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| 1 | EGTA reduces the inflorescence stem mechanical strength of herbaceous peony by modifying secondary wall biosynthesis显示文摘The mechanical strength of inflorescence stems is an important trait in cut flowers.Calcium ions(Ca^(2+))play a pivotal role in maintaining stem strength,but little is known about the underlying molecular mechanisms.In this study,we treated herbaceous peony(Paeonia lactiflora Pall.)with ethyl glycol tetraacetic acid(EGTA),an effective Ca^(2+)chelator,and used morphology indicators,spectroscopic analysis,histochemical staining,electron microscopy,and proteomic techniques to investigate the role of Ca^(2+)in inflorescence stem mechanical strength.The EGTA treatment reduced the mechanical strength of inflorescence stems,triggered the loss of Ca^(2+)from cell walls,and reduced lignin in thickened secondary walls in xylem cells as determined by spectroscopic analysis and histochemical staining.Electron microscopy showed that the EGTA treatment also resulted in significantly fewer xylem cell layers with thickened secondary walls as well as in reducing the thickness of these secondary walls.The proteomic analysis showed 1065 differentially expressed proteins(DEPs)at the full-flowering stage(S4).By overlapping the Kyoto encyclopedia of genes and genomes(KEGG)and gene ontology(GO)analysis results,we identified 43 DEPs involved in signal transduction,transport,energy metabolism,carbohydrate metabolism,and secondary metabolite biosynthesis.Using quantitative real-time polymerase chain reaction(qRT-PCR)analysis,we showed that EGTA treatment inhibited Ca^(2+)sensors and secondary wall biosynthesis-related genes.Our findings revealed that EGTA treatment reduced the inflorescence stem mechanical strength by reducing lignin deposition in xylem cells through altering the expression of genes involved in Ca^(2+)binding and secondary wall biosynthesis. | Yuhan Tang Daqiu Zhao Jiasong Meng Jun Tao | 2019 | Horticulture Research2019，6，1： | 2 |
| 2 | Environmentally benign chitosan as reductant and supporter for synthesis of Ag/AgCI/chitosan composites by one-step and their photocatalytic degradation performance under visible-light irradiation显示文摘 | Hao WANG Yuhan WU Pengcheng WU Shanshan CHEN Xuhong GUO Guihua MENG Banghua PENG Jianning WU Zhiyong LIU | 2017 | Frontiers of Materials Science2017，11，2： | 2 |
| 3 | LATS1 K751 acetylation blocks activation of Hippo signalling and switches LATS1 from a tumor suppressor to an oncoprotein显示文摘Large tumor suppressor 1(LATS1)is the key kinase controlling activation of Hippo signalling pathway.Post-translational modifications of LATS1 modulate its kinase activity.However,detailed mechanism underlying LATS1 stability and activation remains elusive.Here we report that LATS1 is acetylated by acetyltransferase CBP at K751 and is deacetylated by deacetylases SIRT3 and SIRT4.Acetylation at K751 stabilized LATS1 by decreasing LATS1 ubiquitination and inhibited LATS1 activation by reducing its phosphorylation.Mechanistically,LATS1 acetylation resulted in inhibition of YAP phosphorylation and degradation,leading to increased YAP nucleus translocation and promoted target gene expression.Functionally,LATS1-K751 Q,the acetylation mimic mutant potentiated lung cancer cell migration,invasion and tumor growth,whereas LATS1-K751 R,the acetylation deficient mutant inhibited these functions.Taken together,we demonstrated a previously unidentified post-translational modification of LATS1 that converts LATS1 from a tumor suppressor to a tumor promoter by suppression of Hippo signalling through acetylation of LATS1. | Siyuan Yang Weizhi Xu Cheng Liu Jiaqi Jin Xueying Li Yuhan Jiang Lei Zhang Xianbin Meng Jun Zhan Hongquan Zhang | 2022 | Science China(Life Sciences)2022，65，1： | 1 |
| 4 | Preparation of expanded graphite/poly (phenylene sulfide) composites with high thermal and electrical conductivity by rotating solid-state premixing and melt processing显示文摘 | Jinwen Wang Meng Wu Yuhan Li | 2013 | Journal ofMaterialsScience2013，48，5： | 1 |
