学术报告
Title：Novel Approach: From Molecular and Cellular Mechanisms to Therapeutic Development
Time: 14:30- 16:30 PM, October 31, 2014 (Fri.)
Venue: Rm 101, New Life Sciences Building
Host: Prof. Chenjian Li

 

Talk title: Mechanisms and Therapeutic Potential of Autophagy
Speaker: Prof. Xuejun Jiang
Memorial Sloan-Kettering Cancer Center
Abstract:
Autophagy is a basic cellular function for many physiological processes. The molecular and cellular mechanisms of autophagy have been under intense study in the recent years. These mechanisms, when defective, are also pathogenic events for human diseases. Autophagy provides us with targets for therapeutic developments.

 

Talk title: Two Side of g-Secretase: Alzheimer`s disease and Cancer
Speaker: Prof. Yueming Li
Memorial Sloan-Kettering Cancer Center
Abstract:
γ-secretase, a catalyst of Alzheimer disease (AD) and Notch signaling, has become an appealing drug target for AD and cancer therapies. γ-secretase is a large multi-protein complex composed of at least four proteins possessing 19 putative transmembrane domains. Elucidating the structure and function of γ-secretase has been a formidable challenge that requires novel chemical insights. We have developed a series of γ-secretase inhibitors and applied them as probes for characterization of γ-secretase. The use of these inhibitors in understanding the reaction mechanism and signaling of γ-secretase under physiological and pathological conditions will be discussed.

 

Talk title: Ubiquitin-proteolytic control of DNA repair and carcinogenesis
Speaker: Prof. Pengbo Zhou
Cornell University
Abstract:
The cullin 4A (CUL4A) ubiquitin ligase regulates nucleotide excision repair (NER) through proteolytic destruction of the heterodimeric DNA damage sensor: damaged DNA binding proteins 1 and 2 (DDB1 and DDB2). Recent studies revealed a second function of DDBs as integral components of the CUL4A ubiquitin ligase complex: DDB1 is the specific adaptor that bridges CUL4A and the DCAF (DDB1, CUL4A associated factors) substrate receptors, and DDB2 is a DCAF that recruits substrates to the DDB1-CUL4A complex for ubiquitination. However, the physiological role of CUL4A in DNA repair and tumorigenesis remains unknown. I will discuss the critical physiological function of CUL4A in suppressing nucleotide excision repair and antagonizing the DNA damage-responsive cell cycle checkpoint, and highlight the benefit of attenuating CUL4A in protection against UVB- or chemical carcinogen-induced skin carcinogenesis.