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检索条件"任意字段=中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议"

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The crystal structure of PERK luminal domain complexed with the peptide substrate suggests the ligand-driven model for ER stress activation

The crystal structure of PERK luminal domain complexed with ...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Peng Wang Jingzhi Li Jiahui Tao Bingdong Sha Institute of Molecular Biology and Biotechnology College of Life SciencesAnhui Normal University Department of Cell Developmental and Integrative Biology(CDIB)University of Alabama at Birmingham

PERK is one of the major sensor proteins which can detect the protein folding imbalance during ER *** remains unclear how the sensor protein PERK is activated by ER stress to initiate the downstream unfolded protein *** data have demonstrated that PERK luminal domain can recognize and selectively interact with the misfolded proteins but not native *** have identified a peptide substrate P16 for PERK luminal domain by screening the phase display *** peptide P16 can efficiently compete with misfolded proteins to bind with PERK luminal *** illustrate the mechanism how PERK luminal domain interacts with the misfolded proteins,we have determined the crystal structure of bovine PERK luminal domain complexed with its peptide substrate P16 to 2.8? *** structure reveals that PERK luminal domain utilizes a conserved hydrophobic groove to bind the *** within the hydrophobic regions of PERK luminal domain abolish the binding between PERK and the misfolded model *** peptide substrate binding results in major conformational changes in the PERK luminal domain which may favor the oligomerization of *** crystal structure of PERK luminal domain and the peptide substrate complex suggests a novel stacking format for the PERK luminal domain to oligomerize after ligand ***,the structural and biochemical data strongly supported the ligand-driven hypothesis that PERK luminal domain can interact directly with misfolded proteins to induce ER stress signaling.

关键词： ER stress PERK luminal domain peptide substrate complex structure

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Regulation of Cytochrome P450 Enzymes by Reversible Oxidation of Thiols to Sulfenic Acids

Regulation of Cytochrome P450 Enzymes by Reversible Oxidatio...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： F.Peter Guengerich Matthew E.Albertolle Department of Biochemistry Vanderbilt University School of Medicine

Cytochrome P450(P450) enzymes are the major catalysts involved in the metabolism of drugs,steroids,chemical carcinogens,and fat-soluble *** they are involved in >95% of oxidation/reduction reactions of *** signature spectroscopic properties and the catalytic activities are related to a conserved cysteine thiolate ligand binding to the proximal side of the heme *** found that the activity of one human P450 enzyme,P450 4 A11,was stimulated by the addition of mild reducing agents,***,and attenuated by H2 *** analyzed the enzyme and did not find disulfides but did find that the cysteine sulfur was oxidized to a sulfenic acid(-SOH),a reversible *** then found numerous drug metabolizing enzymes that contained sulfenic acids,including several mouse and human P450 s with the heme-cysteinyl sulfenic *** sulfenic acid was found in mouse and human liver and kidney samples in situ,suggesting physiological *** dynamics simulations suggest roles for specific amino acids in modulating the oxidation of the *** part of our continuing efforts in characterization of these systems in cells,we have synthesized new heavy isotope-labeled reagents with much faster kinetics than dimedone and iodoacetamide,which can be used to label sulfenic acids and disulfides,using liquid chromatography-mass *** phenomenon represents a potential new means of post-transcriptionally regulating the activities of P450 enzymes,although more in vivo evidence is in order.

关键词： Cytochrome P450 redox control sulfenic acid drug metabolism steroidogenesis heme ligands

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Single-step bioproduction of the simvastatin precursor monacolin J in an industrial strain of Aspergillus terreus

Single-step bioproduction of the simvastatin precursor monac...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Xuenian Huang Bo Liang Yajing Liang Yong Yang Yun Teng Linghui Zhang Xuefeng Lu Key Laboratory of Biofuels Qingdao Institute of Bioenergy and Bioprocess TechnologyChinese Academy of Sciences Shandong Provincial Key Laboratory of Synthetic Biology Qingdao Institute of Bioenergy and Bioprocess TechnologyChinese Academy of Sciences Zhejiang Hisun Pharmaceutical Co. Ltd.

