Junho Lee
Korea University · 生化学・遺伝学・分子生物学
研究室紹介
Professor Junho Lee's research lab focuses on molecular and cellular mechanisms underlying neurodegenerative diseases, mitochondrial dysfunction, and plant flowering regulation. The lab investigates the role of amyloid-beta in mitochondrial toxicity and neuronal apoptosis, explores the regulation of flowering time through transcription factors like SOC1 and their interaction with environmental and hormonal signals, and develops advanced functional materials such as thermoelectric polymers for energy applications. The integration of molecular biology, neuroscience, and materials science defines the interdisciplinary nature of the lab's research.
Research Overview
Research Output Trend
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Selected Papers
15SOC1, encoding a MADS box transcription factor, integrates multiple flowering signals derived from photoperiod, temperature, hormone, and age-related signals. SOC1 is regulated by two antagonistic flowering regulators, CONSTANS (CO) and FLOWERING LOCUS C (FLC), which act as floral activator and repressor, respectively. CO activates SOC1 mainly through FT but FLC represses SOC1 by direct binding to the promoter. SOC1 is also activated by an age-dependent mechanism in which SPL9 and microRNA156 ar
Amyloid beta peptide (Abeta) is a neurotoxic metabolic product of the amyloid precursor protein (APP). Abeta is strongly implicated in the pathology of Alzheimer's disease (AD) and can be formed intracellularly. In this study, we show that the addition of Abeta to isolated mouse brain mitochondria can directly induce cytochrome c (Cyt c) release and mitochondrial swelling, which were partially inhibited by cyclosporin A (CsA). These results suggest that the Abetaaccumulated intracellularly by AP
Chloroplasts and mitochondria are endosymbiotic organelles thought to be derived from endosymbiotic bacteria. In present-day eukaryotic cells, these two organelles play pivotal roles in photosynthesis and ATP production. In addition to these major activities, numerous reactions, and cellular processes that are crucial for normal cellular functions occur in chloroplasts and mitochondria. To function properly, these organelles constantly communicate with the surrounding cellular compartments. This
A semicrystalline p-type thermoelectric conjugated polymer based on a polymer backbone of cyclopentadithiophene and benzothiadiazole, poly[(4,4′-(bis(hexyldecylsulfanyl)methylene)cyclopenta[2,1-b:3,4-b′]dithiophene)-alt-(benzo[c][1,2,5]thiadiazole)] (PCPDTSBT), is designed and synthesized by replacing normal alkyl side-chains with bis(alkylsulfanyl)methylene substituents. The sp2-hybridized olefinic bis(alkylsulfanyl)methylene side-chains and the sulfur–sulfur (S–S) chalcogen interactions extend
AIMS: Autoimmunity plays an important role in the pathogenesis of viral myocarditis and giant cell myocarditis. Experimental autoimmune myocarditis (EAM) is a mouse model of myocarditis that is induced by cardiac myosin. Tolerogenic dendritic cells (tDCs) are used as anti-inflammatory and immunosuppressive targets in a number of autoimmune disease models, but their effect on EAM has not been addressed. The aim of this study was to investigate whether tDC therapy in an EAM mouse model can suppres
In previous reports we demonstrated that ginsenosides, active ingredients of Panax ginseng, affect some subsets of voltage-dependent Ca(2+) channels in neuronal cells expressed in Xenopus laevis oocytes. However, the major component(s) of ginseng that affect cloned Ca(2+) channel subtypes such as alpha(1C) (L)-, alpha(1B) (N)-, alpha(1A) (P/Q)-, a1E (R)- and a1G (T) have not been identified. Here, we used the two-microelectrode volt-age clamp technique to characterize the effects of ginsenosides
In previous reports we demonstrated that ginsenosides, active ingredients of Panax ginseng, affect some subsets of voltage-dependent Ca2+ channels in neuronal cells expressed in Xenopus laevis oocytes. However, the major component(s) of ginseng that affect cloned Ca2+ channel subtypes such as α1C (L)-, α1B (N)-, α1A (P/Q)-, α1E (R)- and α1G (T) have not been identified. Here, we used the two-microelectrode voltage clamp technique to characterize the effects of ginsenosides and ginsenoside metabo
Intensive glucose control increases the all-cause mortality in type 2 diabetes mellitus (T2DM); however, the underlying mechanisms remain unclear. We hypothesized that strict diet control to achieve euglycemia in diabetes damages major organs, increasing the mortality risk. To evaluate effects on major organs when euglycemia is obtained by diet control, we generated a model of end-stage T2DM in 13-week-old Sprague-Dawley rats by subtotal pancreatectomy, followed by ad libitum feeding for 5 weeks
Abstract Semiconductors have long been perceived as a prerequisite for solid-state transistors. Although switching principles for nanometer-scale devices have emerged based on the deployment of two-dimensional (2D) van der Waals heterostructures, tunneling and ballistic currents through short channels are difficult to control, and semiconducting channel materials remain indispensable for practical switching. In this study, we report a semiconductor-less solid-state electronic device that exhibit
As the global population ages, the prevalence of Parkinson's disease (PD) is steadily on the rise. PD demonstrates chronic and progressive characteristics, and many cases can transition into dementia. This increases societal and economic burdens, emphasizing the need to find effective treatments. Among the widely recognized causes of PD is the abnormal accumulation of proteins, and autophagy dysfunction accelerates this accumulation. The resultant Lewy bodies are also commonly found in Alzheimer