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Author

Jong Soon Kang

Other affiliations: KAIST
Bio: Jong Soon Kang is an academic researcher from Korea Research Institute of Bioscience and Biotechnology. The author has contributed to research in topics: Cytotoxicity & Tumor necrosis factor alpha. The author has an hindex of 38, co-authored 196 publications receiving 4083 citations. Previous affiliations of Jong Soon Kang include KAIST.


Papers
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TL;DR: It is demonstrated that the SLC1A5 variant is a mitochondrial glutamine transporter for cancer metabolic reprogramming by transporting glutamine into mitochondria.

180 citations

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TL;DR: PG-mediated induction of NO production and iNOS mRNA expression in macrophages is mediated, at least in part, by TLR4/NF-kappa B signaling pathway.

125 citations

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TL;DR: It is demonstrated that silymarin has a protective effect against endotoxin-induced sepsis, and suggested that this is mediated, at least in part, by the inhibitory effect of sily marin on the production of IL-1beta and PGE2.

124 citations

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TL;DR: It is suggested that silymarin inhibits nitric oxide production and inducible nitric-oxide synthase (iNOS) gene expression in macrophages by inhibiting NF-kappaB/Rel activation.
Abstract: Silymarin, a polyphenolic flavonoid antioxidant, is known to have anti-inflammatory, hepatoprotective, and anticarcinogenic effects. In the present study, we report the inhibitory effect of silymarin on nitric oxide production and inducible nitric-oxide synthase (iNOS) gene expression in macrophages. In vivo administration of silymarin attenuated nitric oxide production by peritoneal macrophages in lipopolysaccharide (LPS)-treated mice. Silymarin also dose dependently suppressed the LPS-induced production of nitric oxide in isolated mouse peritoneal macrophages and RAW 264.7, a murine macrophage-like cell line. Moreover, iNOS mRNA and its protein expression were completely abrogated by silymarin in LPS-stimulated RAW 264.7 cells. To further investigate the mechanism responsible for the inhibition of iNOS gene expression by silymarin, we examined the effect of silymarin on LPS-induced nuclear factor-kappaB (NF-kappaB)/Rel activation, which regulates various genes involved in immune and inflammatory response. In RAW 264.7 cells, the LPS-induced DNA binding activity of NF-kappaB/Rel was significantly inhibited by silymarin, and this effect was mediated through the inhibition of the degradation of inhibitory factor-kappaB. Silymarin also inhibited tumor necrosis factor-alpha-induced NF-kappaB/Rel activation, whereas okadaic acid-induced NF-kappaB/Rel activation was not affected. NF-kappaB/Rel-dependent reporter gene expression was also suppressed by silymarin in LPS-stimulated RAW 264.7 cells. Further study showed that silymarin suppressed the production of reactive oxygen species generated by H(2)O(2) in RAW 264.7 cells. Collectively, these results suggest that silymarin inhibits nitric oxide production and iNOS gene expression by inhibiting NF-kappaB/Rel activation. Furthermore, the radical-scavenging activity of silymarin may explain its inhibitory effect on NF-kappaB/Rel activation.

97 citations

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TL;DR: Results indicate that PCP activates macrophages through theTLR4 signaling pathway, which suggests that TLR4 is the membrane receptor for PCP.

94 citations


Cited by
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Journal ArticleDOI
TL;DR: This review covers the literature published in 2014 for marine natural products, with 1116 citations referring to compounds isolated from marine microorganisms and phytoplankton, green, brown and red algae, sponges, cnidarians, bryozoans, molluscs, tunicates, echinoderms, mangroves and other intertidal plants and microorganisms.

4,649 citations

01 Mar 2017
TL;DR: Recent advances in understanding of mTOR function, regulation, and importance in mammalian physiology are reviewed and how the mTOR-signaling network contributes to human disease is highlighted.
Abstract: The mechanistic target of rapamycin (mTOR) coordinates eukaryotic cell growth and metabolism with environmental inputs, including nutrients and growth factors. Extensive research over the past two decades has established a central role for mTOR in regulating many fundamental cell processes, from protein synthesis to autophagy, and deregulated mTOR signaling is implicated in the progression of cancer and diabetes, as well as the aging process. Here, we review recent advances in our understanding of mTOR function, regulation, and importance in mammalian physiology. We also highlight how the mTOR signaling network contributes to human disease and discuss the current and future prospects for therapeutically targeting mTOR in the clinic.

2,014 citations

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TL;DR: The authors show that the PHD1 controls muscle mass in a hydroxylation-independent manner and prevents the degradation of leucine sensor LRS during oxygen and amino acid depletion to ensure effective mTORC1 activation in response to leucines.
Abstract: mTORC1 is an important regulator of muscle mass but how it is modulated by oxygen and nutrients is not completely understood. We show that loss of the prolyl hydroxylase domain isoform 1 oxygen sensor in mice (PHD1KO) reduces muscle mass. PHD1KO muscles show impaired mTORC1 activation in response to leucine whereas mTORC1 activation by growth factors or eccentric contractions was preserved. The ability of PHD1 to promote mTORC1 activity is independent of its hydroxylation activity but is caused by decreased protein content of the leucyl tRNA synthetase (LRS) leucine sensor. Mechanistically, PHD1 interacts with and stabilizes LRS. This interaction is promoted during oxygen and amino acid depletion and protects LRS from degradation. Finally, elderly subjects have lower PHD1 levels and LRS activity in muscle from aged versus young human subjects. In conclusion, PHD1 ensures an optimal mTORC1 response to leucine after episodes of metabolic scarcity.

1,466 citations

Journal ArticleDOI
TL;DR: The evaluation of botanical polysaccharide isolated from a wide array of different species of flora provides a unique opportunity for the discovery of novel therapeutic agents and adjuvants that exhibit beneficial immunomodulatory properties.

1,075 citations

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TL;DR: This review summarizes the phytochemical, pharmacological and pharmacokinetics data, together with the clinical and adverse effects of licorice and its bioactive components.
Abstract: The roots and rhizomes of licorice (Glycyrrhiza) species have long been used worldwide as a herbal medicine and natural sweetener. Licorice root is a traditional medicine used mainly for the treatment of peptic ulcer, hepatitis C, and pulmonary and skin diseases, although clinical and experimental studies suggest that it has several other useful pharmacological properties such as antiinflammatory, antiviral, antimicrobial, antioxidative, anticancer activities, immunomodulatory, hepatoprotective and cardioprotective effects. A large number of components have been isolated from licorice, including triterpene saponins, flavonoids, isoflavonoids and chalcones, with glycyrrhizic acid normally being considered to be the main biologically active component. This review summarizes the phytochemical, pharmacological and pharmacokinetics data, together with the clinical and adverse effects of licorice and its bioactive components.

1,053 citations