Junho Kim
Sungkyunkwan University · Biochemistry, Genetics and Molecular Biology
About the Lab
Professor Junho Kim's research lab specializes in biomedical and bioengineering research, focusing on the molecular mechanisms of inflammatory diseases and cancer, particularly through the investigation of natural compounds and their pharmacological effects. The lab explores the therapeutic potential of flavonoids and synthetic derivatives in modulating immune responses and signaling pathways, such as NF-κB and iNOS, in macrophage and cancer cell models. Additionally, the lab engages in clinical research related to post-surgical complications, such as post-thyroidectomy hypocalcemia, aiming to identify early predictors and improve patient outcomes. The integration of molecular biology, immunology, and biomedical device development—such as soft-switching power converters—demonstrates a multidisciplinary approach to advancing health technologies.
Research Overview
Research Output Trend
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Selected Papers
15Flavonoids, such as fisetin (3,7,3’,4’-tetrahydroxyflavone), are plant secondary metabolites. It has been reported that fisetin is able to perform numerous pharmacological roles including anti-inflammatory, anti-microbial, and anti-cancer activities; however, the exact anti-inflammatory mechanism of fisetin is not understood. In this study, the pharmacological action modes of fisetin in lipopolysaccharide (LPS)-stimulated macrophage-like cells were elucidated by using immunoblotting analysis, ki
Purpose: The molecular mechanisms that are responsible for the initiation and progression of breast cancers are largely unknown. This study was to analyze the cyclin B1, cdc2, p53 and p16 tumor suppressor genes in human breast cancer. Materials and Methods: To investigate the role of cyclin B1, cdc2, p53 and p16 in the pathogenesis and progression of breast carcinomas, 98 cases of breast cancers were examined by immunohistochemical method. The correlations of cyclin B1, cdc2, p53 and p16 express
Objectives. High incidence of hypocalcemia after thyroidectomy is a major determinant in delay of discharge. Even though many studies have focused on the search for reliable early predictors of postoperative hypocalcemia, definitions of hypocalcemia are diverse; therefore, interpretation and application of previously reported findings may not be easy. We aimed to elucidate diverse patterns of post-thyroidectomy hypocalcemia and to provide reliable early predictors for these different types of hy
This paper presents a new soft-switching boost converter based on the LC resonance and passive clamping technique without additional active switches. The circuit achieves high efficiency and low voltage stress by adopting a soft switching method using LC resonance. This paper gives a mathematical analysis of each mode and a detailed design procedure of the proposed boost converter. First of all, the operational principles are verified through simulation results. Then, according to the design pro
Summary Alzheimer’s disease (AD) is an age-associated neurodegenerative disorder characterized by progressive neuronal loss and pathological accumulation of the misfolded proteins amyloid-β and tau 1,2 . Neuroinflammation mediated by microglia and brain-resident macrophages plays a crucial role in AD pathogenesis 1–5 , though the mechanisms by which age, genes, and other risk factors interact remain largely unknown. Somatic mutations accumulate with age and lead to clonal expansion of many cell
(E)-3-Phenyl-1-(2-pyrrolyl)-2-propenone (PPP) is a pyrrole derivative of chalcone, in which the B-ring of chalcone linked to bcarbon is replaced by pyrrole group. While pyrrole has been studied for possible Src inhibition activity, chalcone, especially the substituents on the B-ring, has shown pharmaceutical, anti-inflammatory, and anti-oxidant properties via inhibition of NF-kB activity. Our study is aimed to investigate whether this novel synthetic compound retains or enhances the pharmaceutic
Amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer's disease (AD) represent two major categories of neurodegenerative disorders—TDP-43 and tau proteinopathies—for which the mechanisms driving neuronal death remain unclear. Single-cell whole-genome sequencing of 469 neurons from C9ORF72 ALS, C9ORF72 FTD, AD, and control brains revealed increased somatic single nucleotide variants (sSNVs) and insertions/deletions (sIndels) in all three diseases. Mutational signature
Abstract While ATM loss-of-function has long been identified as the genetic cause of Ataxia Telangiectasia (A-T), how this genetic mutation leads to selective and progressive degeneration of cerebellar Purkinje and granule neurons remains unclear. ATM expression is enriched in microglia, the resident immune cell of the central nervous system, throughout cerebellar development and adulthood. Microglial activation has been strongly implicated in neurodegenerative disease and observed in rodent and
Previously, we found that KTH-13 isolated from the butanol fraction of Cordyceps bassiana (Cb-BF) displayed anti-cancer activity. To improve its antiproliferative activity and production yield, we employed a total synthetic approach and derivatized KTH-13 to obtain chemical analogs. In this study, one KTH-13 derivative, 4-(tert-butyl)-2,6-bis(1-phenylethyl)phenol (KTH-13-t-Bu), was selected to test its anti-cancer activity. KTH-13-t-Bu diminished the proliferation of C6 glioma, MDA-MB-231, LoVo,
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease linked to exposure to repetitive head impacts (RHI), yet little is known about its pathogenesis. Applying two single-cell whole-genome sequencing methods to hundreds of neurons from prefrontal cortex of 15 individuals with CTE and 4 with RHI without CTE, we revealed increased somatic single-nucleotide variants in CTE, exhibiting a pattern previously reported in Alzheimer's disease (AD). Furthermore, we discovered high burdens
Abstract Mutations that occur in cells of the body, called somatic mutations, cause human diseases including cancer and some neurological disorders 1 . In a recent study published in Nature, Lee et al. 2 (hereafter “the Lee study”) reported somatic copy number gains of the APP gene, a known risk locus of Alzheimer’s disease (AD), in the neurons of AD-patients and controls (69% vs 25% of neurons with at least one APP copy gain on average). The authors argue that the mechanism of these copy number
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that is linked to exposure to repetitive head impacts (RHI), yet little is known about its pathogenesis. Applying two single-cell whole-genome sequencing methods to hundreds of neurons from prefrontal cortex of 15 individuals with CTE, and 4 with RHI without CTE, revealed increased somatic single-nucleotide variants in CTE, resembling a pattern previously reported in Alzheimer's disease (AD). Furthermore, we discovered remarka
Alzheimer's disease (AD) is a neurodegenerative condition characterized by microglia-mediated neuroinflammation. Deep (>1,000×) panel sequencing of 311 brain samples revealed enrichment of somatic single-nucleotide variants (sSNVs) in cancer driver genes in AD brains, especially in genes associated with clonal hematopoiesis (CH). These sSNVs were associated with clonal expansion and carried by both microglia-like brain macrophages (MLBMs) in multiple brain regions as well as paired blood, sugges
Low-level somatic mutations in the human brain are implicated in various neurological disorders. The contribution of low-level brain somatic mutations to autism spectrum disorder (ASD), however, remains poorly understood. Here, we performed high-depth exome sequencing with an average read depth of 559.3x in 181 cortical, cerebellar, and peripheral tissue samples to identify brain somatic single nucleotide variants (SNVs) in 24 ASD subjects and 31 controls. We detected ~2.4 brain somatic SNVs per
Research Areas
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