Bing Ren

Affiliation: UCSD SOM

Assistant Professor of Cellular and Molecular Medicine

Biography

Dr. Ren received his B.S. degree from the University of Science and Technology of China, Hefei, in 1991, a masters in computer sciences from Harvard, and a Ph.D. in Biochemistry from Harvard in 1998. He did post-doctoral work at the Whitehead Institute for Biomedical Research at MIT and became head of the Laboratory of Gene Regulation at the Ludwig Institute for Cancer Research in 2001.

Research Summary

Of the roughly 3 billion nucleotides in the human genome, it is estimated that 2-3% may correspond to the transcriptional regulatory elements that define a highly specific gene expression program in human cells (Lander et al., 2001; Waterston et al., 2002). These DNA sequences allow each gene to be transcribed at the appropriate time and place during development, and allow each cell in the body to respond appropriately to environmental cues. These sequences also allow the human being to evolve from its ancestors. Delineating the identity and function of the transcriptional regulatory elements is therefore the key to understanding human biology and the molecular basis of diseases.

One research project in the lab is to discover the transcriptional regulatory elements in human genome using a novel high throughput approach that we developed, known as genome-wide location analysis (GWLA) or ChIP-on-chip. This method involves immunoprecipitation of the DNA associated with a particular protein from crosslinked cells, followed by quantitative amplification and simultaneous detection of the enriched sequences with DNA microarray technologies (Figure 1).

We are currently applying GWLA to a panel of well-characterized regulatory proteins and histones with specific modifications that are known to generally associate with transcriptional regulatory elements in vivo, with a goal to determine the sequence features in the human genome that carry out transcriptional regulatory function.

Another area of research in the lab is to understand genetic programs of tumorigenesis. Cancer is a disease characterized by aberrant gene expression that result from genetic alterations in cell1s transcriptional regulatory networks. Many transcriptional regulators have been linked to the causes of cancer, and identification of their genomic binding sites in cells offers a great opportunity to delineate the molecular pathways of malignant transformation and develop better treatment. To this end, we have formed an integrated approach to investigate the genome-wide location and function of c-Myc, a transcription factor responsible for many human cancers. Our initial experiments have resulted in the identification of a complex transcriptional regulatory program controlled by c-Myc that involves more than 700 c-Myc targets. These genes participate in a wide spectrum of cellular processes, including protein biosynthesis, DNA replication, cell cycle check-point control, DNA damage repair, and apoptic signaling pathways. We are currently examining the role that each gene play in the c-Myc transformation process.

References

References From PubMed (NCBI)