Naeun Yoon
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Naeun Yoon has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
- Byung Hwa Jung
Molecular Recognition Research Center, Korea Institute of Science and Technology, Seoul, Republic of Korea
2 shared publications - Ah-Kyung Jang
Molecular Recognition Research Center, Korea Institute of Science and Technology, Seoul 02792, Korea
1 shared publication - Eun Hye Kim
Therapeutics & Biotechnology Division Korea Research Institute of Chemical Technology Daejeon Republic of Korea
1 shared publication - Geonhee Lee
Advanced Materials Division, Korea Research Institute of Chemical Technology, Daejeon 34114, Korea
1 shared publication - Hyunbeom Lee
Center for Advanced Biomolecular Recognition, Korea Institute of Science and Technology, Seoul, Republic of Korea.
1 shared publication - Jeong-O Lee
Advanced Materials Division, Korea Research Institute of Chemical Technology, Daejeon 34114, Korea
1 shared publication
Latest Publications
- Open Access
- 29 November 2021
- Published by MDPI AG in Metabolites
- Vol. 11 (12) , 812
Metabolomics in Autoimmune Diseases: Focus on Rheumatoid Arthritis, Systemic Lupus Erythematous, and Multiple Sclerosis
The metabolomics approach represents the last downstream phenotype and is widely used in clinical studies and drug discovery. In this paper, we outline recent advances in the metabolomics research of autoimmune diseases (ADs) such as rheumatoid arthritis (RA), multiple sclerosis (MuS), and systemic lupus erythematosus (SLE). The newly discovered biomarkers and the metabolic mechanism studies for these ADs are described here. In addition, studies elucidating the metabolic mechanisms underlying these ADs are presented. Metabolomics has the potential to contribute to pharmacotherapy personalization; thus, we summarize the biomarker studies performed to predict the personalization of medicine and drug response.
- 29 November 2021
- Published by MDPI AG in Metabolites
- Vol. 11 (12) , 812
Open AccessMetabolomics in Autoimmune Diseases: Focus on Rheumatoid Arthritis, Systemic Lupus Erythematous, and Multiple Sclerosis
The metabolomics approach represents the last downstream phenotype and is widely used in clinical studies and drug discovery. In this paper, we outline recent advances in the metabolomics research of autoimmune diseases (ADs) such as rheumatoid arthritis (RA), multiple sclerosis (MuS), and systemic lupus erythematosus (SLE). The newly discovered biomarkers and the metabolic mechanism studies for these ADs are described here. In addition, studies elucidating the metabolic mechanisms underlying these ADs are presented. Metabolomics has the potential to contribute to pharmacotherapy personalization; thus, we summarize the biomarker studies performed to predict the personalization of medicine and drug response.
- Open Access
- 7 October 2021
- Published by MDPI AG in Metabolites
- Vol. 11 (10) , 689
A Metabolomics Investigation of the Metabolic Changes of Raji B Lymphoma Cells Undergoing Apoptosis Induced by Zinc Ions
Zinc plays a pivotal role in the function of cells and can induce apoptosis in various cancer cells, including Raji B lymphoma. However, the metabolic mechanism of Zn-induced apoptosis in Raji cells has not been explored. In this study, we performed global metabolic profiling using UPLC−Orbitrap−MS to assess the apoptosis of Raji cells induced by Zn ions released from ZnO nanorods. Multivariate analysis and database searches identified altered metabolites. Furthermore, the differences in the phosphorylation of 1380 proteins were also evaluated by Full Moon kinase array to discover the protein associated Zn−induced apoptosis. From the results, a prominent increase in glycerophosphocholine and fatty acids was observed after Zn ion treatment, but only arachidonic acid was shown to induce apoptosis. The kinase array revealed that the phosphorylation of p53, GTPase activation protein, CaMK2a, PPAR−γ, and PLA−2 was changed. From the pathway analysis, metabolic changes showed earlier onset than protein signaling, which were related to choline metabolism. LC−MS analysis was used to quantify the intracellular choline concentration, which decreased after Zn treatment, which may be related to the choline consumption required to produce choline-containing metabolites. Overall, we found that choline metabolism plays an important role in Zn-induced Raji cell apoptosis.
- 7 October 2021
- Published by MDPI AG in Metabolites
- Vol. 11 (10) , 689
Open AccessA Metabolomics Investigation of the Metabolic Changes of Raji B Lymphoma Cells Undergoing Apoptosis Induced by Zinc Ions
Zinc plays a pivotal role in the function of cells and can induce apoptosis in various cancer cells, including Raji B lymphoma. However, the metabolic mechanism of Zn-induced apoptosis in Raji cells has not been explored. In this study, we performed global metabolic profiling using UPLC−Orbitrap−MS to assess the apoptosis of Raji cells induced by Zn ions released from ZnO nanorods. Multivariate analysis and database searches identified altered metabolites. Furthermore, the differences in the phosphorylation of 1380 proteins were also evaluated by Full Moon kinase array to discover the protein associated Zn−induced apoptosis. From the results, a prominent increase in glycerophosphocholine and fatty acids was observed after Zn ion treatment, but only arachidonic acid was shown to induce apoptosis. The kinase array revealed that the phosphorylation of p53, GTPase activation protein, CaMK2a, PPAR−γ, and PLA−2 was changed. From the pathway analysis, metabolic changes showed earlier onset than protein signaling, which were related to choline metabolism. LC−MS analysis was used to quantify the intracellular choline concentration, which decreased after Zn treatment, which may be related to the choline consumption required to produce choline-containing metabolites. Overall, we found that choline metabolism plays an important role in Zn-induced Raji cell apoptosis.