Dr. Novina received his M.D. from Columbia University, College of Physicians and Surgeons in 2000 and his Ph.D. from Tufts University, Sackler School of Graduate Biomedical Sciences in 1998. His graduate work resulted in 10 publications examining transcriptional regulation of TATA-less promoters in Ananda Roy’s laboratory. As a postdoctoral fellow in Phillip Sharp’s laboratory at the Massachusetts Institute of Technology, Dr. Novina studied the basic mechanisms of microRNAs, demonstrated the use of siRNAs to inhibit HIV infection (Nat Med. 8:681, 2002) and developed one of the first lentiviruses for the delivery of siRNAs to non-dividing mammalian cells (RNA 9:493, 2003), which became the host vector for The RNAi Consortium’s collection of lentivirus-expressed siRNAs.
In 2004, Dr. Novina joined the faculty at Dana-Farber Cancer Institute and Harvard Medical School. His laboratory has made several seminal insights into the fundamental biology of microRNAs and their dysregulation in cancers. His group reported the first fully cell-free microRNA-dependent translational repression reactions (Mol. Cell 22:553, 2006), used these reactions to reveal how microRNAs repress translation initiation by blocking 60S subunit joining to 40S ribosomes (PNAS 105:5343, 2008), discovered an RNA chaperone activity intrinsic to human Argonaute proteins (NSMB 16:1259, 2009) and an alternate mechanism of RISC assembly by Argonaute recruitment to microRNA-mRNA duplexes in vitro and in cells (RNA 18:2041, 2012), demonstrated the first example of an intronic microRNA (miR-211) that assumes the tumor suppressor role of its host gene (melastatin; Mol. Cell 40:841, 2010) and direct coupling between melastatin splicing and miR-211 microprocessing (PLoS Genet. (7)10:e10023302011, 2011). His group recently uncovered a potential tumor suppressor role for ribosomes in regulating microRNA function (Mol. Cell 46:171, 2012).