In fond remembrance and tribute to Dr. Kuan-Teh Jeang, M.D., Ph.D.
In fond remembrance and tribute to Dr. Kuan-Teh Jeang, M.D., Ph.D.
复制标题
谨向医学博士、博士江宽德博士致以深切的怀念和敬意。
DOI：
10.1007/s13365-013-0157-y
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发表时间：
2013
影响因子：
3.2
通讯作者：
Rappaport,Jay
中科院分区：
文献类型：
--
作者：
Rappaport,Jay
In the neurovirology community, we are deeply saddened by the sudden passing of Dr. Kuan-Teh Jeang. Teh was a dear colleague and friend who I came to know, initially as postdoctoral fellows in the laboratory of the esteemed Dr. George Khoury in the Laboratory of Molecular Virology at NIH. This was a dynamic time in the Khoury Lab, as Gilbert Jay was a section head and several other senior postdocs and investigators in the lab included John Brady (who we also lost too soon), Ravi Dhar, Jeff Green, Chou-Zen (Joe) Giam, Kamel Khalili, Lou Laimins (who had recently finished), and Michael Nerenberg, among others. Having trained in Dr. Khoury’s laboratory where the concept of transcriptional enhancers was established using SV40 as a model, Teh had embarked on studies demonstrating the activation of HTLVI transcription by the viral Tax protein. He further demonstrated that transcriptional activation occurred through interaction with cellular factors recognizing the 21 base pair repeats within the HTLV-I long terminal repeat/promoter. After Dr. Khoury’s untimely death (also at a young age), Teh moved to the Laboratory of Molecular Microbiology at NIH and became Chief of the Molecular Virology Section. Here, Teh made highly important contributions to our understanding of HTLV-I (the causative agent of adult T cell leukemia) and HIV. In his further studies with HTLV-1, Teh identified an important mechanism involved in carcinogenesis. In these studies, Teh demonstrated the interaction of Tax with the centrosome machinery during mitosis, providing a means for generating chromosomal abnormalities leading to cancer. He also demonstrated the role of Tax in abrogating the function of the mitotic checkpoint protein, MAD1, as a means for escape of cells with chromosomal abnormalities, leading to tumor formation. In his studies related to HIV, he was one of the first investigators to describe the interaction of Tat with the “nascent” HIV-1 Tat activation response element (TAR) RNA as part of the mechanism leading to transactivation of HIV transcription. Tat proved also to interact with TAR in the context of coactivating cellular factors. Teh further described the interaction of Tat with other proteins including RNAse III or Dicer, an enzyme that processes micro RNAs (miRNA) and short interfering RNAs. Based on Teh’s studies, one of the important roles of Tat in the viral life cycle, in addition to transcription activation, appears to be the suppression of RNA-mediated (ie, miRNA) silencing mechanisms. Teh’s studies were highly sophisticated and innovative. He had undertaken a major effort to identify cellular genes contributing to HIV replication by implementing a short hairpin RNA inhibition screening approach using T cell clones transduced with shRNAs. These studies revealed 252 genes that contribute to productive HIV infection in T cells. These genes could be attractive targets for HIV therapy. His work was also supported by the Bill and Melinda Gates foundation’s “Grand Challenges in Global Health” during the past few years, where Teh was testing the feasibility of a viral interference approach as a way to prevent or cure HIV infection. Teh was a highly energetic and dynamic individual who was a respected leader in both his pursuit of scientific discovery as well as his service to the scientific community. He established the highly successful and prestigious open access journal, Retrovirology, and received the Biomed Central’s “Editor of the Year” award in 2010. He also was honored at the 15th International Conference on Human Retrovirology in 2011, receiving the Dale McFarlin Award of the International Retrovirology Association. Teh was also an editor …
