Robert Nickells, PhD
Professor
1300 University Ave
Madison, WI 53706-1510
| Appointments: | Physiology, UW Comprehensive Cancer Center, Institute on Aging. Eye Research Institute, Department of Ophthalmology Vice Chair of Research. |
| Degrees: | B.S. 1983, University of Victoria
|
| Fellowships: | Postdoctoral Fellowship, 1987-90, California Institute of Technology |
| Research: | Glaucoma is one of the leading causes of blindness world-wide. Although an increase in intraocular pressure is often associated with this disease, it is marked by the progressive death of retinal ganglion cells. Previous studies by my laboratory and others have shown that ganglion cell death occurs by a mechanism that is characteristic of apoptosis - a form of programmed cell death that is regulated by a successive activation of genes from within the dying cell. Hypothetically, neuronal cell death can be blocked or prevented by agents that interrupt key biochemical pathways that are controlled by these genes. This form of treatment, termed "neuroprotection" may provide important avenues of therapy for many neurodegenerative disorders which includes glaucoma. My laboratory studies some of the earliest events that occur in retinal ganglion cells during the cell death process. For these studies we make use of mice lacking genes critical for the cell death process. Our current focus is on epigenetic changes that lead to silencing of normal gene expression well in advance of the committed step in the apoptotic pathway. |
| Recent Publications: |
Silencing of Fem1cR3 gene expression in the DBA/2J mouse precedes retinal ganglion cell death and is associated with Histone Deacetylase activity.
Accelerated retinal ganglion cell death in mice deficient in the Sigma-1 receptor.
The apoptotic response in HCT116BAX-/- cancer cells becomes rapidly saturated with increasing expression of a GFP-BAX fusion protein.
Histone H4 deacetylation plays a critical role in early gene silencing during neuronal apoptosis.
A single nucleotide polymorphism in the Bax gene promoter affects transcription and influences retinal ganglion cell death. |