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Mon, 23 Jan 2017
Seminar (2) : From Salvarsan to Penicillin: Was Fleming a genius, a lucky guy, or neither?

Time: 11.30 AM - 12.15 PM

Venue: Cysteine, Level 7 (30 Biopolis Street, Matrix)

Speaker: Prof. David Engelberg, Associate Professor, Department of Biological Chemistry, The Hebrew University of Jerusalem / Adjunct Professor, Department of Microbiology, The National University of Singapore (NUS).


Many important scientific discoveries are attributed to an unusual and fortuitous serendipity. Careful analysis of such cases, however, reveals luck to be just one parameter, not necessarily the most important one, in the route leading to the breakthrough. In the case of Sir Alexander Fleming and the discovery of penicillin, the story of the petri dish left on the bench when he was on vacation, is well known and serves as a legendary example of one such fortunate coincidence. In this lecture I will try to show that chance in fact played a very minor role in the discovery of what is perhaps the most important drug known to date. I will show how the personal and professional life of Fleming in fact prepared him to be the discoverer of penicillin. I will raise the following questions: Did Fleming understand at all the implications of what he had discovered? Did the scientific community draw lessons from Fleming's discovery to identify more antibiotics and other drugs?

About The Speaker
The molecular basis of inflammatory diseases is complex and far from being understood. Unlike the case of cancer, in which genes and mutations that cause the disease were identified, the trigger and the etiology of chronic inflammation is unknown. However, several biochemical pathways are abnormally overactive in most inflammatory diseases and serve as prime suspects for causing the disease. Such critical pathways are those of the p38 stress/MAP kinase and the ERK MAP kinase. Yet, although considered a target for therapy and is strongly associated with inflammation, the exact role of p38 and ERK in inflammation is not known. It is not even known if their activation would be sufficient to impose inflammation in cells, animals or humans. Such experiments cannot be performed because it is not known how to activate p38 individually in cells or animals. My group is focusing on engineering p38 and other MAP kinases to render them intrinsically active. Using specifically designed Molecular Evolution approaches we were able to isolate intrinsically active variants of p38 and ERK. When these engineered molecules are expressed in biological systems, they are spontaneously active, namely, without the need to expose the system to any stimulation. Thus, only the transgenic molecule is active disclosing most accurately the very specific functions of p38. Using transgenic cells and mice expressing these molecules we shall now be able to answer the question of the linkage between p38, ERK and inflammatory diseases.

Dr. Frank Eisenhaber, Executive Director

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