Recently we reported that the initiation of eukaryotic mRNAs occurs by 'RNA looping' rather than by 'ribosome scanning'. According to the RNA looping hypothesis, translation begins with the association of a 405 ribosomal subunit with translation enhancing elements such as 5' cap, poly(A) tail and an IRES element. The association of a 405 ribosomal subunit to an mRNA, which is called 435 ribosomal preinitiation complex formation, is mediated by translational initiation factors such as elF4E, elF4G, PABP and elF3. At this stage, various parts of the mRNA collide with the 435 ribosomal complex associated with the mRNA. The probability of collision between the 435 ribosome and a particular region on the mRNA depends on the length and the stiffness of the intervening segment between the target region and the 435 ribosome. And the effectiveness of the collision between the 435 ribosome and the initiation codon for the successful engagement of translation is affected by the single-strandedness and nucleotide sequence (Koza k's context) of around the initiation codon. We provided several lines of evidence proving the 'RNA looping hypothesis' using biochemical, molecular biological and mathematical approaches. We also investigate into the translational regulation mechanism under stress conditions. Particularly we are interested in how some of eukaryotic mRNAs are translationally active when translation of most mRNAs is repressed by various stresses. We found a new carrier of initiator tRNA (tRNAi) named elF2A that facilitates loading of tRNAi onto the 405 ribosomal subunit under stress conditions. We found that c-Src mRNA, which is refractory to translational repression by stress, utilizes elF2A for translation under stress conditions and that the elF2A-mediated translation is essential for proliferation of cancer cells under stress conditions.
HCV is a pathogenic virus causing hepatitis, liver cirrhosis, and hepatocellular carcinoma. More than 170 million people are suffering from this virus infection worldwide. We are investigating the molecular basis of the pathogenic processes of HCV including the induction of inflammatory response and fibrogenesis. Moreover, we are trying to develop an antiHCV drug based on the inhibition of NS5A activities required for viral RNA replication and virus assembly.

• ㆍHepatitis C Virus (HCV): Development of anti-HCV drugs
• ㆍTranslation initiation mechanisms via cap and IRES elements
• ㆍDevelopment of a subtype specific diagnostic tool for influenza virus using aptamers

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• ㆍB.S., Seoul National University, Seoul, Korea (1982)
• ㆍM.S., Seoul National University, Seoul, Korea (1984)
• ㆍPh.D., University of New York, Stony Brook, USA (1989)

• ㆍ1989-1991 : Postdoctoral associate, University of New York at Stony Brook
• ㆍ1991-2003 : Assistant and associate professor, POSTECH
• ㆍ2001-2003 : CEO, Panbionet Inc.
• ㆍ2003-Present : Professor, POSTECH
• ㆍ2009-Present : CSO, Aptamer Sciences Inc.
• ㆍ2013-2014 : Head, Department of Life Sciences
• ㆍ2014-Present : Director, POSTECH Biotech Center
• ㆍ2018-Present : Fellow, Korean Academy of Science of Technology