Important Info
To apply, please forward the required application materials to Thomas Quertermous (tomq1@stanford.edu).
The goal of our laboratory is to identify the mechanisms by which coronary artery disease (CAD)- associated alleles contribute to disease risk. To this end, our studies integrate not only human genetics and genomics, but also in vitro cell culture, and mouse genetic models. We employ genomics tools including HiChIP and ATAC-seq to identify and annotate epigenetic mechanisms upstream of causal regulatory variation that we and our collaborators have identified in largescale human genome-wide association studies (Nat Comm. 2016;7:12092, Nat Genet. 2017; 49:1602, Genome Biol. 2020; 21:135). In addition, our interest in CAD-associated transcription factors that are active in the blood vessel wall has led us to integrate single cell technologies into our studies. The depth of data that single cell technologies has provided allows us to characterize the gene regulatory program mediated by these transcription factors as well as the transcriptional mechanisms by which these factors modulate cell state changes (Nat Med. 2019; 25:1280).
We are seeking highly collaborative postdoctoral fellows with experience in the study of transcriptional regulatory mechanisms and cell biology and interest in cardiovascular disease. Interest in and experience with genetic and genomics computational methods is highly desirable, but not a requirement for this position. The Division of Cardiovascular Medicine and the Stanford University School of Medicine provide superlative training opportunities at the post-doctoral level in a highly stimulating and interactive environment.
- Doctoral degree (PhD, MD, or equivalent) conferred by start date
- CV
- Personal Statement