时间：4月19日上午10:00 

地点：药学院224

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Abstract:

Malaria parasites are exquisitely adapted for survival within human red blood cells. Understanding how malaria parasites enter red blood cells is essential for developing strategies to stop blood stage infection. An important feature of Plasmodium invasion is the host cell selectivity that the different species have for cells of the erythroid lineage. Indeed, Plasmodium vivax preferentially invades reticulocytes which are young red blood cells. Several members of P. vivax Reticulocyte Binding Protein (PvRBP) family bind specifically to reticulocytes suggesting that they play a crucial role in restricted host cell selectivity. We report the first crystal structures of the erythrocyte-binding domain from the PvRBP family and present our findings on the a new entry receptor that allows Plasmodium vivax to invade the youngest human red blood cells.

Biosketch:

Dr. Wai-Hong Thamobtained her Ph.D from Princeton University and is a group leader at the Walter and Eliza Hall Institute since 2013. Her research focuses on the discovery of new host-pathogen interactions that govern successful malaria infection. She studies P. falciparum and P. vivax parasite adhesins that are required for entry into red blood cells as well as merozoite surface proteins that bind to human complement proteins. Her lab combines molecular, cellular and structural biology methods to study the mechanisms of parasite invasion and complement evasion strategies of malaria parasites. The overarching aim is to rationally design and generate new inhibitors or antibodies that are able to block these interactions and hence, stop the recurrent infection in the host.

Re-defining the Molecular Control of Apoptotic Cell Death

DrGrant Dewson

Laboratory Head, Cell Signalling and Cell Death Division

Walter and Eliza Hall Institute

Apoptosis is the fundamental process of programmed cell suicide. Normally exquisitely controlled by the Bcl-2 family, defects in the apoptosis machinery contribute to the development of cancer whilst excessive or inappropriate cell death also contribute to degenerative disorders and tissue damage following stroke. Thus the apoptotic machinery is becoming an increasing focus of therapeutic targeting, exemplified by the development of small molecule antagonists of the anti-apoptotic proteins as powerful cancer treatments. However, if the full potential of targeting apoptosis is to be exploited, we need to know precisely how apoptosis is tightly controlled in healthy cells and how this control is lostin disease. Using diverse and innovative approaches, Grant’s lab aims to clarify the molecular mechanisms regulating apoptosis, in particular understanding how the two deadly effector proteins Bak and Bax are unleashed to damage mitochondria to kill cells, and also how mitochondrial dynamics and quality control may influence apoptosis. The ultimate aim of his research is to exploit this knowledge to identify novel therapeutic avenues to augment or inhibit apoptosis in diseases including cancer, neurodegeneration and stroke.

Grant obtained his PhD from the University of Leicester (UK) studying the molecular mechanisms of eosinophil persistence in asthma. Following a post-doctoral position investigating chronic lymphocytic leukemia with Prof. Gerry Cohen at the Medical Research Centre Leicester, he joined Dr Ruth Kluck at the Walter and Eliza Hall Institute to investigate the basic mechanisms of apoptotic cell death. In 2011 he was appointed laboratory head in the Cell Signalling and Cell Death Division.