| 5 | LncRNA-Airn alleviates acute liver injury by inhibiting hepatocyte apoptosis via the NF-κB signaling pathway显示文摘Acute liver injury is a common and serious syndrome caused by multiple factors and unclear pathogenesis.If the injury persists,liver injury can lead to cirrhosis and liver failure and ultimately results in the development of liver cancer.Emerging evidence has indicated that long noncoding RNAs(lncRNAs)play an important role in the development of liver injury.However,the role of antisense Igf2r RNA(Airn)in acute liver injury and its underlying mechanism remain largely unclear.In this study,we show that Airn is upregulated in liver tissue and primary hepatocytes from an acute liver injury mouse model.Consistently,Airn is also overexpressed in serum samples of patients with acute-on-chronic liver failure and is negatively correlated with the Model for End-Stage Liver Disease(MELD)score.Moreover,gene knockout and rescue assays reveal that Airn alleviates CCl_(4)-induced liver injury by inhibiting hepatocyte apoptosis and oxidative stress in vivo.Further investigation reveals that Airn decreases H_(2)O_(2)-induced hepatocyte apoptosis in vitro.Mechanistically,we reveal that Airn represses CCl_(4)-and H_(2)O_(2)-induced enhancement of phosphorylation of p65 and IκBα,suggesting that Airn inhibits hepatocyte apoptosis by inactivating the NF-κB pathway.In conclusion,our results demonstrate that Airn can alleviate acute liver injury by inhibiting hepatocyte apoptosis via inactivating the NF-κB signaling pathway,and Airn could be a potential biomarker for acute liver injury. | Shuai Shao Yu Zhang Feng Zhou Xiaoxiang Meng Zhenjun Yu Guantong Li Lina Zheng Kun Zhang Yuhan Li Beichen Guo Qi Liu Mengxia Zhang Xiaoxiao Du Wei Hong Tao Han | 2022 | Acta Biochimica et Biophysica Sinica2022，54，11： | 1 |
| 6 | Genomic insights into versatile lifestyle of three new bacterial candidate phyla显示文摘Metagenomic explorations of the Earth's biosphere enable the discovery of previously unknown bacterial lineages of phylogenetic and ecological significance.Here,we retrieved 11 metagenomic-assembled genomes(MAGs)affiliated to three new monophyletic bacterial lineages from the seawater of the Yap Trench.Phylogenomic analysis revealed that each lineage is a new bacterial candidate phylum,subsequently named Candidatus Qinglongiota,Candidatus Heilongiota,and Candidatus Canglongiota.Metabolic reconstruction of genomes from the three phyla suggested that they adopt a versatile lifestyle,with the potential to utilize various types of sugars,proteins,and/or short-chain fatty acids through anaerobic pathways.This was further confirmed by a global distribution map of the three phyla,indicating a preference for oxygen-limited or particle-attached niches,such as anoxic sedimentary environments.Of note,Candidatus Canglongiota genomes harbor genes for the complete WoodLjungdahl pathway and sulfate reduction that are similar to those identified in some sulfate-reducing bacteria.Evolutionary analysis indicated that gene gain and loss events,and horizontal gene transfer(HGT)play important roles in shaping the genomic and metabolic features of the three new phyla.This study presents the genomic insight into the ecology,metabolism,and evolution of three new phyla,which broadens the phylum-level diversity within the domain Bacteria. | Xinxu Zhang Zongbao Liu Wei Xu Jie Pan Yuhan Huang Mingwei Cai Zhuhua Luo Meng Li | 2022 | Science China(Life Sciences)2022，65，8： | 0 |
| 7 | Ginsenoside F1 administration promotes UCP1-dependent fat browning and ameliorates obesity-associated insulin resistance显示文摘Obesity-induced type 2 diabetes is mainly due to excessive free fatty acids leading to insulin resistance.Increasing thermogenesis is regarded as an effective strategy for hypolipidemia and hypoglycemia.Ginsenoside is a natural active component in Panax ginseng C.A.Meyer,and some of them enhance thermogenesis.However,there are few studies on the mechanism and target of ginsenosides enhancing thermogenesis.Using thermogenic protein uncoupling protein 1(UCP1)-luciferase reporter assay,we identifi ed ginsenoside F1 as a novel UCP1 activator in the ginsenosides library.Using pull down assay and inhibitor interference,we found F1 binds toβ3-adrenergic receptors(β3-AR)to enhance UCP1 expression via cAMP/PKA/CREB pathway.We also investigated the ability of F1 on energy metabolism in obesity-induced diabetic mice,including body weight,body composition and energy expenditure.The results of proteomics showed that F1 signifi cantly up-regulated thermogenesis proteins and lipolytic proteins,but down-regulated fatty acid synthesis proteins.Ginsenoside F1 increased thermogenesis and ameliorated insulin resistance specifi cally by promoting the browning of white adipose tissue in obese mice.Additionally,ginsenoside F1 improves norepinephrine-induced insulin resistance in adipocytes and hepatocytes,and shows a stronger mitochondria respiration ability than norepinephrine.These fi ndings suggest that ginsenoside F1 is a promising lead compound in the improvement of insulin resistance. | Yuhan Meng Weili Li Chenxing Hu Si Chen Haiyang Li Feifei Bai Lujuan Zheng Ye Yuan Yuying Fan Yifa Zhou | 2023 | Food Science and Human Wellness2023，12，6： | 0 |
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