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DURAIPRASANNAVENKATESH,maria batool,Masaud Shah,최상돈 생화학분자생물학회 2015 Experimental and molecular medicine Vol.47 No.-
Middle East respiratory syndrome coronavirus (MERS-CoV) causes high fever, cough, acute respiratory tract infection and multiorgan dysfunction that may eventually lead to the death of the infected individuals. MERS-CoV is thought to be transmitted to humans through dromedary camels. The occurrence of the virus was first reported in the Middle East and it subsequently spread to several parts of the world. Since 2012, about 1368 infections, including ~ 487 deaths, have been reported worldwide. Notably, the recent human-to-human ‘superspreading’ of MERS-CoV in hospitals in South Korea has raised a major global health concern. The fatality rate in MERS-CoV infection is four times higher compared with that of the closely related severe acute respiratory syndrome coronavirus infection. Currently, no drug has been clinically approved to control MERS-CoV infection. In this study, we highlight the potential drug targets that can be used to develop anti-MERS-CoV therapeutics.
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Durai, Prasannavenkatesh,Govindaraj, Rajiv Gandhi,Choi, Sangdun Published by Blackwell Pub. on behalf of the Feder 2013 The FEBS journal Vol.280 No.23
<P>Proinflammatory responses by Toll‐like receptors (TLRs) to malaria infection are considered to be a significant factor in suppressing pathogen growth and in disease control. The key protozoan parasite <I>Plasmodium falciparum</I> causes malaria through glycosylphosphatidylinositols (GPIs), which induce the host immune response mainly via TLR2 signalling. Experimental studies have suggested that malarial GPIs from <I>P. falciparum</I> are recognized by the TLR2 subfamily. However, the interaction site and their involvement in the activation mechanism are still unknown. A better understanding of the detailed structure of the TLR–GPI interaction is important for the design of more effective anti‐malarial therapeutics. We used a molecular docking method to predict the binding regions of malarial GPIs with the TLR2 subfamily members. We also employed molecular dynamics simulations and principal component analysis to understand ligand‐induced conformational changes of the TLR2 subfamily. We observed the expected structural changes upon ligand binding, and significant movements were found in loop regions located in the ligand‐binding site of the TLR2 subfamily. We further propose that the binding modes of malarial GPIs are similar to lipopeptides, and that the lipid portions of the ligands could play an essential role in selective dimerization of the TLR2 subfamily.</P>
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Durai, Prasannavenkatesh,Batool, Maria,Shah, Masaud,Choi, Sangdun Nature Publishing Group 2015 Experimental and molecular medicine Vol.47 No.8
<P>Middle East respiratory syndrome coronavirus (MERS-CoV) causes high fever, cough, acute respiratory tract infection and multiorgan dysfunction that may eventually lead to the death of the infected individuals. MERS-CoV is thought to be transmitted to humans through dromedary camels. The occurrence of the virus was first reported in the Middle East and it subsequently spread to several parts of the world. Since 2012, about 1368 infections, including ~487 deaths, have been reported worldwide. Notably, the recent human-to-human ‘superspreading' of MERS-CoV in hospitals in South Korea has raised a major global health concern. The fatality rate in MERS-CoV infection is four times higher compared with that of the closely related severe acute respiratory syndrome coronavirus infection. Currently, no drug has been clinically approved to control MERS-CoV infection. In this study, we highlight the potential drug targets that can be used to develop anti-MERS-CoV therapeutics.</P>
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3,6-Dihydroxyflavone Has Antituberculosis Activity and Suppresses Lung Inflammation
곽철희,이영준,전다솜,DURAIPRASANNAVENKATESH,류성원,김양미 대한화학회 2017 Bulletin of the Korean Chemical Society Vol.38 No.8
The antimycobacterial and anti-inflammatory effects of 3,6-dihydroxyflavone (3,6-DHF), a flavonoid with anticancer and antibacterial activities, were investigated in lipopolysaccharide (LPS)-stimulated human lung fibroblast MRC-5 cells. 3,6-DHF had antimycobacterial effects on Mycobacterium tuberculosis (Mtb) H37Rv, multidrug-resistant, and extensively drug-resistant clinical isolates with mean minimum inhibitory concentrations of 25, 100, and 100 µg/mL, respectively. 3,6-DHF bound Mtb β-ketoacyl-acyl carrier protein synthase III (mtKASIII) with high affinity through hydrogen bonding of 3,6-DHF of A-ring 6-hydroxyl and C-ring 3-hydroxyl groups with Tyr304 and Gly209 of mtKASIII. Comparison of 3,6-DHF and 3,6,3′,4′-tetrahydroxyflavone (3,6,3′,4′-THF) activities revealed that 3,6,3′,4′-THF did not have anti-tuberculosis (TB) activity, implying that increased hydrophilicity decreases TB membrane permeabilization. 3,6-DHF reduced tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-12, IL-1β, and matrix metalloproteinase (MMP)-1 mRNA levels and suppressed phosphorylation levels of extracellular signal-regulated kinase (ERK) in LPS-stimulated MRC-5 cells. These data indicate that 3,6-DHF could be developed as a potential anti-TB drug, which also suppresses lung inflammation.
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Pavithra K. Balasubramanian,김지은,손까비,DURAIPRASANNAVENKATESH,김양미 대한화학회 2019 Bulletin of the Korean Chemical Society Vol.40 No.1
Toll-like receptors are membrane-bound proteins which plays a vital role in the regulation of innate immune response which is involved in various inflammatory disorders. 3,6-Dihydroxyflavone (3,6-DHF) is a known chemo preventive agent which is used in the treatment of various cancers including breast cancer and an effective JNK kinase inhibitor which can efficiently block the TLR2-mediated signaling pathways. In this current study, we have explored inhibition of 3,6-DHF in TLR2/TLR1 heterodimerization. We stimulated HEK cells by Pam3CSK4 which specifically induced inflammation through TLR2/TLR1 binding. Secretion of the inflammatory cytokine in Pam3CSK4-induced HEK293-hTLR2 cells was considerably reduced by 3,6-DHF, implying that 3,6-DHF inhibited Pam3CSK4-induced TLR2/TLR1 signaling specifically. In addition, 3,6-DHF did not cause severe cytotoxicity against human embryonic kidney (HEK) cells at high concentration up to 100??M. The binding affinity of 3,6-DHF to TLR2 and TLR1 was explored with 10?5 affinity using bio-layer interferometry and molecular docking studies identified the important active site residues that participate in the inhibition of TLR2/TLR1 heterodimerization. Our results showed that 3,6-DHF inhibits TLR2-mediated inflammatory signaling by direct binding and the insights in designing more potent drug candidates by targeting the interacting crucial active site residues in TLR2/TLR1.
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