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Faculty Detail    
Name GERALD M FULLER
 
Campus Address VH 220 Zip 0019
Phone 205-934-7596
E-mail gmfuller@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor Emeritus

Biographical Sketch 
Dr. Gerald Fuller, Professor of Cell Biology, received his Ph.D. degree in biology from the University of California at San Diego in 1968 and then carried out postdoctoral studies at the Massachusetts Institute of Technology. In 1970, he was appointed to the faculty of Medicine in the Department of Human Genetics at the University of Texas medical School at Galveston, where he remained from 1970 to 1985 and attained the rank of Professor. Dr. Fuller joined the UAB faculty in 1985 as a Professor of Cell Biology.

Research/Clinical Interest
Title
Description
The central focus of my laboratory is to understand the molecular details of how plasma protein genes in the liver are regulated. Our model protein, fibrinogen, is the product of three separate genes. Extensive information shows that increased fibrinogen levels may be involved in coronary artery disease, stroke and renal failure; however, many details of how its synthesis is controlled are unknown. We do know that its transcription, translation and assembly is stringently coordinated. Fibrinogen is up-regulated by the cytokine interleukin-6 (IL-6) and glucocorticoids as well as other members of this cytokine family but the specifics of these events have yet to be elucidated. Using primary hepatocytes, we are studying the promoter regions of each gene to identify the IL-6 responsive elements and to isolate, clone and sequence the IL-6 transcription factors. We have cloned the IL-6 signal transducing protein in the liver cell and are studying the intracellular signaling pathway(s) stimulated by IL-6 that leads to upregulating fibrinogen gene transcription. We recently identified a feedback pathway involving fibrin fragments that stimulates both IL-6 expression in leukocytes and fibrinogen biosynthesis directly in hepatocytes. These hepatocyte receptors of the fragments have been identified but not studied. Understanding how this critical molecule is regulated will provide much needed information that will be useful in several human diseases.