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brennerProfessor Emeritus
Research Areas: 
Transcriptional regulation of GFAP, development of GFAP promoters for transgene expression in astrocytes, and GFAP mutations as a cause of Alexander disease 



Dr. Brenner ceased laboratory research in 2015 when he transitioned to Emeritus status. However, he remains engaged with teaching, committee work and writing.

Michael Brenner received his Ph.D. in Biochemistry from the University of California, Berkeley. He served on the faculty of Harvard College and Temple University Medical School, and was a Research Scientist at the National Institutes of Health before joining UAB in 1998. He is presently Professor Emeritus of Neurobiology.

His prior research investigated both the transcriptional regulation of the gene encoding glial fibrillary acidic protein (GFAP), an intermediate filament protein used as a marker for astrocytes, and the biological role of this protein. Initial findings from the transcriptional studies included identification of the GFAP mRNA and protein start sites and analysis of the GFAP basal promoter. Subsequent investigations used site-directed mutation and deletions in GFAP promoter driven mouse transgenes to identify multiple interacting upstream sites affecting transcription, revealing a surprisingly complex regulatory system for this gene. Several of the promoter constructs developed are extensively used by other laboratories for directing gene expression to astrocytes. These include gfa2, which extends 2.2kb upstream of the mRNA start site, and the smaller 681 bp gfaABC1D promoter, which also expresses in astrocytes throughout the CNS, and is useful for viral delivery systems with limited DNA capacity. Another promoter of interest is gfaABD, whose expression is largely limited to the cortex and hippocampus and has compromised astrocyte specificity, thus revealing an unexpected regional heterogeneity among astrocytes and suggesting that astrocytes in different areas of the brain use different regulatory regions of the GFAP gene. GFAP promoters developed in the Brenner laboratory have been used by more than 500 laboratories in 32 countries. Several are presently available through AddGene.

Investigation of the biological role of GFAP revealed that its absence in mice renders them hypersensitive to traumatic spinal cord injury, indicating a novel role for GFAP in structural support. The laboratory also discovered that mutations within the coding sequence of the GFAP gene are responsible for nearly all cases of Alexander disease, a rare but often fatal neurodegenerative disorder of humans. This was the first identification of a genetic disorder attributable to a primary defect in astrocytes. This discovery made possible a simple diagnostic genetic test for the disease, and provided a therapeutic target that may lead to effective treatment. Dr. Brenner has written 103 peer reviewed publications, 16 book chapters, and holds a US patent. His work has over 7,000 citations, and an H-factor of 47.


Graduate School
Ph.D., Biochemistry, University of California, Berkeley



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