Young Jin Jeon

Gwangju University

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Ho Jin You

Gwangju University

In Youb Chang

Gwangju University

Sang‐Bae Han

Chungbuk National University

Kun Yeong Lee

Mayo Clinic in Arizona

Hwan Mook Kim

Korea Research Institute of Bioscience and Biotechnology

Sang Pil Yoon

Jeju National University

Seung Hyun Han

Seoul National University Dental Hospital

Kyu‐Hwan Yang

Kyungdong University

Jong Soon Kang

Korea Research Institute of Bioscience and Biotechnology

Sung Su Yea

Inje University

Cooperative Institutions

Seoul National University

Chosun University

Korea Research Institute of Bioscience and Biotechnology

Korea Advanced Institute of Science and Technology

Yonsei University

Kyung Hee University

Seoul National University Hospital

Korea University

Sungkyunkwan University

Hormel (United States)

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Activation of NF-κB/Rel in angelan-stimulated macrophages

Immunopharmacology (1999)

Young Jin Jeon Sang‐Bae Han Kyung Seop Ahn Hwan Mook Kim

Transcription

10.1016/s0162-3109(99)00032-6

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Citations (48)

Paclitaxel causes mouse splenic lymphocytes to a state hyporesponsive to lipopolysaccharide stimulation

International Journal of Immunopharmacology (2000)

Michael Lee Sung Su Yea Young Jin Jeon

10.1016/s0192-0561(00)00024-2

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Citations (32)

Down-regulation of protein kinase C: a potential mechanism for 2-amino-3-methylimidazo[4,5-f]quinoline-mediated immunosuppression

Toxicology Letters (1998)

Yong Woo Lee Seung Hyun Han Jae Hong Suh Young Jin Jeon Kyu‐Hwan Yang

Ionomycin

Quinoline

Immunosuppression

Transcription

10.1016/s0378-4274(98)00289-6

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Citations (4)

Radicicol Suppresses Expression of Inducible Nitric-Oxide Synthase by Blocking p38 Kinase and Nuclear Factor-κB/Rel in Lipopolysaccharide-Stimulated Macrophages

Journal of Pharmacology and Experimental Therapeutics (2000)

Young Jin Jeon Young K. Kim Michael Lee Sun M. Park Sang‐Bae Han

Blocking (statistics)

10.1016/s0022-3565(24)39105-0

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Citations (1)

Papain-like 2 protease of coronavirus and innate immune response

Medical Biological Science and Engineering (2020)

Young Jin Jeon

Over the past few decades, certain coronaviruses have become threat to humans.Coronaviruses such as severe acute respiratory syndrome-related coronavirus (SARS-CoV) and Middle East respiratory syndrome-related coronavirus (MERS-CoV) have caused lethal outbreaks in 2003 and 2012, respectively.In 2019, severe infectious coronavirus outbreak with unusual pneumonia was reported in Wuhan, China, which later became pandemic.Due to the similarity of coronavirus disease 2019 (COVID-19) to SARS-CoV, the virus was termed as SARS-CoV-2.Although viral proteases such as papain-like 2 protease (PL2 Pro ) are essential for virulence of SARS-CoV, limited information is available on the role of protease in viral pathogenesis.This article highlights the significance of ubiquitination in signal transduction for innate immune responses and the importance of deubiquitinase activity of PL2 Pro in inhibiting host antiviral activities.

Coronavirus

Deubiquitinating enzyme

10.30579/mbse.2020.3.2.31

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Citations (1)

Deletion of PAX5 Is Frequently Accompanied by CDKN2A Deletion but Not by ETV6-RUNX1 Rearrangement In B-Lineage Acute Lymphoblastic Leukemia

Blood (2010)

Miyoung Kim Young Jin Jeon Cha Ja She Sang Mee Hwang Hyoung Jin Kang

PAX5

breakpoint cluster region

ETV6

Gene rearrangement

10.1182/blood.v116.21.4841.4841

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Citations (0)

Silymarin Inhibits Morphological Changes in LPS-Stimulated Macrophages by Blocking NF-κB Pathway

Korean Journal of Physiology and Pharmacology (2015)

