Research in my lab focuses on studies of the regulation of mRNA stability in the mammalian cell. Our efforts currently focus on two mechanisms that trigger rapid decay of mRNAs. One pathway is called nonsense-mediated mRNA decay (NMD) by which the mammalian cell recognizes and selectively degrades premature termination codon (PTC)-containing defective transcripts before they generate potentially deleterious truncated proteins. The other pathway is called Staufen1-mediated mRNA decay (SMD) by which the cellular protein Staufen1 binds to the specific mRNAs and thereby recruits mRNA decay machinery at the 3’ untranslated region (3’UTR). We are also examining the basic physiologic importance of NMD and SMD through the identification of several trans -acting factors essential for mRNA degradation. Specific interactions of these factors are being analyzed by genetic and biochemical approaches.

NMD(Nonsense-mediated mRNA decay)에 관여하는 새로운 인자 PNRC2(Prolin-rich Nuclear Receptor Coregulatory Protein2)가 decapping complex와의 결합을 통해 NMD를 조절한다는 역할을 규명[Cho et al., 2009, Molecular Cell]

CBP80/20-dependent translation를 조절하는 새로운 개시인자 CTIF(CBP80/20-dependent translation initiation factor)을 발굴, CBP80/20-dependent translation 에만 특이적으로 작용하는 인자임을 규명. 위 그림은 CTIF의 역할을 보여주는 모식도[Kim et al., 2009, Genes and Develpment]