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| 1 | Chromosome-level genome of Himalayan yew provides insights into the origin and evolution of the paclitaxel biosynthetic pathway显示文摘Taxus,commonly known as yew,is a well-known gymnosperm with great ornamental and medicinal value.In this study,by assembling a chromosome-level genome of the Himalayan yew(Taxus wallichiana)with 10.9 Gb in 12 chromosomes,we revealed that tandem duplication acts as the driving force of gene family evolution in the yew genome,resulting in the main genes for paclitaxel biosynthesis,i.e.those encoding the taxadiene synthase,P450s,and transferases,being clustered on the same chromosome.The tandem duplication may also provide genetic resources for the nature to sculpt the core structure of taxoids at different positions and subsequently establish the complex pathway of paclitaxel by neofunctionalization.Furthermore,we confirmed that there are two genes in the cluster encoding isoenzymes of a known enzyme in the paclitaxel biosynthetic pathway.The reference genome of the Himalayan yew will serve as a platform for decoding the complete biosynthetic pathway of paclitaxel and understanding the chemodi-versity of taxoids in gymnosperms. | Jian Cheng Xiao Wang Xiaonan Liu Xiaoxi Zhu Zihe Li Huanyu Chu Qian Wang QianQian Lou Bijun Cai Yiqun Yang Xiaoyun Lu Kai Peng Dingyu Liu Yuwan Liu Lina Lu Huan Liu Ting Yang Qijin Ge Chengcheng Shi Guichun Liu Zhiwei Dong Xun Xu Wen Wang Huifeng Jiang Yanhe Ma | 2021 | Molecular Plant2021，14，7： | 6 |
| 2 | Raising the production of phloretin by alleviation of by-product of chalcone synthase in the engineered yeast显示文摘Phloretin is an important skin-lightening and depigmenting agent from the peel of apples. Although de novo production of phloretin has been realized in microbes using the natural pathway from plants, the efficiency of phloretin production is still not enough for industrial application. Here, we established an artificial pathway in the yeast to produce phloretin via assembling two genes of p-coumaroyl-CoA ligase(4CL) and chalcone synthase(CHS). CHS is a key enzyme which conventionally condenses a CoA-tethered starter with three molecules of malonyl-CoA to form the backbone of flavonoids. However, there was 33% of byproduct generated via CHS by condensing two molecules of malonyl-CoA during the fermentation process. Hence, we introduced a more efficient CHS and improved the supply of malonyl-CoA through two pathways;the by-product ratio was decreased from 33% to 17% and the production of phloretin was improved from 48 to 83.2 mg L^(-1). Finally, a fed-batch fermentation process was optimized and the production of phloretin reached 619.5 mg L^(-1), which was 14-fold higher than that of the previous studies. Our work established a platform for the biosynthesis of phloretin from the low-cost raw material 3-(4-hydroxyphenyl) propanoic acid and also illustrated the potential for industrial scale bio-manufacturing of phloretin. | Chunmei Jiang Xiaonan Liu Xianqing Chen Yi Cai Yibin Zhuang Tian Liu Xiaoxi Zhu Hui Wang Yuwan Liu Huifeng Jiang Wen Wang | 2020 | Science China(Life Sciences)2020，63，11： | 3 |
| 3 | Three-dimensional silk fibroin scaffolds enhance the bone formation and angiogenic differentiation of human amniotic mesenchymal stem cells:a biocompatibility analysis显示文摘Silk fibroin(SF)is a fibrous protein with unique mechanical properties,adjustable biodegradation,and the potential to drive differentiation of mesenchymal stem cells(MSCs)along the osteogenic lineage,making SF a promising scaffold material for bone tissue engineering.In this study,hAMSCs were isolated by enzyme digestion and identified by multiple-lineage differentiation.SF scaffold was fabricated by freeze-drying,and the adhesion and proliferation abilities of hAMSCs on scaffolds were determined.Osteoblast differentiation and angiogenesis of hAMSCs on scaffolds were further evaluated,and histological staining of calvarial defects was performed to examine the