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On January 10, 2010, the community of leukocyte biologists suffered a great loss with the passing of a colleague and friend, Gary Michael Bokoch, who died unexpectedly at the age of 55. Gary's contributions to scientific research in general, and to the field of leukocyte biology specifically, were substantial and often represented major breakthroughs that advanced the field and pushed it in new directions. In addition, Gary was a dedicated mentor, and his guidance fostered the development of a number of junior investigators who have gone on to make important contributions in the field of leukocyte biology. He will be missed by us all.

Gary was born on April 15, 1954, and grew up in Erie, PA, USA. Even in high school, Gary had a passion for science, and he pursued this interest as an undergraduate at The Pennsylvania State University, where he earned a B.S. degree in biology and graduated with highest honors in 1976. That same year, Gary entered the graduate program at Vanderbilt University, where he pursued a Ph.D. in pharmacology. While at Vanderbilt, he was awarded a prestigious National Science Foundation Predoctoral Fellowship. During graduate school, Gary worked in the laboratory of Dr. Peter Reed, where he investigated arachidonic acid metabolism in neutrophils activated by chemotactic peptides. He was a very productive graduate student at Vanderbilt and published four first-author papers, and three of these were in the Journal of Biological Chemistry. Following graduate school, Gary moved to the University of Texas Health Science Center, were he was awarded a National Institutes of Health Postdoctoral Fellowship to work in the laboratory of Dr. Alfred Gilman, one of the world's foremost pharmacologists. During his time in Dr. Gilman's laboratory, Gary purified and characterized the biochemical properties of the inhibitory guanine nucleotide-binding regulatory component of adenylate cyclase, which is now known as Gi. This work represented a major advance in the field, leading to a better understanding of the mechanism of action of Gi, and resulted in the publication of four back-to-back papers in the Journal of Biological Chemistry. Subsequently, Gary published a paper in Cell, demonstrating that pertussis toxin inhibited N-formyl peptide receptor-mediated release of arachidonic acid and granular enzymes by neutrophils and that this inhibition was secondary to ribosylation of Gi. This study was among the first to demonstrate that G proteins can participate in receptor-mediated signal transduction by mechanisms that do not involve cAMP. Overall, Gary published six papers from his postdoctoral work, all in top-tier journals. This work also provided a strong background for Gary's future work on the role of GTP-binding proteins in leukocyte signal transduction and activation.

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