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3篇 您的检索式:作者名="Aijia Song"
    题名 作者 年代 出处 被引量
1aunalysis of the Genome Sequence of the Medicinal Plant Salvia miltiorrhiza显示文摘Haibin Xu Jingyuan Song Hongmei Luo Yujun Zhang Qiushi Li Yingjie Zhu Jiang Xu Ying Li Chi Song Bo Wang Wei Sun Guoan Shen Xin Zhang Jun Qian Aijia Ji Zhichao Xu Xiang Luo Liu He Chuyuan Li Chao Sun Haixia Yah Guanghong Cui Xiwen Li Xian 'en Li Jianhe Wei Juyan Liu Yitao Wang Alice Hayward David Nelson Zemin Ning Reuben J. Peters Xiaoquan Qi Shilin Chen 2016Molecular Plant2016,9,6:70
2Genomic survey of bZIP transcription factor genes related to tanshinone biosynthesis in Salvia miltiorrhiza显示文摘Tanshinones are a class of bioactive components in the traditional Chinese medicine Salvia miltiorrhiza, and their biosynthesis and regulation have been widely studied. Current studies show that basic leucine zipper(bZIP) proteins regulate plant secondary metabolism, growth and developmental processes. However, the b ZIP transcription factors involved in tanshinone biosynthesis are unknown.Here, we conducted the first genome-wide survey of the b ZIP gene family and analyzed the phylogeny,gene structure, additional conserved motifs and alternative splicing events in S. miltiorrhiza. A total of 70 Smb ZIP transcription factors were identified and categorized into 11 subgroups based on their phylogenetic relationships with those in Arabidopsis. Moreover, seventeen Smb ZIP genes underwent alternative splicing events. According to the transcriptomic data, the Smb ZIP genes that were highly expressed in the Danshen root and periderm were selected. Based on the prediction of b ZIP binding sites in the promoters and the co-expression analysis and co-induction patterns in response to Ag^+ treatment via quantitative real-time polymerase chain reaction(qRT-PCR), we concluded that Smb ZIP7 and Smb ZIP20 potentially participate in the regulation of tanshinone biosynthesis. These results provide a foundation for further functional characterization of the candidate Smb ZIP genes, which have the potential to increase tanshinone production.Yu Zhang Zhichao Xu Aijia Ji Hongmei Luo Jingyuan Song 2018Acta Pharmaceutica Sinica B2018,8,2:14
3Liquiritigenin promotes osteogenic differentiation and prevents bone loss via inducing auto-lysosomal degradation and inhibiting apoptosis显示文摘Osteoporosis(OP)is a debilitating skeletal abnormality involving bone remodeling and bone cell homeostasis characterized by decreased bone strength and high fracture risk.A novel therapeutic intervention for OP by manipulating cellular autophagy-apoptosis processes to promote skeletal homeostasis is presented.Protective effects of the naturally occurring plant extract Liquiritigenin(LG)were demonstrated in an ovariectomy(OvX)-OP mouse model and preosteoblast MC3T3-E1 cells.Micro-CT and histological staining assessments of skeletal phenotype were applied alongside detection of autophagy activity in osteocytes and MC3T3-E1 cells by transmission electron microscopy(TEM).The effects of LG on chloroquine(CQ)-and the apoptosis-inducing TS-treated osteogenic differentiations and status of lysosomes within MC3T3-E1 cells were analyzed by Neutral red,Alizarin red S and alkaline phosphatase(ALP)staining and Western blot assays.Treatment with LG prevented bone loss,increased osteogenic differentiation in vivo and in vitro,and inhibited osteoclast formation to some extent.TEM analyses revealed that LG can improve auto-lysosomal degradation within osteocytes from OVX mice and MC3T3-E1 cells.The abnormal status of lysosomes associated with CQ and TS treatments was notably alleviated by LG which also reduced levels of apoptosis-induced inhibition of osteogenic differentiation and averted abnormal osteogenic differentiation as a consequence of a blockage in autolysosome degradation.Overall,LG stimulates bone growth in Oovx mice through increased osteogenic differentiation and regulation of autophagyapoptosis mechanisms,presenting an auspicious natural therapy for Op.Yu Qiu Yueyang Zhao Zhimin Long Aijia Song Peng Huang Kejian Wang Ling Xu David Paul Molloy Guiqiong He 2023Genes & Diseases2023,10,1:0
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