Postdoctoral Fellow-MSH

• 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 effects and therapeutic utility of PRMT inhibitors for specific genetic subsets of cancers may have incredible therapeutic importance. The health relatedness is that our studies may identify new therapeutic opportunities for a variety of cancer types that have no curative therapies for the majority of patients with these diseases.

Requirements:

• Strong background in Mouse models of cancer, Molecular Biology and RNA biology is appreciated.
• Ph.D. degree in molecular biology or similar. Strong background in cancer, RNA/chromatin biology and familiarity with recent advances in these fields and NGS technologies. Excellent communication and teaching skills. Must be able to work as an individual while part of a small team.

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