Nak-Kyun Kim
Yonsei University
About the Lab
Professor Nak-Kyun Kim's research lab focuses on innate immunity and host defense mechanisms, with a particular emphasis on the regulation of inflammatory responses in chronic lung diseases, microbial infections, and cancer. The lab investigates key molecular players such as pattern recognition receptors (e.g., Mincle), signaling adaptors (e.g., CD11b), and interferon-stimulated genes (e.g., OASL1) in shaping immune responses. It also explores epigenetic and non-coding RNA regulation in cell fate determination and disease pathogenesis, especially in the context of aging, viral infection, and hepatocellular carcinoma. The lab integrates immunology, virology, and systems biology to uncover novel regulatory mechanisms underlying chronic inflammation and immune homeostasis.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
8Although chronic obstructive pulmonary disease (COPD) is regarded as a chronic inflammatory lung disease, the disease mechanismis still not known. Intriguingly, aging lungs are quite similar to COPD-affected lungs in many ways, and COPD has beenviewed as a disease of accelerated premature aging of the lungs. In this paper, based on a literature review, we would like to proposeimmunosenescence, age-associated decline in immunity, as a critical mechanism for the development of COPD. Immunosenescen
During mycobacteria infection, anti-inflammatory responses allow the host to avoid tissue damage caused by overactivation of the immune system; however, little is known about the negative modulators that specifically control mycobacteria-induced immune responses. Here we demonstrate that integrin CD11b is a critical negative regulator of mycobacteria cord factor-induced macrophage-inducible C-type lectin (Mincle) signaling. CD11b deficiency resulted in hyperinflammation following mycobacterial i
Oligoadenylate synthetase (OAS) protein family is the major interferon (IFN)-stimulated genes responsible for the activation of RNase L pathway upon viral infection. OAS-like (OASL) is also required for inhibition of viral growth in human cells, but the loss of one of its mouse homolog, OASL1, causes a severe defect in termination of type I interferon production. To further investigate the antiviral activity of OASL1, we examined its subcellular localization and regulatory roles in IFN productio
Cell type specification is a delicate biological event in which every step is under tight regulation. From a molecular point of view, cell fate commitment begins with chromatin alteration, which kickstarts lineage-determining factors to initiate a series of genes required for cell specification. Several important neuronal differentiation factors have been identified from ectopic over-expression studies. However, there is scarce information on which DNA regions are modified during induced pluripo
The complement is a part of the immune system that plays several roles in removing pathogens. Despite the importance of the complement system, the exact role of each component has been overlooked because the complement system was thought to be a nonspecific humoral immune mechanism that worked against pathogens. Decay-accelerating factor (DAF or CD55) is a known inhibitor of the complement system and has recently attracted substantial attention due to its role in various diseases, such as cancer
Enhancers have been conventionally perceived as cis-acting elements that provide binding sites for trans-acting factors. However, recent studies have shown that enhancers are transcribed and that these transcripts, called enhancer RNAs (eRNAs), have a regulatory function. Here, we identified putative eRNAs by profiling and determining the overlap between noncoding RNA expression loci and eRNA-associated histone marks such as H3K27ac and H3K4me1 in hepatocellular carcinoma (HCC) cell lines. Of th
Cells must fine-tune their gene expression programs for optimal cellular activities in their natural growth conditions. Transcriptional memory, a unique transcriptional response, plays a pivotal role in faster reactivation of genes upon environmental changes, and is facilitated if genes were previously in an active state. Hyper-activation of gene expression by transcriptional memory is critical for cellular differentiation, development, and adaptation. TREM (Transcriptional REpression Memory), a
Hepatocellular carcinoma is a major health burden, and thoughvarious treatments through much research are available, difficultiesin early diagnosis and drug resistance to chemotherapy-basedtreatments render several ineffective. Cancer stem cell model hasbeen used to explain formation of heterogeneous cell populationwithin tumor mass, which is one of the underlying causesof high recurrence rate and acquired chemoresistance, highlightingthe importance of CSC identification and understandingthe mol
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