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Michael A. Erb, Ph.D.

Scripps Fellow
Department of Chemistry
California Campus
Scripps VIVO Scientific Profile
(858) 784-7034

Scripps Research Joint Appointments

Faculty, Graduate Program

Research Focus

Our hypothesis: The coordinated rewiring of cellular state during oncogenesis is reliant upon dysregulated transcriptional programs.

Our approach: We are principally focused on the basic research and therapeutic discovery of targets controlling chromatin-dependent transcriptional signaling in cancer. Ultimately, our studies are aimed at accelerating new understandings of pathogenic transcription and advancing novel chemical tools and therapeutic directions. Ongoing projects are placed within several stages of preclinical drug discovery and include: (1) functional genomics to identify transcriptional regulators involved in cancer growth or drug resistance, (2) chemical discovery to fashion biologically useful small-molecule probes, and (3) mechanistic study of transcriptional target biology using kinetically acute chemical perturbations. We prefer a chemical biology approach to cancer and chromatin biology for two reasons. First, chemical probes can serve as therapeutically relevant starting points for the advancement of drug-like derivatives into the clinic. Second, the rapid effect of pharmacologic tools offers the ability to attribute cellular phenotypes to the primary mechanisms of action of perturbed proteins. However, the vast majority of proteins involved in transcriptional signaling have proved, thus far, intractable to pharmacologic disruption. To overcome this limitation, we employ a chemical/genetic strategy that can, in principal, rapidly target any protein of interest for proteolytic degradation. This system, dTAG, utilizes a highly specific chemical probe to direct the ubiquitin proteasome system toward targets that feature a small protein tag. The pharmacologic nature of the dTAG system offers a kinetic resolution that supports the study of first-order phenotypes, enabling facile study of transcriptional mechanisms in cells.

Our mission: To innovate new cancer medicines and to train scientists to operate at the interface of functional genetics, transcriptional genomics, and chemical discovery.


B.A., Biochemistry, Claremont McKenna College, 2014
Ph.D., Biological and Biomedical Sciences, Harvard University, 2017

Awards & Professional Activities

2014 Phi Beta Kappa Academic Honor Society, Member
2014 Best Thesis in Physical Sciences, Claremont McKenna
2013 Rose Hills Foundation Summer Research Fellowship, Claremont McKenna
2013 Goldwater Scholar, Honorable Mention, Barry Goldwater Scholarship and Excellence in Education Foundation
2007 John Stauffer Scholarship for Academic Merit in Chemistry, Claremont McKenna

Selected References

All Publications

Winter GE*, Mayer A*, Buckley DL*, Erb MA*, Roderick JE, Vittori S, Reyes J, Iuilo J d, Souza A, Ott CJ, Roberts JM, Zeid R, Scott TG, Paulk J, Lachance K, Olson Calla, Dastjerdi S, Bauer S, Lin CY, Gray NS, Kelliher MA, Churchman LS†, Bradner JE†. BET bromodomain proteins function as master transcription elongation factors independent of CDK9 recruitment. Molecular Cell 67, 5–8.e19 (2017). PMCID: PMC5663500. *Equal contribution. †Corresponding author.

Erb MA, Scott TG, Li BE, Xie H, Paulk J, Seo H-S, Souza A, Roberts JM, Dastjerdi S, Buckley DL, Sanjana NE, Shalem O, Nabet B, Zeid R, Offei-Addo NK, Dhe-Paganon S, Zhang F, Orkin SH, Winter GE, Bradner JE. Transcription control by the ENL YEATS domain in acute leukemia. Nature 543, 270-274 (2017). PMCID: PMC5497220.