We are also working to increase the utility of the GFAP expression system by developing cassettes that direct expression to particular subregions of the brain, are more compact, have higher expression levels, can be regulated, and permit astrocyte-specific gene knockouts. In continuing studies of the GFAP protein we are extending our sequencing of the GFAP gene of Alexander disease patients to discover new mutations which might contribute to an understanding of how protein aggregate diseases develop. We also plan to investigate why mice lacking GFAP are hypersensitive to cervical cord injury. References Cited 1. Multiple interacting sites regulate astrocyte-specific transcription of the human gene for glial fibrillary acidic protein.
GFAP promoter directs astrocyte-specific expression in transgenic mice.
Conditional ablation of cerebellar astrocytes in postnatal transgenic mice. Galbreath, E., Kim, S-J., Park, K., Brenner, M., and Messing. Astrocyte-specific expression of tyrosine hydroxylase after intracerebral gene transfer induces behavioral recovery in experimental Parkinsonism. Trejo, F., Vergara, P., Brenner, M. and Segovia, J. Gene therapy in a rodent model of Parkinson's disease using differentiated C6 cells expressing a GFAP-tyrosine hydroxylase transgene. Mice lacking GFAP are hypersensitive to traumatic cerebrospinal injury.