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Ben Shen - One of the best experts on this subject based on the ideXlab platform.
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Adipostatins A–D from Streptomyces sp. 4875 inhibiting Brugia malayi asparaginyl-tRNA synthetase and killing adult Brugia malayi parasites
The Journal of antibiotics, 2015Co-Authors: Mostafa E. Rateb, Dong Yang, Sanja Vodanovic-jankovic, Michael A. Kron, Ben ShenAbstract:Adipostatins A–D from Streptomyces sp. 4875 inhibiting Brugia malayi asparaginyl-tRNA synthetase and killing adult Brugia malayi parasites
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new ws9326a congeners from streptomyces sp 9078 inhibiting Brugia malayi asparaginyl trna synthetase
Organic Letters, 2012Co-Authors: Sanja Vodanovicjankovic, Michael A. Kron, Ben ShenAbstract:Lymphatic filariasis is caused by the Brugia malayi parasite. Three new congeners of the depsipeptide WS9326A (1), WS9326C (2), WS9326D (3), and WS9326E (4), were isolated from Streptomyces sp. 9078 by using a B. malayi asparaginyl-tRNA synthetase (BmAsnRS) inhibition assay. WS9326D specifically inhibits the BmAsnRS, kills the adult B. malayi parasite, and does not exhibit significant general cytotoxicity to human hepatic cells, representing a new lead scaffold for antifilarial drug discovery.
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tirandamycins from streptomyces sp 17944 inhibiting the parasite Brugia malayi asparagine trna synthetase
Organic Letters, 2011Co-Authors: Sanja Vodanovicjankovic, Michael A. Kron, Nathan A Ledeboer, Shengxiong Huang, Scott R Rajski, Ben ShenAbstract:Lymphatic filariasis is caused by the parasitic nematodes Brugia malayi and Wuchereria bancrofti, and asparaginyl-tRNA synthetase (AsnRS) is considered an excellent antifilarial target. The discovery of three new tirandamycins (TAMs), TAM E (1), F (2), and G (3), along with TAM A (4) and B (5), from Streptomyces sp. 17944 was reported. Remarkably, 5 selectively inhibits the B. malayi AsnRS and efficiently kills the adult B. malayi parasite, representing a new lead scaffold to discover and develop antifilarial drugs.
Michael A. Kron - One of the best experts on this subject based on the ideXlab platform.
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Adipostatins A–D from Streptomyces sp. 4875 inhibiting Brugia malayi asparaginyl-tRNA synthetase and killing adult Brugia malayi parasites
The Journal of antibiotics, 2015Co-Authors: Mostafa E. Rateb, Dong Yang, Sanja Vodanovic-jankovic, Michael A. Kron, Ben ShenAbstract:Adipostatins A–D from Streptomyces sp. 4875 inhibiting Brugia malayi asparaginyl-tRNA synthetase and killing adult Brugia malayi parasites
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new ws9326a congeners from streptomyces sp 9078 inhibiting Brugia malayi asparaginyl trna synthetase
Organic Letters, 2012Co-Authors: Sanja Vodanovicjankovic, Michael A. Kron, Ben ShenAbstract:Lymphatic filariasis is caused by the Brugia malayi parasite. Three new congeners of the depsipeptide WS9326A (1), WS9326C (2), WS9326D (3), and WS9326E (4), were isolated from Streptomyces sp. 9078 by using a B. malayi asparaginyl-tRNA synthetase (BmAsnRS) inhibition assay. WS9326D specifically inhibits the BmAsnRS, kills the adult B. malayi parasite, and does not exhibit significant general cytotoxicity to human hepatic cells, representing a new lead scaffold for antifilarial drug discovery.
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tirandamycins from streptomyces sp 17944 inhibiting the parasite Brugia malayi asparagine trna synthetase
Organic Letters, 2011Co-Authors: Sanja Vodanovicjankovic, Michael A. Kron, Nathan A Ledeboer, Shengxiong Huang, Scott R Rajski, Ben ShenAbstract:Lymphatic filariasis is caused by the parasitic nematodes Brugia malayi and Wuchereria bancrofti, and asparaginyl-tRNA synthetase (AsnRS) is considered an excellent antifilarial target. The discovery of three new tirandamycins (TAMs), TAM E (1), F (2), and G (3), along with TAM A (4) and B (5), from Streptomyces sp. 17944 was reported. Remarkably, 5 selectively inhibits the B. malayi AsnRS and efficiently kills the adult B. malayi parasite, representing a new lead scaffold to discover and develop antifilarial drugs.