Monacolin J is a key precursor for the synthesis of simvastatin(Zocor),an important drug for treating ***,monacolin J is manufactured through alkaline hydrolysis of lovastatin,a fungal polyketide produced by Aspergillus *** chemical processes for the conversion of lovastatin to simvastatin are laborious,cost expensive and environmentally unfriendly.A biocatalysis process for monacolin J conversion to simvastatin has been ***,direct bioproduction of monacolin J has not yet been ***,we identified a lovastatin hydrolase from Penicillium chrysogenum,which displays a 232-fold higher catalytic efficiency for the in vitro hydrolysis of lovastatin compared to a previously patented hydrolase,but no activity for ***,we showed that an industrial *** strain heterologously expressing this lovastatin hydrolase can produce monacolin J through single-step fermentation with approximately 95% of the biosynthesized lovastatin was hydrolyzed to monacolin *** further troubleshoot the nearly 6% residual lovastatin in the above engineered *** strain,we then performed several rounds of directed evolution to this specific lovastatin ***,the engineered *** strain overexpressing Q140 L mutant realized almost 100% bioconversion of the produced lovastatin to monacolin ***,our results realize single-step bioproduction of monacolin J in a more efficient way,providing an attractive and eco-friendly substitute over the existing chemical synthetic routes of monacolin J and promotes complete bioproduction of simvastatin at industrial scale.

关键词： Monacolin J Simvastatin lovastatin hydrolase Aspergillus terreus directed evolution Microbial cell factory

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Interleukin-22 promotes autophagy and inhibits apoptosis in rheumatoid arthritis through targeting the STAT3 pathway in synovial fibroblasts

Interleukin-22 promotes autophagy and inhibits apoptosis in ...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Bo Wang Weikun Hou Center for Translational Medicine the First Affiliated Hospital of Xi'an Jiaotong University Osteonecrosis and joint Reconstruction Ward Joint SurgeryXi'an Honghui Hospital

Rheumatoid arthritis(RA) is a common chronic autoimmune inflammatory *** role of autophagy and apoptosis in the pathogenesis of RA is ***-22(IL-22) as a cytokine of Th22 plays a significant and complicated role in inflammatory and autoimmune rheumatic *** propose that IL-22 regulates activation of autophagy and exerts inhibition of apoptosis in synovial fibroblasts,and is thereby essential for development of *** results showed that the concentration of IL-22 in RA was significantly higher than in HC and *** synovial fibroblasts and chondrocytes treated with rhIL-22,the apoptosis was significantly decreased in synovial fibroblasts,but not in *** protein expression of Bcl-2 was increased in a dose-dependent manner,and cleaved Caspase-3 was ***-22 triggered autophagic flux in synovial fibroblasts,which led to autophagy-related proteins Beclin 1 and LC3(8)were significantly *** induced autophagy and inhibited apoptosis were associated with STAT3 phosphorylation though expression of Bcl-2 and Beclin *** and inhibiting STAT3 by inhibitor or by siRNA led to synovial fibroblasts abrogated the effects of *** importantly,the STAT3 pathway could regulate the balance of apoptosis and autophagy in RA synovial *** conclude that IL-22 inhibited apoptosis and promoted autophagy,and this balance was regulated though STAT3 pathway leading to upreglation of Bcl-2 and Beclin 1 in RA synovial *** pathogenic mechanism suggest a strategy for using anti-STAT3 approach to RA treatment.

关键词： Interleukin-22 Apoptosis Autophagy STAT3 Rheumatoid arthritis

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Development of a Deep Learning Model for Binding Affinity Prediction and Fragment-based de novo Drug Design

Development of a Deep Learning Model for Binding Affinity Pr...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Shiwei Wang Jianfeng Pei Luhua Lai PTN Joint Graduate Program Academy for Advanced Interdisciplinary StudiesPeking University Center for Quantitative Biology Academy for Advanced Interdisciplinary StudiesPeking University BNLMS State Key Laboratory for Structural Chemistry of Unstable and Stable Speciesand Peking-Tsinghua Center for Life Sciences at College of Chemistry and Molecular EngineeringPeking University

The traditional drug design and discovery methods were time-consuming and expensive,which largely reduced the efficiency of drug design ***-based de novo drug design was applied to accelerate the procedure of drug *** a complementary of high-throughput screening technology,de novo drug design method is confronted with a virtually infinite search *** drug-like molecules can be discovered by exploring the chemical space with specific combinational search strategies,which provides a new approach to find novel ***,challenges including combinatorial explosion,scoring function and so on hinder the development and application of de novo drug *** this work,we hope to construct a reinforcement-learning model by combing Monto Carlo Tree Search method and deep neural network to solve the combinatorial explosion *** order to achieve our goals,we updated our Pocket program to extract more accurate pharmacophore models,which can help to extract features of 3 D structure information of protein-ligand ***,we developed a new scoring function to predict binding affinity of protein-ligand complex based on the 3 D structure *** further improving and optimizing,the new scoring function could be applied to binding affinity prediction and will be integrated to our fragment-based de novo drug design method.

