Gerardo A Morfini

    Email Address: gmorfini@uic.edu
    College: Medicine Department: Anatomy and Cell Biology
    Title: Associate Profesor
    Office: COMRB 7053 Phone: 312-996-6869
    Participating in the Chancellor’s Undergraduate Research Awards program: Yes

    Research Interest:
    The unique ability of neurons to receive, process, and transmit information depends upon the organized distribution of cellular organelles at discrete subcellular compartments (i.e., axons and dendrites). Such distribution in turn depends upon intracellular trafficking events collectively referred to as axonal transport (AT), which are carried by molecular motor proteins. An illumination of molecular mechanisms regulating axonal transport is critical for a comprehensive understanding of neuronal function.

    Within this context above, our studies over the last years identified specific signaling pathways that regulate AT through phosphorylation of motor proteins. Significantly, genetic evidence revealed that alterations in AT may play a critical role in various human neurodegenerative diseases including Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and Amyotrophic Lateral Sclerosis. Based on these observations, our current research aims to evaluate the contribution of specific protein kinases to the progressive loss of neuronal connectivity that characterizes these diseases. Knowledge derived from this work will provide a conceptual framework for the development of novel therapeutic strategies for neurodegenerative diseases based on preservation of neuronal connectivity.

    Selected publications

    1. Gatto et al (2015). Analysis of YFP(J16)-R6/2 reporter mice and postmortem brains reveals early pathology and increased vulnerability of callosal axons in Huntington's disease. Hum Mol Genet. 24(18):5285-98.

    2. Morfini et al (2013). Inhibition Of Fast Axonal Transport By Pathogenic SOD1 Involves Activation of P38 MAP Kinase. PLOS One 8(6):e65235.

    3. Kanaan et al (2011) Pathogenic Forms of Tau Inhibit Kinesin-Dependent Axonal Transport Through a Mechanism Involving Activation of Axonal Phosphotransferases. J. Neurosci. 31(27):9858-68.

    4. Bosco et al (2010) Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS. Nat. Neurosci. 13(11):1396-403.

    5. Pigino, et al. (2009) Disruption of fast axonal transport is a pathogenic mechanism for intraneuronal amyloid beta. Proc. Natl. Acad. Sci. USA 106, 5907-5912.

    6. Morfini et al (2009) Axonal transport defects in neurodegenerative diseases. J. Neurosci. 29, 12776-12786.

    7. Morfini et al (2009) Pathogenic huntingtin inhibits fast axonal transport by activating JNK3 and phosphorylating kinesin. Nat. Neurosci. 12, 864-871.

    Minimum time commitment in hours per week: 15

    Qualifications of a Student:
    Priority is given primarily to Biology/Chemistry majors with top GPAs (>3.5), which have taken a course in at least one and preferably two of the following areas: neuroscience, cell biology, biochemistry or molecular biology.
    Sophomores pursuing Medical/Graduate school are encouraged to apply. Prior research experience is an advantage but not necessary. Applicant should have excellent communication and team-work skills, be mature, organized and reliable.

    Brief Summary of what is expected from the student:
    The student should be willing to make a sustained commitment with a regular schedule during the school year. Summer research options are only available to students that have been involved during the academic year. Students interested in a multiyear experience are preferred .Lab time is expected to be devoted to lab activities only. Students should expect to start a training period where they will be under the supervision of a senior lab member to learn general lab duties and techniques. After this period and with evidence of gained precision, commitment and trouble-shooting skills, students are expected to become fully embedded in a particular project under the direction of a project leader.

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