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Title: The Capable Abl : Old Dog New Tricks
Originating Office: IAS
Speaker: Wang, Jean Yin-Jen
Issue Date: 12-Dec-2013
Event Date: 12-Dec-2013
Group/Series/Folder: Record Group 8.15 - Institute for Advanced Study
Series 3 - Audio-visual Materials
Location: 8.15:3 EF
Notes: IAS Distinguished Lecture.
Title from opening screen.
Co-sponsored by Division of Life Science.
Abstract: The ubiquitously expressed Abl gene encodes a non-receptor tyrosine kinase that is required for embryonic development but dispensable to adult viability because CML or GIST cancer patients can tolerate continuous treatments with drugs that inhibit the Abl tyrosine kinase. Since its cloning three decades ago, the many studies of Abl by numerous investigators have linked it to a variety of signaling pathways that regulate a wide range of biological processes. Results from the Abl studies have supported the concept that Abl is a capable signal transducer with many context-dependent biological functions. In recent years, the speaker and his research group have focused their studies of Abl on its nuclear function, particularly in the regulation of DNA damage response. They have knock-in mutated the three nuclear localization signals in the mouse Abl gene and shown that nuclear Abl is required for cisplatin to induce apoptosis in the mouse kidneys. In this lecture, the speaker will discuss the nuclear Abl tyrosine kinase function with emphasis on its roles in the post-transcriptional regulation of PUMA and microRNA in genotoxin-stressed cells.
Prof Jean Wang received her PhD in Biochemistry from the University of California at Berkeley in 1980. She was a postdoctoral fellow at the Massachusetts Institute of Technology from 1980 to 1983. She joined the University of California at San Diego in 1983, and is currently Distinguished Professor of the Department of Medicine.
Prof Wang’s research interests include genetic and epigenetic regulation of cell death decision. Her current research focuses on understanding how cells recognize, assess and respond to lesions in DNA and the molecular mechanisms by which a damaged cell can distinguish between continued proliferation, permanent growth arrest and suicide. Defects in these regulatory mechanisms contribute to tumor development, because mistakes made in DNA damage responses will likely cause genome instability. The functions of these pathways will also influence how normal cells and tumor cells respond to radiotherapy and chemotherapy. Understanding of these regulatory mechanisms may affect how people treat cancer in the future.
Prof Wang received numerous awards including the Merit Award from the US National Cancer Institute and the Distinguished Scholar Award from the National Taiwan University. She is a Fellow of the American Academy of Arts and Sciences and the American Academy of Microbiology.
Duration: 83 min.
Appears in Series:8.15:3 - Audio-visual Materials
Videos for Public -- Distinguished Lectures