cocultured scaffolds.We found that hAMSCs expressed the basic surface markers of MSCs.Collagen type I(COLI)expression was observed on scaffolds cocultured with hAMSCs.The scaffolds potentiated the proliferation of hAMSCs and increased the expression of COL-I in hAMSCs.The scaffolds also enhanced the alkaline phosphatase activity and bone mineralization,and upregulated the expressions of osteogeniorelated factors in vitro.The scaffolds also enhanced the an gioge nic differe ntiati on of hAMSCs.The cocultured scaffolds in creased bone formati on in treating critical calvarial defects in mice.This study first demonstrated that the application of 3D SF scaffolds co-cultured with hAMSCs greatly enhaneed osteogenic differentiation and angiogenesis of hAMSCs in vitro and in vivo.Thus,3D SF scaffolds cocultured with hAMSCs may be a better alter native for bone tissue engin eering. | Yuwan Li Ziming Liu Yaping Tang Qinghong Fan Wei Feng Changqi Luo Guangming Dai Zhen Ge Jun Zhang Gang Zou Yi Liu Ning Hu Wei Huang | 2020 | Acta Biochimica et Biophysica Sinica2020，52，6： | 2 |
| 4 | Preparation and evaluation of an imidazole-coated capillary column for the electrophoretic separation of aromatic acids显示文摘 | LIU Chuenying HO Yuwan PAI Yifen | 2000 | J Chromatogr:A2000，897，12： | 1 |
| 5 | Chaperone-mediated Autophagy Regulates Cell Growth by Targeting SMAD3 in Glioma显示文摘Previous studies suggest that the reduction of SMAD3(mothers against decapentaplegic homolog 3)has a great impact on tumor development,but its exact pathological function remains unclear.In this study,we found that the protein level of SMAD3 was greatly reduced in human-grade IV glioblastoma tissues,in which LAMP2A(lysosome-associated membrane protein type 2A)was significantly up-regulated.LAMP2A is a key ratelimiting protein of chaperone-mediated autophagy(CMA),a lysosome pathway of protein degradation that is activated in glioma.We carefully analyzed the amino-acid sequence of SMAD3 and found that it contained a pentapeptide motif biochemically related to KFERQ,which has been proposed to be a targeting sequence for CMA.In vitro,we confirmed that SMAD3 was degraded in either serum-free or KFERQ motif deleted condition,which was regulated by LAMP2A and interacted with HSC70(heat shock cognate 71 kDa protein).Using isolated lysosomes,amino-acid residues 75 and 128 of SMAD3 were found to be of importance for this process,which affected the CMA pathway in which SMAD3 was involved.Similarly,down-regulating SMAD3 or up-regulating LAMP2A in cultured glioma cells enhanced their proliferation and invasion.Taken together,these results suggest that excessive activation of CMA regulates glioma cell growth by promoting the degradation of SMAD3.Therefore,targeting the SMAD3-LAMP2Amediated CMA-lysosome pathway may be a promising approach in anti-cancer therapy. | Hanqun Liu Yuxuan Yong Xingjian Li Panghai Ye Kai Tao Guoyou Peng Mingshu Mo Wenyuan Guo Xiang Chen Yangfu Luo Yuwan Lin Jiewen Qiu Ziling Zhang Liuyan Ding Miaomiao Zhou Xinling Yang Lin Lu Qian Yang Pingyi Xu | 2022 | Neuroscience Bulletin2022，38，6： | 0 |
| 6 | Combination of Evodiamine with Berberine Reveals a Regulatory Effect on the Phenotypic Transition of Colon Epithelial Cells Induced by CCD-18Co显示文摘Objective Transdifferentiation exists between stromal cells or between stromal cells and cancer cells.Evodiamine and berberine are predominant pharmacological components of Zuojin pill,a prescription of Traditional Chinese Medicine,playing crucial functions in remolding of tumor microenvironment.This study aimed to explore the effect of combination of evodiamine with berberine(cBerEvo)on the phenotypic transition of colon epithelial cells induced by tumor-associated fibroblasts,as well as the involved mechanisms.Methods Human normal colon epithelial cell line HCoEpiC cells were treated with the prepared conditioned medium of CCD-18 Co,a human colon myofibroblast line,to induce epithelial-mesenchymal transition.Phase contrast microscope was used to observe