We have long-standing interest in the regulation of RNA metabolism, particularly with respect to the control of alternative pre-mRNA splicing in development and disease. Our initial research contributed to the establishment of the SR (for serine-arginine rich) family of splicing regulators and demonstrated that SR proteins are responsible for committing pre-mRNA to the splicing pathway. ...
Our lab was also responsible for the discovery of SR protein-specific kinases (SRPKs), and demonstrated that these kinases regulate nuclear import of SR proteins and SR protein-mediated protein-protein interactions during splicing. We found that SRPKs are partitioned between the cytoplasm and the nucleus,serving as critical transducers of external signals to regulate splicing in the nucleus. ...
Our research has uncovered additional functions of splicing factors and regulators in gene expression at the chromatin levels, demonstrating, for example, that the classic SR protein SC35 (a.k.a. SRSF2) has a direct role in transcriptional pause release by facilitating the recruitment of the Pol II CTD kinase pTEFb, and that RBFox2 interacts with nascent ...
During our basic research of the PTB family of RNA binding proteins in regulated RNA metabolism, we unexpectedly found that depletion of PTB is able to potently convert various non-neuronal cells to neurons. Pursuing this intriguing phenomenon, we revealed that PTB suppresses a key neuronal induction pathway whereas its neuronal paralog nPTB provides a critical checkpoint ...