The Bresnick laboratory is recruiting one or two postdoctoral fellows to join our research group at the Wisconsin Institutes For Medical Research (WIMR) in the University of Wisconsin School of Medicine and Public Health in Madison, WI. The WIMR provides a cutting-edge scholarly environment for conducting innovative basic and translational research.
We use multidisciplinary approaches to understand important biological processes, including stem/progenitor cell function, blood cell development, and vascular biology. Such approaches include genomics, proteomics, chemical genetics, and computational analysis, as well as traditional molecular, cellular, and biochemical methodologies. In addition to elucidating biological principles, we aim to develop innovative therapeutic strategies based on targeting novel mechanisms. Projects include: (1) Mechanisms of hematopoiesis. Defining such mechanisms has enormous importance, as deviations from hematopoietic programs yield leukemias, lymphomas and other blood disorders. We are analyzing the function and regulation of GATA transcription factors that control hematopoietic stem and progenitor cell function, hematopoiesis, and additional important processes. Transcriptional profiling and chromatin immunoprecipitation studies have identified a large cohort of novel GATA factor target g enes, including genes encoding proteins that bear no obvious similarity to known proteins. Loss-of-function and gain-of-function studies are being conducted in mice, zebrafish, and cultured cells to elucidate new biological pathways, which will provide key insights into mechanisms of development, differentiation, and human disease. (2) Transcriptional control of hemoglobin synthesis. These studies address fundamental mechanistic questions on how chromatin modification/remodeling regulates transcription of endogenous loci and also how hemoglobin synthesis is dysregulated in human hemoglobinopathies. Many questions remain unanswered regarding how dynamic changes in chromatin are orchestrated during development, differentiation, and pathophysiological processes. (3) Linking GATA factor mechanisms to human disease. GATA-1 mutations cause human leukemias, while GATA-2 mutations occur in leukemia as well as coronary artery disease. We discovered a link between GATA-2 function and P arkinson’s disease and also a GATA-1-regulated endogenous suppressor of angiogenesis that functions via a novel mechanism. Studying GATA factors can yield important insights of considerable relevance to human disease.
The successful candidate will develop both independent and collaborative experiments in one or more of our focal areas.
Please apply to email@example.com with your cv, and comments about potential areas of interest.