Ji-Hwan Ryu
연세대학교 생화학과 · 생화학·유전·분자생물학
Ji-Hwan Ryu 교수의 연구실은 장내 미생물과 숙주의 상호작용을 규명하는 데 초점을 맞추고 있으며, 특히 Caudal 유전자와 NF-κB 경로를 중심으로 장내 면역 반응의 조절 메커니즘을 연구하고 있습니다. 곤충 모델을 활용해 장내 미생물 군집의 균형을 유지하는 숙주 인자와 항생제 유사 단백질의 조절 기전을 밝혀내고 있으며, 이는 장내 미생물총과 숙주의 공진화적 상호작용을 이해하는 데 기여합니다. 최근에는 산화 스트레스와 세포 사멸, 바이러스 감염 메커니즘 등으로 연구 영역을 확장하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Although commensalism with gut microbiota exists in all metazoans, the host factors that maintain this homeostatic relationship remain largely unknown. We show that the intestinal homeobox gene Caudal regulates the commensal-gut mutualism by repressing nuclear factor kappa B–dependent antimicrobial peptide genes. Inhibition of Caudal expression in flies via RNA interference led to overexpression of antimicrobial peptides, which in turn altered the commensal population within the intestine. In pa
In Drosophila melanogaster, although the NF-kappaB transcription factors play a pivotal role in the inducible expression of innate immune genes, such as antimicrobial peptide genes, the exact regulatory mechanism of the tissue-specific constitutive expression of these genes in barrier epithelia is largely unknown. Here, we show that the Drosophila homeobox gene product Caudal functions as the innate immune transcription modulator that is responsible for the constitutive local expression of antim
Although commensalism with gut microbiota exists in all metazoans, the host factors that maintain this homeostatic relationship remain largely unknown. We show that the intestinal homeobox gene Caudal regulates the commensal-gut mutualism by repressing nuclear factor kappa B-dependent antimicrobial peptide genes. Inhibition of Caudal expression in flies via RNA interference led to overexpression of antimicrobial peptides, which in turn altered the commensal population within the intestine. In pa
Here, we present the novel finding that DUOX2-generated ROS induce AEC death, leading to hyperoxia-induced lung injury.
As an enveloped virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) delivers its viral genome into host cells via fusion of the viral and cell membranes. Here, we show that ANO6/TMEM16F-mediated cell surface exposure of phosphatidylserine is critical for SARS-CoV-2 entry and that ANO6-selective inhibitors are effective against SARS-CoV-2 infections. Application of the SARS-CoV-2 Spike pseudotyped virus (SARS2-PsV) evokes a cytosolic Ca<sup>2+</sup> elevation and ANO6-dependent ph