Eun Jeong Kim Min Young Lee Young Jin Jeon

The present study showed that silymarin, a polyphenolic flavonoid isolated from milk thistle (Silybum marianum), inhibited lipopolysaccharide (LPS)-induced morphological changes in the mouse RAW264.7 macrophage cell line. We also showed that silymarin inhibited the nuclear translocation and transactivation activities of nuclear factor-kappa B (NF-κB), which is important for macrophage activation-associated changes in cell morphology and gene expression of inflammatory cytokines. BAY-11-7085, an NF-κB inhibitor, abrogated LPS-induced morphological changes and NO production, similar to silymarin. Treatment of RAW264.7 cells with silymarin also inhibited LPS-stimulated activation of mitogen-activated protein kinases (MAPKs). Collectively, these experiments demonstrated that silymarin inhibited LPS-induced morphological changes in the RAW264.7 mouse macrophage cell line. Our findings indicated that the most likely mechanism underlying this biological effect involved inhibition of the MAPK pathway and NF-κB activity. Inhibition of these activities by silymarin is a potentially useful strategy for the treatment of inflammation because of the critical roles played by MAPK and NF-κB in mediating inflammatory responses in macrophages.

Silybum marianum

IκBα

Proinflammatory cytokine

10.4196/kjpp.2015.19.3.211

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Citations (55)

Prodigiosin blocks T cell activation by inhibiting interleukin-2Ralpha expression and delays progression of autoimmune diabetes and collagen-induced arthritis.

PubMed (2001)

Sang‐Bae Han Se Hyung Park Young Jin Jeon Young Kook Kim Hwan Mook Kim

Prodigiosin (PDG) was previously reported to be a T cell-specific immunosuppressant. Here we describe the mechanism of action of PDG in T cells and the effect of PDG on autoimmune diseases. PDG selectively suppresses concanavalin A (Con A)-induced T cell proliferation, but has little effect on lipopolysaccharide-induced proliferation of B cells and nitric oxide production of macrophages. Although PDG does not block interleukin (IL)-2 production, it efficiently inhibits interleukin-2 receptor alpha-chain (IL-2Ralpha) expression, and this results in a disruption of the IL-2/IL-2R signaling pathway, on which a great part of the regulation of T cell activation depends. PDG blocks T cell differentiation into effector helper T cells secreting interferon-gamma and IL-4 as well as into effector cytotoxic T lymphocytes expressing perforin, which is at least in part resulting from inhibition of the IL-2/IL-2R signaling. PDG indirectly blocks signal transducer and activator of transcription activation by inhibiting cytokine signalings in Con A-activated T cells, although it does not inhibit the activation of nuclear factor-kappaB, nuclear factor of activated T cells, and activator protein-1. As direct evidence of immunosuppression in vivo, we show that PDG markedly reduced blood glucose levels and cellular infiltration into the pancreatic islets in nonobese diabetic mice, and that it also delays the onset of collagen-induced arthritis in DBA/1 mice. In conclusion, our results demonstrate that PDG has a unique mode of action, namely, that it blocks T cell activation by inhibiting primarily IL-2Ralpha expression in the IL-2/IL-2R signaling, and show that this compound represents a promising immunosuppressant candidate for the treatment of autoimmune diseases.

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Citations (62)

Radicicol Inhibits iNOS Expression in Cytokine-Stimulated Pancreatic Beta Cells

Korean Journal of Physiology and Pharmacology (2013)

Cha Kyung Youn Seon Joo Park Mei Hong Li Min Young Lee Kun Yeong Lee

Here, we show that radicicol, a fungal antibiotic, resulted in marked inhibition of inducible nitric oxide synthase (iNOS) transcription by the pancreatic beta cell line MIN6N8a in response to cytokine mixture (CM: TNF-α, IFN-γ, and IL-1β). Treatment of MIN6N8a cells with radicicol inhibited CM-stimulated activation of NF-κB/Rel, which plays a critical role in iNOS transcription, in a dose-related manner. Nitrite production in the presence of PD98059, a specific inhibitor of the extracellular signal-regulated protein kinase-1 and 2 (ERK1/2) pathway, was dramatically diminished, suggesting that the ERK1/2 pathway is involved in CM-induced iNOS expression. In contrast, SB203580, a specific inhibitor of p38, had no effect on nitrite generation. Collectively, this series of experiments indicates that radicicol inhibits iNOS gene expression by blocking ERK1/2 signaling. Due to the critical role that NO release plays in mediating destruction of pancreatic beta cells, the inhibitory effects of radicicol on iNOS expression suggest that radicicol may represent a useful anti-diabetic activity.

10.4196/kjpp.2013.17.4.315

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Citations (4)

Hydrophobic Fractions of Triticum aestivum L. Extracts Contain Polyphenols and Alleviate Inflammation by Regulating Nuclear Factor-kappa B

Biotechnology and Bioprocess Engineering (2021)

Moon‐Hee Choi Min Young Lee Seung-Hwa Yang Hyun‐Jae Shin Young Jin Jeon

Anti-inflammatory

10.1007/s12257-020-0352-7

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Citations (10)