关键词： scoring function Representation of binding pocket de novo drug design Reinforcement learning

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O-GlcNAcylation destabilizes the active tetrameric PKM2 to promote the Warburg effect

O-GlcNAcylation destabilizes the active tetrameric PKM2 to p...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Yang Wang Jia Liu Xin Jin Dapeng Zhang Dongxue Li Fengqi Hao Yunpeng Feng Shan Gu Fanlin Meng Miaomiao Tian Yi Zheng Ling Xin Xinbo Zhang Xue Han L.Aravind Min Wei Key Laboratory of Molecular Epigenetics of the Ministry of Education (MOE) Northeast Normal University Department of Biology and Program of Bioinformatics and Computational Biology Saint Louis University National Center for Biotechnology Information National Library of MedicineNational Institutes of Health

The Warburg effect,characterized by increased glucose uptake and lactate production,is a well-known universal across cancer-and other ***2,a splice isoform of the pyruvate kinase（PK） specifically expressed in these cells,serves as a major regulator of this metabolic reprogramming with an adjustable activity subjected to numerous allosteric effectors and posttranslational *** we have identified a novel posttranslational modification on PKM2,O-GlcNAcylation,which specifically targets Thr and Ser,residues of the region encoded by the alternatively spliced exon 10 in cancer *** show that PKM2 O-GlcNAcylation is upregulated in various types of human tumor cells and patient tumor *** modification destabilized the active tetrameric PKM2,reduced PK activity and led to nuclear translocation of *** also observed that the modification is associated with an increased glucose consumption and lactate production,and enhanced level of lipid and DNA synthesis,indicating that O-GlcNAcylation promotes the Warburg *** vivo experiments showed that blocking PKM2 O-GlcNAcylation attenuated tumor ***,we demonstrate that O-GlcNAcylation is a new regulatory mechanism for PKM2 in cancer cells and serves as a bridge between PKM2 and metabolic reprogramming typical of the Warburg effect.

关键词： PKM2 O-GlcNAcylation Warburg effect cancer metabolism

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Cell-surface Translocation of Annexin A2 contributes to bleomycin-induced pulmonary fibrosis by mediating inflammatory response in mice

Cell-surface Translocation of Annexin A2 contributes to bleo...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Yunlong Lei Department of Biochemistry and Molecular Biology Molecular Medicine and Cancer Research CenterChongqing Medical University

Bleomycin,a widely used cancer drug,may give rise to a serious side effect,pulmonary fibrosis which is associated with significant morbidity and *** the intensive efforts,the precise pathogenic mechanisms still remain to be *** previous study showed that bleomycin bound directly to annexin A2(ANXA2,p36),leading to development of pulmonary fibrosis by impeding TFEB-induced autophagic ***,we demonstrated that ANXA2 also played a critical role in bleomycin-induced inflammation,which represents another major cause of bleomycin-induced pulmonary *** found that bleomycin could induce the cell surface translocation of ANXA2 in lung epithelial cells through exosomes secretion associated with enhanced interaction between ANXA2 and *** of ANXA2 or blocking membrane ANXA2 by small peptide TM601 mitigated bleomycin-induced activation of NF-κB pathway and production of proinflammatory cytokine IL-6 in lung epithelial ***2-deficient(ANXA2-/-) mice treated with bleomycin exhibit reduced pulmonary fibrosis along with decreased cytokine production compared with bleomycin-challenged wild-type ***,the surface ANXA2 inhibitor TM601,could ameliorate fibrotic and inflammatory response in bleomycin-treated *** together,our results indicated that,in addition to disturb autophagic flux,ANXA2 can contribute to bleomycininduced pulmonary fibrosis by mediating inflammatory response.

