Nahyun Kim
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Nahyun Kim has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Chae-Min Lim
Department of Bioscience and Biotechnology, Konkuk University, Seoul, Republic of Korea
2 shared publications - Do-Young Yoon
Department of Bioscience and Biotechnology, Konkuk University, Seoul 05029, Republic of Korea
2 shared publications - Hong-Gyum Kim
NovelVita Inc., #310, Bio-2-dong, 32, Soyanggang-ro, Chuncheon 24232, Gangwon-do, Republic of Korea
2 shared publications - Jin Tae Hong
College of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju 28160, Republic of Korea
2 shared publications - Jinju Kim
Department of Bioscience and Biotechnology, Konkuk University, Seoul, Republic of Korea
2 shared publications - Young Yang
Department of Biological Sciences Sookmyung Women's University Seoul Republic of Korea
2 shared publications
Latest Publications
- Open Access
- 26 March 2025
- Published by Springer Nature in Scientific Reports
- Vol. 15 (1) , 1
Author Correction: Mutated IL-32θ (A94V) inhibits COX2, GM-CSF and CYP1A1 through AhR/ARNT and MAPKs/NF-κB/AP-1 in keratinocytes exposed to PM10
- 26 March 2025
- Published by Springer Nature in Scientific Reports
- Vol. 15 (1) , 1
Open AccessAuthor Correction: Mutated IL-32θ (A94V) inhibits COX2, GM-CSF and CYP1A1 through AhR/ARNT and MAPKs/NF-κB/AP-1 in keratinocytes exposed to PM10
- Open Access
- 15 January 2025
- Published by Springer Nature in Scientific Reports
- Vol. 15 (1) , 1-13
Mutated IL-32θ (A94V) inhibits COX2, GM-CSF and CYP1A1 through AhR/ARNT and MAPKs/NF-κB/AP-1 in keratinocytes exposed to PM10
Exposure to particulate matter (PM) in the air harms human health. Most studies on particulate matter’s (PM) effects have primarily focused on respiratory and cardiovascular diseases. Recently, IL-32θ, one of the IL-32 isoforms, has been demonstrated to modulate cancer development and inflammatory responses. This study revealed that one-point mutated IL-32θ (A94V) plays an important role in attenuating skin inflammation. IL-32θ (A94V) inhibited PM-induced COX-2, a pro-inflammatory cytokine GM-CSF and CYP1A1 in PM-exposed human keratinocytes HaCaT cells. IL-32θ (A94V) modulating effects were mediated via down-regulating ERK/p38/NF-κB/ AP-1 and AhR/ARNT signaling pathways. Our study indicates that PM triggers skin inflammation by upregulating COX-2, GM-CSF and CYP1A1 expression. IL-32θ (A94V) suppresses the expressions of COX-2, GM-CSF, and CYP1A1 by blocking the nuclear translocation of NF-κB and AP-1, as well as inhibiting the activation of the AhR/ARNT signaling pathway. Our findings offer valuable insights into developing therapeutic strategies and potential drugs to mitigate PM-induced skin inflammation by inhibiting the ERK/p38/NF-κB/AP-1 and AhR/ARNT signaling pathways.
- 15 January 2025
- Published by Springer Nature in Scientific Reports
- Vol. 15 (1) , 1-13
Open AccessMutated IL-32θ (A94V) inhibits COX2, GM-CSF and CYP1A1 through AhR/ARNT and MAPKs/NF-κB/AP-1 in keratinocytes exposed to PM10
Exposure to particulate matter (PM) in the air harms human health. Most studies on particulate matter’s (PM) effects have primarily focused on respiratory and cardiovascular diseases. Recently, IL-32θ, one of the IL-32 isoforms, has been demonstrated to modulate cancer development and inflammatory responses. This study revealed that one-point mutated IL-32θ (A94V) plays an important role in attenuating skin inflammation. IL-32θ (A94V) inhibited PM-induced COX-2, a pro-inflammatory cytokine GM-CSF and CYP1A1 in PM-exposed human keratinocytes HaCaT cells. IL-32θ (A94V) modulating effects were mediated via down-regulating ERK/p38/NF-κB/ AP-1 and AhR/ARNT signaling pathways. Our study indicates that PM triggers skin inflammation by upregulating COX-2, GM-CSF and CYP1A1 expression. IL-32θ (A94V) suppresses the expressions of COX-2, GM-CSF, and CYP1A1 by blocking the nuclear translocation of NF-κB and AP-1, as well as inhibiting the activation of the AhR/ARNT signaling pathway. Our findings offer valuable insights into developing therapeutic strategies and potential drugs to mitigate PM-induced skin inflammation by inhibiting the ERK/p38/NF-κB/AP-1 and AhR/ARNT signaling pathways.