Profiles
Earl W. Godfrey, PhD
1984-1999, Assistant and Associate Professor, Cellular Biology and Anatomy, Medical College of Wisconsin
1999-2004, Associate Professor, Pathology and Anatomy, EVMS
2004-2016, Professor, Pathology and Anatomy, EVMS
2007-2016, Director, Biomedical Sciences Graduate Programs, EVMS
Faculty Appointments
Associate to Full Professor, Department of Pathology and Anatomy, EVMS, 1999-2016
Program Director, Biomedical Sciences, EVMS, 2007-2016
Assistant to Associate Professor, Department of Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, 1984-1999
Assistant Professor, Cellular Biology and Anatomy, Texas Tech University Health Sciences Center, 1983-1984
Courses Taught
Reproductive Clinical Sciences, Ph.D., Program: Developmental Biology
Office Hours
By appointment
Undergraduate Degree
B.S., Biochemistry, University of Wisconsin - Madison
Graduate Education
Ph.D., Biology, Johns Hopkins University
Postdoctoral Education
Neurobiology, Stanford University
Lab Location
Lewis Hall, Room 3033
Current Projects
The goal of Dr. Godfrey’s current research is to test a new therapy using cells from patients with amyotrophic lateral sclerosis (ALS, Lou Gehrig’s disease) and frontotemporal dementia (FTD), the second most common cause of dementia. The therapy involves a DNA- and RNA-binding protein, Pur-alpha, discovered by his collaborator at EVMS, Dr. Edward Johnson. The protein binds to an expanded RNA repeat sequence found in cells of patients with the most common genetic form of both ALS and FTD, the C9ORF72 expanded hexanucleotide repeat (GGGGCC). In a fly model of this mutation, overexpression of Pur-alpha has been shown to reduce neurodegeneration. Pur-alpha and Pur peptides developed by Dr. Johnson and Dr. Dianne Daniel bind tightly to the C9ORF72 repeat and partially reverse cellular pathology in cells from C9ORF72 ALS patients. We plan to test Pur peptides in patient cells and neurons expressing the C9ORF72 hexanucleotide repeat expansion. After optimizing the treatment of cells, we plan to test the peptides in mice, with a view toward possible therapy in patients.
Presentations and Scholarships
Selected Publications
Daigle, J.G., Krishnamurthy, K., Ramesh, N., Casci, I., Monaghan, J., McAvoy, K., Godfrey, E.W., Daniel, D.C., Johnson, E.M., Monahan, Z., Shewmaker, F., Passinelli, P., and Pandey, U.B. Pur-alpha regulates cytoplasmic stress granule dynamics and ameliorates FUS toxicity. Acta Neuropathol. 131: 605-20, 2016.
Godfrey, E.W., and Schwarte, R.C. Nitric oxide and cyclic GMP regulate early events in agrin signaling in skeletal muscle cells. Experimental Cell Research 316: 1935-1945, 2010.
Godfrey, E.W., Longacher, M.W., Neiswender, H., Schwarte, R.C., and Browning, D.D. Guanylate cyclase and cyclic GMP-dependent protein kinase regulate agrin signaling at the developing neuromuscular junction. Developmental Biology, 307: 195-201, 2007.
Godfrey, E.W. and Schwarte, R.C. The role of nitric oxide signaling in the formation of the neuromuscular junction. J. Neurocytol. 32: 591-602, 2003.
Schwarte, R.C., and Godfrey, E.W. Nitric oxide synthase activity is required for postsynaptic differentiation of the embryonic neuromuscular junction. Devel. Biol. 273: 276-284, 2004.
Faculty Appointments
Associate to Full Professor, Department of Pathology and Anatomy, EVMS, 1999-2016
Program Director, Biomedical Sciences, EVMS, 2007-2016
Assistant to Associate Professor, Department of Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, 1984-1999
Assistant Professor, Cellular Biology and Anatomy, Texas Tech University Health Sciences Center, 1983-1984
Courses Taught
Reproductive Clinical Sciences, Ph.D., Program: Developmental Biology
Office Hours
By appointment
Undergraduate Degree
B.S., Biochemistry, University of Wisconsin - Madison
Graduate Education
Ph.D., Biology, Johns Hopkins University
Postdoctoral Education
Neurobiology, Stanford University
Lab Location
Lewis Hall, Room 3033
Current Projects
The goal of Dr. Godfrey’s current research is to test a new therapy using cells from patients with amyotrophic lateral sclerosis (ALS, Lou Gehrig’s disease) and frontotemporal dementia (FTD), the second most common cause of dementia. The therapy involves a DNA- and RNA-binding protein, Pur-alpha, discovered by his collaborator at EVMS, Dr. Edward Johnson. The protein binds to an expanded RNA repeat sequence found in cells of patients with the most common genetic form of both ALS and FTD, the C9ORF72 expanded hexanucleotide repeat (GGGGCC). In a fly model of this mutation, overexpression of Pur-alpha has been shown to reduce neurodegeneration. Pur-alpha and Pur peptides developed by Dr. Johnson and Dr. Dianne Daniel bind tightly to the C9ORF72 repeat and partially reverse cellular pathology in cells from C9ORF72 ALS patients. We plan to test Pur peptides in patient cells and neurons expressing the C9ORF72 hexanucleotide repeat expansion. After optimizing the treatment of cells, we plan to test the peptides in mice, with a view toward possible therapy in patients.
Presentations and Scholarships
Selected Publications
Daigle, J.G., Krishnamurthy, K., Ramesh, N., Casci, I., Monaghan, J., McAvoy, K., Godfrey, E.W., Daniel, D.C., Johnson, E.M., Monahan, Z., Shewmaker, F., Passinelli, P., and Pandey, U.B. Pur-alpha regulates cytoplasmic stress granule dynamics and ameliorates FUS toxicity. Acta Neuropathol. 131: 605-20, 2016.
Godfrey, E.W., and Schwarte, R.C. Nitric oxide and cyclic GMP regulate early events in agrin signaling in skeletal muscle cells. Experimental Cell Research 316: 1935-1945, 2010.
Godfrey, E.W., Longacher, M.W., Neiswender, H., Schwarte, R.C., and Browning, D.D. Guanylate cyclase and cyclic GMP-dependent protein kinase regulate agrin signaling at the developing neuromuscular junction. Developmental Biology, 307: 195-201, 2007.
Godfrey, E.W. and Schwarte, R.C. The role of nitric oxide signaling in the formation of the neuromuscular junction. J. Neurocytol. 32: 591-602, 2003.
Schwarte, R.C., and Godfrey, E.W. Nitric oxide synthase activity is required for postsynaptic differentiation of the embryonic neuromuscular junction. Devel. Biol. 273: 276-284, 2004.