关键词： Bleomycin annexin A2 pulmonary fibrosis inflammation IL-6

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Roles of N-terminal Asparagine Amidohydrolase Gene from Apis cerana cerana in Oxidative Stress Responses

Roles of N-terminal Asparagine Amidohydrolase Gene from Apis...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Guangdong Zhao Chen Wang Jie Meng Baohua Xu Xingqi Guo State Key Laboratory of Crop Biology College of Life SciencesShandong Agricultural University College of Animal Science and Technology Shandong Agricultural University

N-terminal asparagine amidohydrolase(Ntan1) is a feature of the ubiquitin-dependent N-end rule pathway of protein degradation which has been implicated in a legion of physiological functions: sensing of heme,oxygen,and nitric oxide;selective elimination of misfolded proteins,DNA *** identified the AccNtan1 gene from Apis cerana cerana and investigated its role in oxidation *** sequence alignments and phylogenetic analysis revealed that AccNtan1 is highly conserved in insect *** results indicated that the expression levels of AccNtan1 in wing,honey sac and abdomen were significantly lower than in other tissues and significantly higher in early development stages,including larve,prepupae and pink-eyed *** further observed that the expression of AccNtan1 was induced by several environmental ***,disc diffusion assays result suggested that overexpression of AccNtan1 enhances the resistance of bacteria to oxidative *** results indicated that AccNtan1 may be involved in the response to oxidative ***,after knockdown of AccNtan1 using RNA interference(RNAi),the expression levels of most antioxidant genes and antioxidant enzymatic activities were significantly ***,we hypothesize that AccNtan1 plays important roles in environmental stress responses and anti-oxidative processes.

关键词： N-terminal asparagine amidohydrolase Oxidative stress RNA inference Apis cerana cerana

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MiR-181b-5p contributes to hepatic glycogen synthesis through EGR1/PTEN/AKT pathway

MiR-181b-5p contributes to hepatic glycogen synthesis throug...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Shuyue Wang Yulun Wu Meiting Yang Yuxin Li National Engineering Laboratory for Druggable Gene and Protein Screening School of Life SciencesNortheast Normal University Research Center of Agriculture and Medicine Gene Engineering of Ministry of Education Northeast Normal University

MiR-181 family plays an important role in the regulation of various cellular ***,whether MiR-181 b-5 p mediates hepatic insulin resistance remains *** this study,we found that miR-181 b-5 p was significantly decreased in the liver of diabetic mice as well as in hepatocytes treated with high ***,inhibition of miR-181 b-5 p expression led to impairment of AKT/GSK pathway and reduced level of glycogenesis,whereas overexpression of miR-181 b-5 p resulted in activated AKT/GSK pathway and increased glycogen levels in *** Addition,up-regulation of miR-181 b-5 p reversed high glucose-induced suppression of glycogenesis in *** study revealed that EGR1 is a target of miR-181 b-5 p by luciferase reporter assay and western *** of EGR1 by transfecting with siRNA targeting EGR1 could significantly suppress the expression of PTEN and then increase glycogen ***1 knockdown reversed miR-181 b-5 p inhibition-induced reduced glycogenesis and activation of AKT/GSK *** conclusion,we found novel evidence suggesting that hepatic miR-181 b-5 p mediated glycogen synthesis through targeting EGR1 to regulate PTEN expression.

关键词： EGR1 hepatic glycogenesis high glucose miR-181b-5p PTEN

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A brief overview of neural tube defects

A brief overview of neural tube defects

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Yuqing Sun Kaili Zhang Juan Zhang Yufei Wang Zhizhen Liu Department of Biochemistry and Molecular Biology Shanxi Medical University

neural tube defects,is a kind of serious congenital birth defects in the central Nervous system disease and is one of the major causes of perinatal fetal death and one of the major causes of the fetal permanent *** average incidence of neural tube defects in the world is 1% to 2%,and China is the country with a high incidence of the disease,the average incidence rate in China is 3%.Clinically,NTDs are mainly divided into four categories,namely,Anencephaly,Encephalocele,Spina bifida(SB),and low spina *** most common type of NTD is spina bifida.A large body of literature indicates that the occurrence of the disease is considered to be a complex process,caused by multiple factors,and is a "multi-cause" *** other words,the development of neural tube itself is a complex multi-step process,strictly controlled by genes,regulated by many environmental factors,involving gene-gene,gene-environment and gene-nutrient interactions,and a large number of studies have confirmed that NTDs are more highly correlated with genetic factors,and the risk of chromosomal abnormalities in fetuses with NTDs is significantly higher than in healthy people,but it is also affected by external *** clinical prevention,early folic acid supplementation can reduce the incidence and recurrence rate of neural tube defects,but for folic acid-resistant pregnant women,if combined with folic acid and inositol(a water-soluble vitamin),neural tube defects The incidence is *** recent years,the research progress has mainly focused on the epigenetic direction,mainly DNA methylation,histone acetylation,etc.;and targeted research on related signaling *** article mainly introduces the concept of neural tube formation,neural tube defects and pathogenesis,research progress and clinical prevention.

关键词： neural tube neural tube malformation folic acid gene homocysteine metabolism epigenetic

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