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Five New Stilbenes from the Stem Bark of Artocarpus communis
Susanna T. S. Chan,Wendy L. Popplewell,Heidi R. Bokesch,Tawnya C. McKee,Kirk R. Gustafson 한국생약학회 2018 Natural Product Sciences Vol.24 No.4
Five new prenylated stilbenes (1 - 5), along with the known compounds cudraflavone C, trans-4-isopentenyl-3,5,2',4'-terahydroxystilbene, trans-4-(3-methyl-E-but-1-enyl)-3,5,2',4'-tetrahydroxystilbene, pannokin G, cycloartobiloxanthone, artonin P, morusin, artocarpin, artonin E, kuwanon C, artobiloxanthone, and artoindonesianin C (6 - 17) were isolated from the stem bark of the tropical tree Artocarpus communis. The structures were established by NMR spectroscopic analysis, MS studies, and comparison with spectral data reported in the literature.
Koo, Taeyoung,Lu-Nguyen, Ngoc B.,Malerba, Alberto,Kim, Eunji,Kim, Daesik,Cappellari, Ornella,Cho, Hee-Yeon,Dickson, George,Popplewell, Linda,Kim, Jin-Soo American Society of GeneCell Therapy 2018 Molecular therapy Vol.26 No.6
<▼1><P>Duchenne muscular dystrophy (DMD) is a fatal, X-linked muscle-wasting disease caused by mutations in the <I>DMD</I> gene. In 51% of DMD cases, a reading frame is disrupted because of deletion of several exons. Here, we show that CjCas9 derived from <I>Campylobacter jejuni</I> can be used as a gene-editing tool to correct an out-of-frame <I>Dmd</I> exon in <I>Dmd</I> knockout mice. Herein, we used Cas9 derived from <I>S. pyogenes</I> to generate <I>Dmd</I> knockout mice with a frameshift mutation in <I>Dmd</I> gene. Then, we expressed CjCas9, its single-guide RNA, and the EGFP gene in the <I>tibialis anterior</I> muscle of the <I>Dmd</I> knockout mice using an all-in-one adeno-associated virus (AAV) vector. CjCas9 cleaved the target site in the <I>Dmd</I> gene efficiently <I>in vivo</I> and induced small insertions or deletions at the target site. This treatment resulted in conversion of the disrupted <I>Dmd</I> reading frame from out of frame to in frame, leading to the expression of dystrophin in the sarcolemma. Importantly, muscle strength was enhanced in the CjCas9-treated muscles, without off-target mutations, indicating high efficiency and specificity of CjCas9. This work suggests that <I>in vivo DMD</I> frame correction, mediated by CjCas9, has great potential for the treatment of DMD and other neuromuscular diseases.</P></▼1><▼2><P>Koo et al. demonstrate that CjCas9 derived from <I>Campylobacter jejuni</I> can be used as a gene-editing tool to correct an out-of-frame <I>Dmd</I> exon in <I>Dmd</I> knockout mice. This study provides the therapeutic utility of CjCas9 for the treatment of Duchenne muscular dystrophy and other neuromuscular diseases.</P></▼2>