**Job Description**

**_Roles & Responsibilities:_**

+ Our group has recently identified that inhibiting spliceosomal assembly through inhibition of arginine methylation provides an effective means of therapeutic splicing inhibition. Specifically, inhibiting either symmetric arginine methylation (mediated by the protein arginine methyltransferase 5 -PRMT5) or asymmetric dimethyl arginine methylation (mediated by type I PRMTs (PRMT1, 3, 4, and 6)) reduces splicing fidelity resulting in strong preferential killing of (i) splicing factor-mutant leukemias and (ii) MYC-overexpressing lymphomas over their wildtype counterparts.In follow-up projects ongoing in the lab we aim to determine the molecular basis for the synthetic lethality between PRMT inhibition and either MYC overexpression or SF mutations.The significance of these studies is that inhibitors of PRMTs are now entering phase I clinical trials in patients with a variety of cancer types and defining the mechanistic ...