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An immunodominant antigen of Brugia malayi is an asparaginyl-tRNA synthetase
FEBS letters, 1995Co-Authors: Michael A. Kron, Kristine Marquard, Michael Härtlein, Steven Price, Reuben LebermanAbstract:Lymphatic filariasis is caused by infection with the filarial nematodes Brugia malayi, Brugia timori, Wuchereria bancrofti and Onchocerca volvulus which collectively infect about 200 million persons throughout the world. Protein sequence homology analysis of a major nematode antigen suggested that it was a class II aminoacyl-tRNA synthetase. The overproduction, purification and verification that the major B. malayi antigen is an asparaginyl-tRNA synthetase is described.
Gary J Weil - One of the best experts on this subject based on the ideXlab platform.
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Effects of Doxycycline on gene expression in Wolbachia and Brugia malayi adult female worms in vivo
Journal of biomedical science, 2012Co-Authors: Ramakrishna U. Rao, Yuefang Huang, Sahar Abubucker, Michael E. Heinz, Seth D. Crosby, Makedonka Mitreva, Gary J WeilAbstract:Background Most filarial nematodes contain Wolbachia symbionts. The purpose of this study was to examine the effects of doxycycline on gene expression in Wolbachia and adult female Brugia malayi.
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Distribution of Brugia malayi larvae and DNA in vector and non-vector mosquitoes: implications for molecular diagnostics.
Parasites & vectors, 2009Co-Authors: Sara M. Erickson, Gary J Weil, Kerstin Fischer, Bruce M. Christensen, Peter U. FischerAbstract:Background The purpose of this study was to extend prior studies of molecular detection of Brugia malayi DNA in vector (Aedes aegypti- Liverpool) and non-vector (Culex pipiens) mosquitoes at different times after ingestion of infected blood.
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Brugia malayi: effects of gamma radiation on adult worms and their intracellular Wolbachia bacteria.
Experimental parasitology, 2005Co-Authors: Ramakrishna U. Rao, Laura J. Atkinson, Robert P. Vanderwall, Gary J WeilAbstract:Prior studies have shown that intracellular Wolbachia endobacteria are necessary for the normal development, reproduction, and survival of filarial nematodes. The purpose of this study was to examine effects of gamma radiation on Wolbachia and reproduction in Brugia malayi adult worms. Worms were exposed to 0, 10, 25, 45, 75, and 105 krad of gamma radiation from a 137cesium source and cultured in vitro for 10 days. Irradiation reduced production of microfilariae in a dose-dependent manner. Embryograms of irradiated female worms showed dose-related abnormalities with arrested development at the early embryo stage. Irradiation reduced the viability of adult worms in a dose-dependent manner, but no lethal effect was observed. Electron microscopy studies showed that irradiation cleared Wolbachia from worm tissues. Real-time polymerase chain reaction studies demonstrated greatly reduced Wolbachia DNA in irradiated worms. These effects are essentially the same as those observed in adult worms treated with doxycycline. These studies suggest that effects of irradiation on reproduction in Brugia malayi may be caused by effects of irradiation on Wolbachia.
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Brugia malayi: effects of antibacterial agents on larval viability and development in vitro.