the morphological changes.Epithelial-mesenchymal transition markers including E-cadherin,vimentin and alpha-smooth muscle actin(α-SMA)were observed with immunofluorescence microscopy.Migration was assessed by wound healing assay.Western blotting was used to detect the expressions of E-cadherin,vimentin,α-SMA,Snail,ZEB1 and Smads.Results In contrast to the control,the tumor-associated fibroblasts-like CCD-18 Co cells induced downregulation of E-cadherin and up-regulation of vimentin,α-SMA,Snail and ZEB1(P<0.05),and promoted migration of HCoEpiCs(P<0.05),with over expression of Smads including Smad2,p-Smad2,Smad3,p-Smad3 and Smad4(P<0.05),which were abolished by a transforming growth factor-β(TGF-β)receptor inhibitor LY364947 and by cBerEvo in a concentration dependent manner.In addition,cBerEvo-inhibited ratios of p-Smad2/Smad2 and p-Smad3/Smad3 were also dose dependent.Conclusion The above results suggest that cBerEvo can regulate the differentiation of colon epithelial cells induced by CCD-18 Co through suppressing activity of TGF-β/Smads signaling pathway. | Chao Huang Keming Xiang Bingjun Liang Weixuan Huang Fanjun Zhang Yuwan Shao Xiulian Wang Haosheng Liu Weizeng Shen | 2020 | Chinese Medical Sciences Journal2020，35，3： | 0 |
| 7 | Inertial Subgradient Extragradient Algorithm for Solving Variational Inequality Problems with Pseudomonotonicity显示文摘In order to solve variational inequality problems of pseudomonotonicity and Lipschitz continuity in Hilbert spaces, an inertial subgradient extragradient algorithm is proposed by virtue of non-monotone stepsizes. Moreover, weak convergence and R-linear convergence analyses of the algorithm are constructed under appropriate assumptions. Finally, the efficiency of the proposed algorithm is demonstrated through numerical implementations. | Yuwan Ding Hongwei Liu Xiaojun Ma | 2023 | Journal of Harbin Institute of Technology(New Series)2023，30，5： | 0 |
| 8 | CHCHD2 Thr61Ile mutation impairs F1F0-ATPase assembly in in vitro and in vivo models of Parkinson's disease显示文摘Mitochondrial dysfunction is a significant pathological alte ration that occurs in Parkinson's disease(PD),and the Thr61lle(T61I)mutation in coiled-coil helix coiled-coil helix domain containing 2(CHCHD2),a crucial mitochondrial protein,has been reported to cause Parkinson's disease.FIFO-ATPase participates in the synthesis of cellular adenosine triphosphate(ATP)and plays a central role in mitochondrial energy metabolism.However,the specific roles of wild-type(WT)CHCHD2 and T611-mutant CHCHD2 in regulating F1FO-ATPase activity in Parkinson's disease,as well as whether CHCHD2 or CHCHD2 T61I affects mitochondrial function through regulating F1FO-ATPase activity,remain unclea r.Therefore,in this study,we expressed WT CHCHD2 and T61l-mutant CHCHD2 in an MPP^(+)-induced SH-SY5Y cell model of PD.We found that CHCHD2 protected mitochondria from developing MPP^(+)-induced dysfunction.Under normal conditions,ove rexpression of WT CHCHD2 promoted F1FO-ATPase assembly,while T61I-mutant CHCHD2 appeared to have lost the ability to regulate F1FO-ATPase assembly.In addition,mass spectrometry and immunoprecipitation showed that there was an interaction between CHCHD2 and F1FO-ATPase.Three weeks after transfection with AAV-CHCHD2 T61I,we intraperitoneally injected 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine into mice to establish an animal model of chronic Parkinson's disease and found that exogenous expression of the mutant protein worsened the behavioral deficits and dopaminergic neurodegeneration seen in this model.These findings suggest that WT CHCHD2 can alleviate mitochondrial dysfunction in PD by maintaining F1F0-ATPase structure and function. | Xiang Chen Yuwan Lin Zhiling Zhang Yuting Tang Panghai Ye Wei Dai Wenlong Zhang Hanqun Liu Guoyou Peng Shuxuan Huang Jiewen Qiu Wenyuan Guo Xiaoqin Zhu Zhuohua Wu Yaoyun Kuang Pingyi Xu Miaomiao Zhou | 2024 | Neural Regeneration Research2024，19，1： | 0 |
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