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Hogyoung Kim

Researcher at Tulane University

Publications -  61
Citations -  2473

Hogyoung Kim is an academic researcher from Tulane University. The author has contributed to research in topics: Microvesicles & Cancer. The author has an hindex of 26, co-authored 54 publications receiving 2026 citations. Previous affiliations of Hogyoung Kim include Louisiana State University & LSU Health Sciences Center New Orleans.

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Cordycepin inhibits lipopolysaccharide-induced inflammation by the suppression of NF-κB through Akt and p38 inhibition in RAW 264.7 macrophage cells

TL;DR: Results suggest that cordycepin inhibits the production of NO production by down-regulation of iNOS and COX-2 gene expression via the suppression of NF-kappaB activation, Akt and p38 phosphorylation, and may provide a potential therapeutic approach for inflammation-associated disorders.
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Manumycin A suppresses exosome biogenesis and secretion via targeted inhibition of Ras/Raf/ERK1/2 signaling and hnRNP H1 in castration-resistant prostate cancer cells.

TL;DR: Manumycin-A (MA), a natural microbial metabolite, was identified as an inhibitor of exosome biogenesis and secretion by castration-resistant prostate cancer (CRPC) C4-2B, but not the normal RWPE-1, cells.
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Poly(ADP-Ribose) Polymerase-1 Is a Determining Factor in Crm1-Mediated Nuclear Export and Retention of p65 NF-κB upon TLR4 Stimulation

TL;DR: It is shown that PARP-1 inhibition by gene knockout, knockdown, or pharmacologic blockade prevented p65 NF-κB nuclear translocation in smooth muscle cells upon TLR4 stimulation, NF-σκB DNA-binding activity, and subsequent inducible NO synthase and ICAM-1 expression.
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Phellinus linteus inhibits inflammatory mediators by suppressing redox-based NF-κB and MAPKs activation in lipopolysaccharide-induced RAW 264.7 macrophage

TL;DR: It is suggested that PLBF inhibits the production of NO and PGE2 through the down-regulation of iNOS and COX-2 gene expression via ROS-based NF-kappaB and MAPKs activation, and may provide a potential therapeutic approach for inflammation-associated disorders.