Combined inhibition of MTAP and MAT2a mimics synthetic lethality in tumor models via PRMT5 inhibition.

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作者： Gabriel T,Bedard ^[1] ; Nord,Gilaj ^[2] ; Karina,Peregrina ^[3] ; Isabella,Brew ^[1] ; Elena,Tosti ^[4] ; Karl,Shaffer ^[5] ; Peter C,Tyler ^[5] ; Winfried,Edelmann ^[4] ; Leonard H,Augenlicht ^[3] ; Vern L,Schramm ^[6]

作者单位： Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York, USA. ^[1] Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York, USA; Department of Chemistry, Lehman College, Bronx, New York, USA. ^[2] Department of Oncology, Albert Einstein College of Medicine, Bronx, New York, USA; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York, USA; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York, USA. ^[3] Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York, USA; Department of Genetics, Albert Einstein College of Medicine, Bronx, New York, USA. ^[4] Ferrier Research Institute, Victoria University of Wellington, Lower Hutt, New Zealand. ^[5] Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York, USA. Electronic address: vern.schramm@einsteinmed.edu. ^[6]

关键词 5'-methylthioadenosine MAT2a MTAP PRMT5 S-adenosyl-L-methionine arginine methylation cancer metabolism colorectal cancer