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Role of σ-factor (orf21) in clavulanic acid production in Streptomyces clavuligerus NRRL3585
Jnawali, H.N.,Liou, K.,Sohng, J.K. G. Fischer 2011 MICROBIOLOGICAL RESEARCH Vol.166 No.5
A putative sigma factor gene, orf21, was disrupted or overexpressed in the wild-type clavulanic acid (CA) producer Streptomyces clavuligerus NRRL3585 and characterized. An orf21 mutant (Streptomyces clavuligerus HN14) of S. clavuligerus was obtained by insertional inactivation via double-crossover. Although there was little reduction of sporulation in the mutant, the growth pattern was similar between mutant and wild-type. The production was reduced by 10-15% in S. clavuligerus HN14 compared to that in wild-type. Overexpression of orf21 in wild-type cells caused hyperproduction of spores on solid medium and increased clavulanic acid production by 1.43-fold. The overexpression of orf21 in wild-type S. clavuligerus stimulated the expression of the early clavulanic acid genes, ceas2 and cas2, and the regulatory gene, ccaR, as demonstrated by RT-PCR. The elevation of the ceas2, cas2 and ccaR transcripts was consistent with the enhanced production of clavulanic acid.
Jnawali, Hum Nath,Lee, Eunjung,Jeong, Ki-Woong,Shin, Areum,Heo, Yong-Seok,Kim, Yangmee American Chemical Society and American Society of 2014 Journal of natural products Vol.77 No.2
<P>Rhamnetin (<B>1</B>), a commonly occurring plant O-methylated flavonoid, possesses antioxidant properties. To address the potential therapeutic efficacy of <B>1</B>, its anti-inflammatory activity and mode of action in mouse macrophage-derived RAW264.7 cells stimulated with lipopolysaccharide (LPS) or interferon (IFN)-γ were investigated. Rhamnetin (<B>1</B>) suppressed mouse tumor necrosis factor (mTNF)-α, mouse macrophage inflammatory protein (mMIP)-1, and mMIP-2 cytokine production in LPS-stimulated macrophages. A nontoxic dose of <B>1</B> suppressed nitric oxide production. It was found that the anti-inflammatory effects of <B>1</B> are mediated by actions on the p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and cyclooxygenase (COX)-2 pathways in LPS- or IFN-γ-stimulated RAW264.7 cells. It was determined that <B>1</B> binds to human JNK1 (9.7 × 10<SUP>8</SUP> M<SUP>–1</SUP>) and p38 MAPK (2.31 × 10<SUP>7</SUP> M<SUP>–1</SUP>) with good affinity. The binding model showed interactions with the 3′- and 4′-hydroxy groups of the B-ring and the 5-hydroxy group of the A-ring of <B>1</B>. Further, <B>1</B> exerted an anti-inflammatory effect, reducing the levels of pro-inflammatory cytokines and mediators.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/jnprdf/2014/jnprdf.2014.77.issue-2/np400803n/production/images/medium/np-2013-00803n_0008.gif'></P>
Jnawali, Hum Nath,Lee, Eunjung,Jeong, Ki-Woong,Heo, Yong-Seok,Kim, Yangmee Korean Chemical Society 2013 Bulletin of the Korean Chemical Society Vol.34 No.9
Fisetin is a naturally occurring flavonoid with some anti-cancer and anti-inflammation capabilities. In this study, we perform docking studies between human c-Jun N-terminal kinase 1 (JNK 1) and fisetin and proposed a binding model of fisetin and JNK 1, in which the hydroxyl groups of the B ring and oxygen at the 4-position of the C ring play key roles in binding interactions with JNK. Fluorescence quenching and saturation-transfer difference (STD) NMR experiments showed that fisetin exhibits good binding affinity to JNK, $1.32{\times}10^8M^{-1}$. The anti-inflammatory activity of fisetin was also investigated. Fisetin significantly suppressed tumor necrosis factor, the NO production, and macrophage inflammatory cytokine release in LPS-stimulated RAW264.7 mouse macrophages. We found that the anti-inflammatory cascade of fisetin was mediated through the JNK, and cyclooxygenase (COX)-2 pathways. Our findings suggest the potential of fisetin as an anti-inflammatory agent.
Binding Model of Fisetin and Human c-Jun NH2-Terminal Kinase 1 and Its Anti-inflammatory Activity
Jnawali Hum Nath,이은정,정기웅,허용석,김양미 대한화학회 2013 Bulletin of the Korean Chemical Society Vol.34 No.9
Fisetin is a naturally occurring flavonoid with some anti-cancer and anti-inflammation capabilities. In this study, we perform docking studies between human c-Jun N-terminal kinase 1 (JNK 1) and fisetin and proposed a binding model of fisetin and JNK 1, in which the hydroxyl groups of the B ring and oxygen at the 4-position of the C ring play key roles in binding interactions with JNK. Fluorescence quenching and saturation-transfer difference (STD) NMR experiments showed that fisetin exhibits good binding affinity to JNK, 1.32 × 108 M−1. The anti-inflammatory activity of fisetin was also investigated. Fisetin significantly suppressed tumor necrosis factor, the NO production, and macrophage inflammatory cytokine release in LPS-stimulated RAW264.7 mouse macrophages. We found that the anti-inflammatory cascade of fisetin was mediated through the JNK, and cyclooxygenase (COX)-2 pathways. Our findings suggest the potential of fisetin as an anti-inflammatory agent.
Jnawali, Hum Nath,Lee, Eunjung,Shin, Areum,Park, Young Guen,Kim, Yangmee Korean Chemical Society 2014 Bulletin of the Korean Chemical Society Vol.35 No.9
Quercetin is a major dietary flavonoid found in onions, apples, tea, and red wine, and potentially has beneficial effects on disease prevention. We carried out this study to investigate the effect of quercetin on UVB-induced matrix metalloproteinase-1 (MMP-1) expression in human keratinocyte HaCaT cells and to further understand the mechanisms of its action. The anti-inflammatory activity of quercetin was investigated and quercetin significantly suppressed the NO production in LPS-stimulated RAW264.7 mouse macrophages. Post treatment of quercetin decreased UV irradiation-induced phosphorylation of JNK, p38 MAPK, and ERK by 91%, 21%, and 17%, respectively. MMP-1 is mainly responsible for the degradation of dermal collagen during the aging process of human skin and quercetin suppressed the UVB-induced MMP-1 by 94%. Binding studies revealed that quercetin binds to p38 with high binding affinity ($1.85{\times}10^6M^{-1}$). The binding model showed that the 4'-hydroxy groups of the B-ring of quercetin participated in hydrogen bonding interactions with the side chains of Lys53, Glu71, and Asp168 and the 5-hydroxy group of the A-ring formed a hydrogen bond with the backbone amide of Met109. The major finding of this study shows that quercetin inhibits phosphorylation of JNK, p38 MAPK, and ERK pathway leading to the prevention of MMP-1 expression in human keratinocyte HaCaT cells. Therefore, our findings suggested the potentials of quercetin as a skin anti-photoaging agent.