Simon developed a way rapidly and reversibly activate or repress any gene using dCas9 and FKBP-FRB tagged regulators. He also discovered that the switch from npBAF to nBAF contributed to the cell cycle exit of neural progenitors and the end of their multipotent state. Simon joined the faculty of the University of Geneva.
was a graduate student in the lab after completing a medical residency at Yale. Paul started the work in our lab on chromatin and was the first to define the mammalian BAF or mSWI/SNF complex (Nature 1993). He also worked with Steve Goff’s group at Columbia to show that the complex functioned as a tumor […]
Ollie was an MD/PhD student in the lab. He discovered that the mammalian SWI/SNF-Like BAF complex binds PIP2 and accelerates the rate of actin filament formation. He also studied the genomic transcriptional response to co-stimulation of T lymphocytes and demonstrated that CD28 induces quantitative rather than qualitative changes in gene activation. His work also lead […]
Oli Bell and Nate Hathaway developed an approach to effectively study chromatin dynamics in living cells. The approach involves using small molecule inducers of proximity to add or quickly remove different chromatin regulatory activities to one allele of a single gene in living cells or even a living mouse. His work showed that one […]
Keji is now a Senior Investigator at the Laboratory of Molecular Immunology at the NIH. He discovered that the mammalian SWI/SNF-like BAF complex contains b-actin as well as an actin-like protein and that actin plays a role in regulating the ATPase activity of the chromatin remodeling complex. One of his recent paper can be found […]
Chris discovered that BAF complexes repress the hox genes in ES cells by a remarkable mechanism in which the complexes evict polycomb at many sites over the genome allowing it to rapidly accumulate and repress the hox genes.
