Yonsei University · 生化学・遺伝学・分子生物学
Professor Ji-Hwan Ryu's research lab focuses on host-microbe interactions, particularly the molecular mechanisms underlying intestinal immune homeostasis and innate immunity in Drosophila and mammalian models. The lab investigates how transcription factors like Caudal regulate tissue-specific immune responses and maintain commensal microbiota balance, with implications for inflammatory diseases and host defense. Recent work also explores host factors involved in viral entry, such as ANO6/TMEM16F in SARS-CoV-2 infection, and oxidative stress responses in lung injury. The lab integrates genetics, cell biology, and host-pathogen interactions to uncover conserved pathways in innate immunity and tissue homeostasis.
Figures are computed from collected data and may differ slightly.
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
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