이지원 교수
Jiwon Lee
고려대학교 · 생화학·유전·분자생물학
연구실 소개
이지원 교수의 연구실은 생체분자 기반의 나노소재를 설계하고 응용하는 데 초점을 맞추고 있습니다. 페린틴, 단백질 입자, 금 나노입자 등을 활용해 암 진료 및 치료에 활용 가능한 다기능성 생체소재를 개발하며, 특히 암세포 표적화, 유전자 치료 물질 전달, 광열 치료 등에 응용 가능한 나노플랫폼을 중심으로 연구를 진행하고 있습니다. 또한 생체 적합성과 기능성의 균형을 고려한 유전자 및 화학적 공학 기반의 나노입자 설계가 핵심입니다.
연구 현황
연구 성과 추이
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주요 논문
15Proteins are fundamentally the most important macromolecules for biochemical, mechanical, and structural functions in living organisms. Therefore, they provide us with diverse structural building blocks for constructing various types of biomaterials, including an important class of such materials, hydrogels. Since natural peptides and proteins are biocompatible and biodegradable, they have features advantageous for their use as the building blocks of hydrogels for biomedical applications. They d
Compared to yeast esterase, fungal cutinase degraded butyl benzyl phthalate (BBP) far more efficiently; i.e., almost 60% of the BBP disappeared within 7.5 h. Also, the final chemical composition significantly depended on the enzyme used. Toxicity monitoring using bioluminescent bacteria showed that butyl methyl phthalate, a major product of degradation by esterase, was an oxidative toxic hazard.
Considering the problems of small interfering RNA (siRNA) delivery using traditional viral and nonviral vehicles, a new siRNA delivery system to enhance efficiency and safety needs to be developed. Here human ferritin‐based proteinticles are genetically engineered to simultaneously display various functional peptides on the surface of proteinticles: cationic peptide to capture siRNA, tumor cell targeting and penetrating peptides, and enzymatically cleaved peptide to release siRNA inside tumor ce
Cancer theragnosis using a single multimodality agent is the next mainstay of modern cancer diagnosis, treatment, and management, but a clinically feasible agent with in vivo cancer targeting and theragnostic efficacy has not yet been developed. A new type of cancer theragnostic agent is reported, based on gold magnetism that is induced on a cancer‐targeting protein particle carrier. Superparamagnetic gold‐nanoparticle clusters (named SPAuNCs) are synthesized on a viral capsid particle that is e
We synthesized fluorescent ferritin nanoparticles (FFNPs) through bacterial expression of the hybrid gene consisting of human ferritin heavy chain (hFTN-H), spacer (glycine-rich peptide), and enhanced green (or red) fluorescent protein [eGFP (or DsRed)] genes. The self-assembly activity of hFTN-H that leads to the formation of nanoparticles (12 nm in diameter), the conformational flexibility of the C-terminus of hFTN-H, and the glycine-rich spacer enabled eGFPs (or DsReds) to be well displayed o
PGCS-NPs (40 nm) with excellent photo-thermal activity are developed, on the surface of which affibody peptides with specific affinity for EGFR and many small gold dots (1-3 nm) are densely presented. The IV-injected PGCS-NPs into EGFR-expressing tumor-bearing mice successfully perform targeted and photothermal therapy of cancer. It seems that the small gold dots released from disassembled PGCS-NPs are easily removed and never cause in vivo toxicity problems.
Here we report a novel assembly structure of near-infrared plasmonic gold nanoparticles (AuNPs), possessing both photoacoustic (PA) and photothermal (PT) properties. The template for the plasmonic AuNP assembly is a bioconjugate between short double-strand DNA (sh-dsDNA) and human methyl binding domain protein 1 (MBD1). MBD1 binds to methylated cytosine-guanine dinucleotides (mCGs) within the sequence of sh-dsDNA. Hexahistidine peptides on the engineered MBD1 function as a nucleation site for Au
As recent advancements in the chimeric antigen receptor-T cells have revolutionized the way blood cancers are handled, potential benefits from producing off-the-shelf, standardized immune cells entail the need for development of allogeneic immune cell therapy. However, host rejection driven by HLA disparity in adoptively transferred allogeneic T cells remains a key obstacle to the universal donor T cell therapy. To evade donor HLA-mediated immune rejection, we attempted to eliminate T cell's HLA
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