Jingwei Cheng
I am interested in transforming proteins and oncogenes targeted by small DNA tumor viruses including polyomaviruses. I am particularly interested in the interplay between two MAX network components in Merkel cell carcinoma oncogenesis: the MCPyV ST, L-MYC and P400 complex (SLaP) mediated transcriptional activation and the Polycomb Repressive Complex 1.6 (PRC1.6) mediated transcriptional repression. I am working on understanding how the m6A RNA methylation and PRMT5-mediated symmetric dimethylarginine (SDMA) formation on splicing factors safeguard proper splicing of proliferation-associated genes in cancers where MYC-driven global excess of pre-mRNA may overwhelm the splicing machinery.
I am interested in transforming proteins and oncogenes targeted by small DNA tumor viruses including polyomaviruses. I am particularly interested in the interplay between two MAX network components in Merkel cell carcinoma oncogenesis: the MCPyV ST, L-MYC and P400 complex (SLaP) mediated transcriptional activation and the Polycomb Repressive Complex 1.6 (PRC1.6) mediated transcriptional repression. I am working on understanding how the m6A RNA methylation and PRMT5-mediated symmetric dimethylarginine (SDMA) formation on splicing factors safeguard proper splicing of proliferation-associated genes in cancers where MYC-driven global excess of pre-mRNA may overwhelm the splicing machinery.