Jong-Bum Kwon
Ewha Womans University · 生化学・遺伝学・分子生物学
研究室紹介
Professor Jong-Bum Kwon's research lab focuses on the molecular mechanisms underlying genome stability, chromatin remodeling, and inflammatory signaling in cancer and neuroinflammatory diseases. The lab investigates the roles of deubiquitinating enzymes—particularly BAP1 and its regulation of chromatin remodelers like INO80—in DNA replication, fork stability, and tumor suppression. A central theme is understanding how post-translational modifications and epigenetic regulators control gene expression and cellular responses to stress, with implications for cancer and central nervous system disorders. The lab also explores novel epigenetic targets, such as non-BET bromodomain proteins, for therapeutic intervention.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15In this study, we demonstrate that TGF-beta inhibits TNF-alpha expression, and induces/enhances IL-6 expression by primary rat astrocytes. Treatment of astrocytes with TGF-beta alone had no effect on TNF-alpha mRNA or protein expression; however, TGF-beta suppressed induction of TNF-alpha expression by three different stimuli (IFN-gamma/LPS, IFN-gamma/IL-1 beta, TNF-alpha) at both the protein and mRNA level. The extent of TGF-beta-mediated inhibition was greatest when astrocytes were pretreated
BAP1 is a ubiquitin C-terminal hydrolase domain-containing deubiquitinase with a wide array of biological activities. Studies in which advanced sequencing technologies were used have uncovered a link between BAP1 and human cancer. Somatic and germline mutations of the BAP1 gene have been identified in multiple human cancers, with a particularly high frequency in mesothelioma, uveal melanoma and clear cell renal cell carcinoma. BAP1 cancer syndrome highlights that all carriers of inherited BAP1-i
The recovery from replication stress by restarting stalled forks to continue DNA synthesis is crucial for maintaining genome stability and thereby preventing diseases such as cancer. We previously showed that BRCA1-associated protein 1 (BAP1), a nuclear deubiquitinase with tumor suppressor activity, promotes replication fork progression by stabilizing the INO80 chromatin remodeler via deubiquitination and recruiting it to replication forks during normal DNA synthesis. However, whether BAP1 funct
Tumor necrosis factor-α (TNF-α) contributes to demyelinating diseases in the central nervous system. Astrocytes, the major glial cells in the CNS, do not constitutively express TNF-α, but the TNF-α gene is transcriptionally activated in response to a variety of stimuli, including TNF-α itself. Because of the importance of TNF-α in the CNS, we examined the mechanisms underlying transcriptional regulation of the TNF-α gene in astrocytes. In transient transfection assays, a plasmid construct contai