Inhibition Of Fast Axonal Transport By Pathogenic SOD1 Involves Activation of P38 MAP Kinase. PLOS One, 8 (2013) e65235.
Morfini, G., et al. (2009) Axonal transport defects in neurodegenerative diseases. J. Neurosci. 29, (2009) 12776-12786.
Morfini, G., et al. Pathogenic huntingtin inhibits fast axonal transport by activating JNK3 and phosphorylating kinesin. Nat. Neurosci., 12 (2009) 864-871.
Morfini, G., et al. 1-Methyl-4-phenylpyridinium affects fast axonal transport by activation of caspase and protein kinase C. PNAS, 104 (2007) 2442-2447.
Morfini, G., et al. JNK mediates pathogenic effects of polyglutamine-expanded androgen receptor on fast axonal transport. Nat. Neurosci., 9 (2006) 907-916.