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研討會公告              ● 生化所行事曆

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2018 / 4 月份 演講
演講題目 Transcription initiation and genetic disorders: Understanding gene expression regulation and providing explanations for the clinic
時間 年/月/日 2018/4/3 11:00 ~ 12:00
地點 生化所114室
主講人 Dr. Jean-Marc Egly
主講人背景 法國IGBMC教授
演講主持人 蔡明道院士
洽詢人員 劉小姐
洽詢電話 02-27855696#1165
洽詢信箱 liukchun@gate.sinica.edu.tw
 
演講題目 [2018年李卓皓院士紀念演講] Synthetic Biochemistry: Making Biofuels and Commodity Chemicals the Cell-Free Way
時間 年/月/日 2018/4/10 10:00 ~ 12:00
地點 生化所103講堂
主講人 Dr. James U. Bowie
主講人背景 美國加州大學洛杉磯分校化學與生化所教授
演講主持人 蔡明道院士
洽詢人員 劉小姐
洽詢電話 02-27855696#1165
洽詢信箱 liukchun@gate.sinica.edu.tw
演講摘要 Considerable effort is currently directed to engineer micro-organisms to produce useful chemicals. The greatest potential environmental benefit of metabolic engineering will be the production of high volume commodity chemicals, such as biofuels. Yet the high yields and concentrations required for the economic viability of low-value chemicals are particularly hard to achieve in microbes due to the myriad competing biochemical pathways and product toxicity. We are developing an alternative approach, which we call synthetic biochemistry. Synthetic biochemistry throws away the cells and builds biochemical pathways in reaction vessels using complex mixtures of isolated enzymes. As the only pathway in the vessel is the desired transformation, yields can approach 100%. The challenge for synthetic biochemistry is to replace the complex regulatory systems that exist in cells in a simplified form. I will describe highly robust systems we have designed and built that can operate continuously for long periods of time.-Dr. James U. Bowie
 
演講題目 Probing glycan function and assembly through the use of structurally-defined glycoconjugates
時間 年/月/日 2018/4/16 10:30 ~ 12:00
地點 生化所114室
主講人 Dr. Todd L. Lowary
主講人背景 加拿大阿爾伯塔大學化學研究所教授
演講主持人 邱繼輝特聘研究員
洽詢人員 劉小姐
洽詢電話 02-27855696#1165
洽詢信箱 liukchun@gate.sinica.edu.tw
演講摘要 Understanding the many biological roles of carbohydrates (glycans) requires access to homogenous probe molecules. Such species are difficult to isolate in sufficient quantity and purity from nature and the recombinant technologies that are widely used to prepare proteins are not available for glycans. Consequently, the synthesis of glycans and conjugates of them (glycoconjugates) by chemical, chemoenzymatic, or enzymatic means is a critical technology for the advancement of glycoscience. This seminar will focus on ongoing investigations in which synthetic molecules are being used to understand the assembly or biological function of glycans. In particular, investigations focused on understanding the interaction between glycans produced by mycobacteria, including the human pathogen Mycobacterium tuberculosis, and the immune system of the host will be discussed. A second study on the assembly of the polysaccharide arabinogalactan, the major structural component of the mycobacterial cell wall, will also be presented. Finally, work towards the preparation of a family structurally-unprecedented N-linked glycans from chlorella viruses will be covered. Chlorella viruses differ from most other viruses in that their genomes encode for carbohydrate synthesizing enzymes (glycosyltransferases). The compounds being prepared are designed to act as substrates for these glycosyltransferases and will be essential in unravelling their function.Dr. Todd L. Lowary
 
演講題目 BRD4 in Transcription Programming and Cancer Therapy
時間 年/月/日 2018/4/17 10:30 ~ 12:00
地點 生化所114室
主講人 江正明博士
主講人背景 美國德州大學達拉斯西南醫學中心生物化學研究所教授
演講主持人 邱繼輝特聘研究員
洽詢人員 劉小姐
洽詢電話 02-27855696#1165
洽詢信箱 liukchun@gate.sinica.edu.tw
演講摘要 Bromodomain-containing protein 4 (BRD4) is an epigenetic regulator and transcription cofactor whose phosphorylation by casein kinase II (CK2) and dephosphorylation by protein phosphatase 2A (PP2A) modulates its function in gene-specific targeting and recruitment of transcriptional regulators and chromatin modifiers. Although BRD4 has emerged as an important cancer therapeutic target, it also plays crucial roles in diverse cellular processes, including cell cycle progression, DNA damage response, chromatin structure maintenance, stem cell reprogramming, cell lineage determination, X-chromosome inactivation, and viral latency and reactivation. While the bromodomains of BET family proteins, including BRD4, BRD2, BRD3 and BRDT, have been the primary targets of small compounds, such as JQ1 and I-BET, that show promising anticancer effects against some hematopoietic cancer and solid tumors, the issue related to drug resistance upon prolonged treatment necessitates a better understanding of alternative pathways underlying not only the resistance but also persistent BET protein dependence. In our studies of BRD4 phosphorylation, we identified three-dozen small compound inhibitors targeting phosphorylation-dependent BRD4 interactions with distinct transcription/replication factors including p53 and cancer-associated human papillomavirus (HPV) E2 proteins. Some of these identified phospho-BRD4-targeting compounds effectively block cancer cell growth and migration and specifically inhibit p53 interaction with BRD4, but not BRD2 and BRD3, highlighting the development of BRD4-specific inhibitors without cross-interference with the other BET family proteins. Genome-wide expression and binding studies as well as mouse cancer models have been developed to define the mechanisms of BRD4 action and compound inhibition. Clearly, phospho-BRD4-targeting compounds are more selective in modulating BRD4 function in gene reprogramming and cancer therapy compared to the widely used JQ1- and I-BET-derived BET bromodomain inhibitors.-Dr. Cheng-Ming Chiang
 
演講題目 Protein ubiquitination in regulating cancer hallmarks and membrane dynamics
時間 年/月/日 2018/4/18 10:30 ~ 12:00
地點 生化所114室
主講人 陳瑞華博士
主講人背景 本所特聘研究員
演講主持人 邱繼輝特聘研究員
洽詢人員 劉小姐
洽詢電話 02-27855696#1165
洽詢信箱 liukchun@gate.sinica.edu.tw
演講摘要 Protein ubiquitination is one of the most powerful and elaborate posttranslational modifications and controls a plethora of cellular processes, such as cell division, differentiation, survival, intracellular trafficking, and stress responses. Dysregulation of protein ubiquitination is associated with a number of disease states, including cancer and neurodegeneration. I will discuss our efforts to dissect the ubiquitination pathways of tumor suppressor proteins DAPK and PML, and their impacts on the malignant features of tumor cells and tumor microenvironment. Our work indicates that regulation of protein ubiquitination pathways could be exploited as anti-cancer strategies. I will also discuss our findings on protein ubiquitination in regulating cellular processes involving membrane dynamics, such as post-Golgi trafficking and autophagy, and our attempt to understand the functional impacts of atypical ubiquitination.-Dr. Ruey-Hwa Chen
 

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