Darmood Wei

Graduate Student

Contact Information Email: weid@email.unc.edu Office: (919) 966-1350 Location:
Education B.A., Molecular Cell Biology, University of California, Berkeley B.S., Molecular Toxicology, University of California, Berkeley Joined the Biological and Biomedical Sciences Program in 2009 Adviser: Bernard Weissman
Research Interests Elucidating the role of BAF180 after SNF5 loss during Malignant Rhabdoid Tumor development. SNF5, a member of the ATP-dependent SWI/SNF complex, is lost in Malignant Rhabdoid Tumors (MRTs), a rare and aggressive form of pediatric cancer.The SNF5 loss is the putative initiating event for the development of these tumors. Previous studies have demonstrated SNF5 re-expression results in a p21 dependent G1 growth arrest. Our lab has re-expressed SNF5 into three MRT cells lines, and observed increased expression of BAF180, a core subunit of SWI/SNF. We also observed concomitant increased levels of SNF5 and BAF180 at the p21 promoter in different cell lines. We are currently using RT-PCR, immunoblotting and chromatin immunoprecipitation (ChIP) analyses to further investigate the role of BAF180 during SNF5 re-expression. Elucidation of this mechanism allows for the further insights into the epigenetic effects associated with the etiology of this cancer.

Contact Information

Email: weid@email.unc.edu
Office: (919) 966-1350
Location:

Education

B.A., Molecular Cell Biology, University of California, Berkeley
B.S., Molecular Toxicology, University of California, Berkeley
Joined the Biological and Biomedical Sciences Program in 2009
Adviser: Bernard Weissman

Research Interests

Elucidating the role of BAF180 after SNF5 loss during Malignant Rhabdoid Tumor development. SNF5, a member of the ATP-dependent SWI/SNF complex, is lost in Malignant Rhabdoid Tumors (MRTs), a rare and aggressive form of pediatric cancer.The SNF5 loss is the putative initiating event for the development of these tumors. Previous studies have demonstrated SNF5 re-expression results in a p21 dependent G1 growth arrest. Our lab has re-expressed SNF5 into three MRT cells lines, and observed increased expression of BAF180, a core subunit of SWI/SNF. We also observed concomitant increased levels of SNF5 and BAF180 at the p21 promoter in different cell lines. We are currently using RT-PCR, immunoblotting and chromatin immunoprecipitation (ChIP) analyses to further investigate the role of BAF180 during SNF5 re-expression. Elucidation of this mechanism allows for the further insights into the epigenetic effects associated with the etiology of this cancer.