Steven B. McMahon, PhD
Philadelphia, PA 19107
PhD, Immunology, University of Pennsylvania
MS, Physiology, Temple University
BS, Biology, Albright College
Expertise and 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.
Most Recent Peer-Reviewed Publications
- A PERK–miR-211 axis suppresses circadian regulators and protein synthesis to promote cancer cell survival
- Delayed Accumulation of H3K27me3 on Nascent DNA Is Essential for Recruitment of Transcription Factors at Early Stages of Stem Cell Differentiation
- Repression of telomerase gene promoter requires human-specific genomic context and is mediated by multiple HDAC1-containing corepressor complexes
- A rare DNA contact mutation in cancer confers p53 gain-of-function and tumor cell survival via TNFAIP8 induction
- Subtelomeric p53 binding prevents accumulation of DNA damage at human telomeres
- Multi-focal control of mitochondrial gene expression by oncogenic MYC provides potential therapeutic targets in cancer
- The retinoblastoma tumor suppressor modulates DNA repair and radioresponsiveness
- Retraction Notice to: Nuclear receptor function requires a TFTC-type histone acetyl transferase complex
- MYC and the control of apoptosis
- USP22 regulates oncogenic signaling pathways to drive lethal cancer progression
- The epigenetic modifier ubiquitin-specific protease 22 (USP22) regulates embryonic stem cell differentiation via transcriptional repression of sex-determining region Y-box 2 (SOX2)
- P53: The TRiC Is Knowing When to Fold 'Em
- 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
- Acetylation of the cell-fate factor dachshund determines p53 binding and signaling modules in breast cancer
- 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
- Enzymatic assays for assessing histone deubiquitylation activity
- Phosphorylation of Tip60 by GSK-3 Determines the Induction of PUMA and Apoptosis by p53