Dr. Arthur D. Riggs is a world-renowned expert in diabetes, best known for his role in the development of technology that led to the first synthetic human insulin for patients. In 1979, Dr. Riggs received the Juvenile Diabetes Foundation Research Award for research that resulted in the bacterial production of human insulin. This work led to the formation of Genentech and the biotechnology industry. Dr. Riggs then turned his attention to recombinant antibodies, setting the stage for their successful use in the treatment of cancer. He has been a pioneer in the field of epigenetics, which is the study of persistent changes in gene expression that do not involve changes in primary base sequence. In recent years, Dr. Riggs’ research has mainly focused on mammalian epigenetic mechanisms and DNA methylation.
Dr. Riggs received his bachelor’s degree from University of California at Riverside and his doctorate in biochemistry from the California Institute of Technology. He was elected to the United States National Academy of Sciences in 2006 and in 2008 received the Distinguished Alumni Award from the California Institute of Technology.
My laboratory research is broad-based, with an emphasis on gene regulation by chromatin-based mechanisms and changes in the genome that take place during mammalian development. Emphasis is given to developing and using new methods for studying and controlling mammalian gene expression, especially during development in tissue culture from a stem or progenitor cell to a mature adult cell. Recent studies, some still ongoing, have included measuring genome-wide DNA methylation patterns, and changes in these patterns, during cancer progression or normal development.
I am particularly interested in improving the efficiency with which embryonic stem cells (ESC), both mouse and human, can be guided towards mature somatic cells, such as insulin-producing beta cells or cardiomyocytes. Three approaches are currently being explored (i) second generation antisense oligonucleotides (ASOs), (ii) transcription factors fused to novel protein transduction domains, and (iii) epigenetic engineering of ESC by gene-specific DNA methylation or demethylation to limit differentiation to the desired pathway. The latter studies are making use of TALES (Transcription Activation Like Effectors) and CRISPRS (Clustered Regularly Interspaced Palindromic Repeats) to produce mutant cell lines and engineer epigenetic changes in cells and mice.
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