Eun-Sung Kim
Kyung Hee University · Medicine
About the Lab
Professor Eun-Sung Kim's research lab focuses on the intersection of cellular biology, autophagy, and melanogenesis, exploring how subcellular organelle dynamics—particularly mitochondrial morphology and autophagic flux—affect pigmentation processes in melanocytes and melanoma cells. The lab investigates signaling pathways such as ROS-ERK and molecular regulators like Drp1, OPA1, ATG5, and ARP101 to elucidate their roles in melanin regulation. Additionally, the lab examines sociotechnical and policy dimensions of science and technology, including technological convergence, risk communication in public health crises (e.g., MERS), and climate policy in the context of developmental state models. This interdisciplinary approach bridges molecular mechanisms with societal implications in health and environmental policy.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Mitochondrial dynamics control mitochondrial functions as well as their morphology. However, the role of mitochondrial dynamics in melanogenesis is largely unknown. Here, we show that mitochondrial dynamics regulate melanogenesis by modulating the ROS-ERK signaling pathway. Genetic and chemical inhibition of Drp1, a mitochondrial fission protein, increased melanin production and mitochondrial elongation in melanocytes and melanoma cells. In contrast, down-regulation of OPA1, a mitochondria fusio
The United States (US), European Union (EU), and South Korea had different definitions and visions of technological convergence before interacting with each other from the late 2000s. The Korean government has used Western policies as a benchmark but produces a distinct concept of technological convergence due to a particular imaginary of technology as a vehicle for national economic growth. This sociotechnical imaginary of technological developmentalism influences Korea’s translation of technol
Autophagy degrades cellular components and organelles through a cooperative process involving autophagosomes and lysosomes. Although autophagy is known to mainly regulate the turnover of cellular components, the role of autophagy in melanogenesis has not been well addressed. Here, we show that inhibition of autophagy suppresses the antimelanogenesis activity of resveratrol (RSV), a well-known antimelanogenic agent. RSV strongly increased autophagy in melanocytes. However, the depletion of ATG5 s
위험소통은 2015년 상반기 발생한 메르스 위기의 가장 큰 문제로 지적되어왔다. 감염자가 방문한 병원의 이름을 정부가 늦게 공개하는 바람에 메르스가 여러 병원으로 확산되었을 뿐만 아니라 대중들의 공포가 증폭되었다. 이 글은 이 메르스 위기 당시 정부에 의해 이루어진 위험소통이 실패하게 된 사회적 원인을 분석하고 그 개선방안을 제시한다. 이 글은 정부의 위험소통전략을 “결핍모델”로 해석하면서 “맥락적 모델”의 관점에서 결핍 모델의 한계와 문제점을 분석한다. 특히 위험소통에서의 과학적 불확실성, 이해관계, 정부의 신뢰, 대중의 정체성 형성 및 낙인효과에 대한 함의를 분석한다. 마지막으로 메르스와 같은 신종전염병 관련 위험소통을 개선하기 위한 방안을 제시한다.
The climate change policy design of the Lee Myung-bak administration was the outcome of interest group politics around the greenhouse gas and energy target management scheme, carbon taxes, and the emission-trading scheme. Using qualitative methods, this research examines powerful stakeholders and their interests at play in Korea’s climate change policymaking processes. It also links the political economy of climate change policy to the legacy of the ‘developmental state’ and examines environment
Autophagy is a cooperative process between autophagosomes and lysosomes that degrades cellular organelles. Although autophagy regulates the turnover of cellular components, its role in melanogenesis is not clearly established. Previously, we reported that ARP101 induces autophagy in various cancer cells. Here, we show that ARP101 inhibits melanogenesis by regulation of autophagy. ARP101 inhibited α-MSH-stimulated melanin synthesis and suppressed the expression of tyrosinase and TRP1 in immortali
Human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) secrete various beneficial molecules, which have anti-apoptotic activity and cell proliferation. However, the effect of hUCB-MSCs in melanogenesis is largely unclear. In this study, we show that conditioned media (CM) derived from hUCB-MSCs inhibit melanogenesis by regulating microphthalmia-associated transcription factor (MITF) expression via the ERK signalling pathway. Treatment of hUCB-MSC-CM strongly inhibited the alpha-me
Research Areas
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