Seung Ja Oh
경희대학교 유전생명공학과 · 생화학·유전·분자생물학
이 교수의 연구실은 혈관 내피 세포의 기능 유지와 염증 반응 조절을 핵심으로 삼아, 세 sepsis, 암의 면역 회피 메커니즘, 그리고 조직 재생에서의 염증 조절을 타깃으로 한 신약 개발과 유전자 편집 기술의 응용을 연구하고 있습니다. 특히 TIE2 수용체 활성화를 통한 혈관 보호, RORα를 통한 T세포 내 콜레스테롤 대사 조절, 그리고 염증 반응에 따라 약물 방출을 제어하는 스마트 수용성 젤리 기반 치료 전략 개발에 주력하고 있습니다. 이는 만성 염증 질환 및 암 치료의 새로운 접근법을 제시하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Protection of endothelial integrity has been recognized as a frontline approach to alleviating sepsis progression, yet no effective agent for preserving endothelial integrity is available. Using an unusual anti-angiopoietin 2 (ANG2) antibody, ABTAA (ANG2-binding and TIE2-activating antibody), we show that activation of the endothelial receptor TIE2 protects the vasculature from septic damage and provides survival benefit in three sepsis mouse models. Upon binding to ANG2, ABTAA triggers clusteri
Cas9 ribonucleoprotein (RNP)-mediated delivery has emerged as an ideal approach for in vivo applications. However, the delivery of Cas9 RNPs requires electroporation or lipid- or cationic-reagent-mediated transfection. Here, we developed a carrier-free Cas9 RNP delivery system for robust gene editing in vivo. For simultaneous delivery of Cas9 and a guide RNA into target cells without the aid of any transfection reagents, we established a multifunctional Cas9 fusion protein (Cas9-LMWP) that forms
ADP-ribosylation actor 6 (ARF6) regulates the endocytosis and recycling of a variety of proteins and also promotes peripheral actin rearrangements and cell motility. ARF6 is activated by a large number of guanine nucleotide exchange factors, which likely regulate ARF6 at different locations and during different processes. In this study we investigate the roles of the cytohesin ADP-ribosylation factor (ARF)-guanine nucleotide exchange factors during the recycling of integrin beta1. Intriguingly,
Retinoic acid-related orphan receptor α (RORα) functions as a transcription factor for various biological processes, including circadian rhythm, inflammation, cancer, and lipid metabolism. Here, we demonstrate that RORα is crucial for maintaining cholesterol homeostasis in CD8<sup>+</sup> T cells by attenuating NF-kB transcriptional activity. Cholesterol sulfate, the established natural agonist of RORα, exhibits cellular cytotoxicity on, and increased effector responses in, CD8<sup>+</sup> T cel