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B iosensor &
S tructural B iology Laboratory

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X-ray Crystallography
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DNA repairing protein

Hereditary nonpolyposis colorectal carcinoma (HNPCC) is caused by inherited mutations in some of the gene encoding components of a base-pair mismatch repair pathway. We focus on the continuous structural studies of three proteins such as MutS, MutL and MutH as well as their human homologs.
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Checkpoint protein

Understanding the nature of interaction along the checkpoint cascade would reveal how malfunctions of those proteins lead to diseases (human cancers). We are targeting more than 30 proteins involved in the damaged DNA checkpoint pathway.
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Telomerase

There has been a vast increase in telomere-telomerase research over past few years since they have been shown to impact on both cancer and aging. Telomeres, a special chromatin structure at both termini of chromosomes, protect chromosomal ends from recombination and degradation. Telomerase, a critical enzyme responsible for the length of telomere in the cell division, is repressed in most somatic cells and activated in approximately 90% of human cancer tissues. Thus telomerase activity is a useful cancer-cell detection marker and a prognostic indicator. For the structural study of telomerase and its interaction with telomere and telomere associated proteins, telomerase is being initially prepared using baculovirus expression system. In order to elucidate the mechanisms of the protein-DNA and protein-protein interactions associated with telomere-telomerase system, electrochemical studies such as cyclic voltammetry and impedometry will be carried out.
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ssDNA binding transcription factors

Transcription activation or repression of RNA polymerase II is often mediated by sequence-specific DNA-binding proteins (i.e. transcription activating factors) that respond to extracellular signals by interacting with critical cis-acting regulatory elements. Here, we will be focusing on structural studies of three key single-strand binding proteins, Purα, Purβ, and MSY1 that affect on the human neurodegenerative disease.
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Presynaptic Protein, Synuclein

Alpha synuclein accumulates in Lewy bodies and two missense mutations, A30P and A53T, have been linked to familial Parkinson’s disease. Neither the normal function of alpha-synuclein, nor the pathomechanism of alpha-synuclein-induced neuropathy are known. So we aim at elucidating the mechanism of alpha-synucleinopathies, also revealing the its three dimensional structure by X-ray crystallography.