Steven B. McMahon, PhD
233 S. Tenth Street, Suite 609
Philadelphia, PA 19107
Most Recent Peer-reviewed Publications
- Dachshund binds p53 to block the growth of lung adenocarcinoma cells
- A high-confidence interaction map identifies SIRT1 as a mediator of acetylation of USP22 and the SAGA coactivator complex
- Dynamic regulation of mitochondrial transcription as a mechanism of cellular adaptation
- MYST protein acetyltransferase activity requires active site lysine autoacetylation
- Inhibition of the single downstream target BAG1 activates the latent apoptotic potential of MYC
PhD, Immunology, University of Pennsylvania
MS, Physiology, Temple University
BS, Biology, Albright College
Expertise & Research Interests
Our group has a long-standing interest in understanding the biochemical events that are deregulated to cause alterations in broad transcriptional programs in human cancer. As such, our research focuses on the two most commonly mutated transcription factors, MYC and p53, that are critical to cancer progression. We are currently focused on defining precisely how MYC and p53 are regulated in cancer cells, how the transcription programs they control are altered in cancer, and ultimately what essential cellular processes are impacted by these changes. Collectively, these studies have identified previously unknown nodes in these pathways that may represent potential therapeutic targets.
Current Research Projects
- Understand the role of altered mitochondrial transcription in the ability of MYC to reprogram cellular metabolism during malignant transformation.
- Identify the mechanism by which post-translational modifications control the ability of the p53 tumor suppressor to selectively activate distinct transcriptomes.
- Define the contribution of genetic lesions in subunits of the human SAGA coactivator complex to human cancer.