Emanuel Hanski 20th Lancefield International Symposium on Streptococci and Streptococcal Diseases 2017

Emanuel Hanski

Emanuel Hanski, received his Ph.D. in Biological Chemistry from the Hebrew University of Jerusalem. He conducted his post-doctoral training in Prof. Alfred G. Gilman’s lab at Texas Southwestern Medical Center in Dallas, investigating signal transduction through beta adrenergic receptors with the emphasis on the role of GTP-binding proteins in the process. He then joined the Weizmann Institute of Science where he studied the mechanism of action of Bordetella pertussis toxins and Bordetella pathogenesis. During a sabbatical at Washington University School of Medicine in Saint Louis, Emanuel has begun studying group A streptococcal (GAS) pathogenesis. In 1992, he joined the faculty of Medicine at the Hebrew University of Jerusalem and was appointed associate Professor. In 1996 he became full Professor and in 2000 the Chairman of the Institute of Microbiology. In 2005 Emanuel was elected as a Howard Hughes International Scholar. In 2011, he joined the National University of Singapore-Hebrew University of Jerusalem (NUS-HUJ) initiative program on Cellular and Molecular Mechanisms of Inflammation funded by the National Research Foundation (NRF) of Singapore. Hanski’s laboratory combines a multitude of approaches to study GAS pathogenesis including genetic, biochemical, cell biology, immunological and others. A specific attempt is made to decipher the role of various virulence factors in animal models relevant to human disease. Through these complementary approaches, the laboratory characterized the fibronectin-binding proteins of GAS. Later on they studied the CXC chemokine-cleaving serine protease that plays a central role in impairing neutrophil recruitment and activation during invasive GAS diseases. His laboratory has also identified and characterized the quorum sensing locus sil. Recently the group discovered and characterized a novel mechanism of host sensing by the bacterium in which GAS creates endoplasmic reticulum stress in the host through the action of streptolysin toxins. This in turn triggers the unfolded protein response and increases the expression of asparagine (ASN). GAS senses ASN and utilizes it to alter its virulence gene expression profile and to increase its rate of multiplication.

Abstracts this author is presenting: