이지오 교수
Ji-O Lee
포항공과대학교 생명과학과 · 생화학·유전·분자생물학
연구실 소개
이지오 교수의 연구실은 식물의 2차 대사와 면역 조절을 중심으로 한 분자 생물학적 메커니즘을 규명하고 있습니다. 특히 식물에서 색소 생성과 스트레스 저항성에 기여하는 안토시아이닌 생합성의 전사적 조절 메커니즘과, 암 치료를 위한 면역세포 활성화를 위한 사이토카인 유전자 변형 기반의 유전자 치료 전략을 동시에 연구하고 있습니다. 이는 식물의 대사 조절 원리와 면역세포 기반 암 치료 기법의 융합적 접근을 목표로 합니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
4Plants have evolved an extensive specialized secondary metabolism. The colorful flavonoid anthocyanins, for example, not only stimulate flower pollination and seed dispersal, but also protect different tissues against high light, UV and oxidative stress. Their biosynthesis is highly regulated by environmental and developmental cues and induced by high sucrose levels. Expression of the biosynthetic enzymes involved is controlled by a transcriptional MBW complex, comprising (R2R3) MYB- and bHLH-ty
Abstract Plants have evolved an extensive specialized secondary metabolism. The colorful flavonoid anthocyanins, for example, not only stimulate flower pollination and seed dispersal but also protect different tissues against high light, UV- and oxidative stress. Their biosynthesis is highly regulated by environmental and developmental cues and induced by high sucrose levels. Expression of the biosynthetic enzymes involved is controlled by a transcriptional MBW complex, comprising (R2R3) MYB- an
Various approaches employing cytokines and cytokine gene–modified tumor cells have been explored to induce antitumor responses, yet their widespread application has been limited due to efficacy concerns and adverse effects. In this study, interleukin-7 was engineered for expression both as a natural secretory form (sIL-7) and as a membrane-bound form fused with the B7.1 type I transmembrane protein (mbIL-7/B7) on CT26 colon cancer cells. Analysis of the resulting cell clones demonstrated that ec
Interferon gamma (IFNγ) is well-known for its ability to stimulate immune cells in response to pathogen infections and cancer. To develop an effective cancer therapeutic vaccine, CT26 colon carcinoma cells were genetically modified to express IFNγ either as a secreted form (sIFNγ) or as a membrane-bound form. For the membrane-bound expression, IFNγ was fused with Fas (mbIFNγ/Fas), incorporating the extracellular cysteine-rich domains, transmembrane, and cytoplasmic domains of Fas. The tumor cell
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