Experimental parasitology, 2002Co-Authors: Ramakrishna U. Rao, Hanaa Moussa, Gary J WeilAbstract:Abstract Recent studies have suggested that intracellular Wolbachia bacteria are necessary for reproduction and survival of adult filarial worms. We now report results of in vitro studies of effects of antibacterial antibiotics (tetracycline, rifampicin, chloramphenicol, azithromycin, and doxycycline) on Brugia malayi infective larvae (L3) motility and molting. All of the antibiotics tested except chloramphenicol decreased L3 motility by 50% or more at 10 days, with minimal effective concentrations (MECs) of 20–100 μg/ml. Tetracyclines, rifampicin, and chloramphenicol inhibited L3 to L4 molting by 12 days in a concentration- and time-dependent manner, with MECs in the range of 1–20 μg/ml. These studies show that antibiotics active against Rickettsiaceae inhibit B. malayi L3 molting at low concentrations in vitro; higher concentrations kill the larvae. While it is possible that antibiotics directly affect filarial L3, we believe it is more likely that the effects seen are indirect effects related to bacterial killing. Index Descriptors and Abbreviations: Brugia malayi; Filarioidea; Rickettsiaceae; Wolbachia; antibiotics; NI-medium; NCTC-135 and IMDM, Iscove’s Modified Dulbecco’s Medium; FCS, fetal calf serum; Tet, tetracycline; Rif, rifampicin; Chlor, chloramphenicol; Azith, azithromycin; Doxy, doxycycline; IM, incomplete molting larvae; MEC, minimum effective concentration; PCR, polymerase chain reaction.
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immune responses to Brugia malayi paramyosin in rodents after dna vaccination
Vaccine, 1999Co-Authors: Benwen Li, Shaorong Zhang, Kurt C Curtis, Gary J WeilAbstract:Immunization with recombinant Brugia malayi paramyosin protein (BM5) induces partial immunity to this filarial nematode in jirds. The present study examined the effects of intramuscular immunization with plasmid DNA that encodes BM5. DNA-immunized mice produced strong antibody and cell-mediated responses to paramyosin. The protective activity of DNA vaccination with BM5 was tested in jirds. Vaccinated jirds produced strong antibody responses to paramyosin, but adult worm recoveries after challenge were not decreased in vaccinated animals relative to controls. These studies show that DNA vaccination can induce immune responses to filarial antigens in rodents. Further efforts will be needed to achieve the goal of inducing protective immunity to filariasis with this promising new technology.
Sanja Vodanovicjankovic - One of the best experts on this subject based on the ideXlab platform.
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new ws9326a congeners from streptomyces sp 9078 inhibiting Brugia malayi asparaginyl trna synthetase
Organic Letters, 2012Co-Authors: Sanja Vodanovicjankovic, Michael A. Kron, Ben ShenAbstract:Lymphatic filariasis is caused by the Brugia malayi parasite. Three new congeners of the depsipeptide WS9326A (1), WS9326C (2), WS9326D (3), and WS9326E (4), were isolated from Streptomyces sp. 9078 by using a B. malayi asparaginyl-tRNA synthetase (BmAsnRS) inhibition assay. WS9326D specifically inhibits the BmAsnRS, kills the adult B. malayi parasite, and does not exhibit significant general cytotoxicity to human hepatic cells, representing a new lead scaffold for antifilarial drug discovery.
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tirandamycins from streptomyces sp 17944 inhibiting the parasite Brugia malayi asparagine trna synthetase
Organic Letters, 2011Co-Authors: Sanja Vodanovicjankovic, Michael A. Kron, Nathan A Ledeboer, Shengxiong Huang, Scott R Rajski, Ben ShenAbstract:Lymphatic filariasis is caused by the parasitic nematodes Brugia malayi and Wuchereria bancrofti, and asparaginyl-tRNA synthetase (AsnRS) is considered an excellent antifilarial target. The discovery of three new tirandamycins (TAMs), TAM E (1), F (2), and G (3), along with TAM A (4) and B (5), from Streptomyces sp. 17944 was reported. Remarkably, 5 selectively inhibits the B. malayi AsnRS and efficiently kills the adult B. malayi parasite, representing a new lead scaffold to discover and develop antifilarial drugs.
Reuben Leberman - One of the best experts on this subject based on the ideXlab platform.
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An immunodominant antigen of Brugia malayi is an asparaginyl-tRNA synthetase
FEBS letters, 1995Co-Authors: Michael A. Kron, Kristine Marquard, Michael Härtlein, Steven Price, Reuben LebermanAbstract:Lymphatic filariasis is caused by infection with the filarial nematodes Brugia malayi, Brugia timori, Wuchereria bancrofti and Onchocerca volvulus which collectively infect about 200 million persons throughout the world. Protein sequence homology analysis of a major nematode antigen suggested that it was a class II aminoacyl-tRNA synthetase. The overproduction, purification and verification that the major B. malayi antigen is an asparaginyl-tRNA synthetase is described.