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Biochemical and biophysical research communication...Biochemical and biophysical research communications 49건

  1. [해외논문]   The structure-activity relationship of ginsenosides on hypoxia-reoxygenation induced apoptosis of cardiomyocytes   SCI SCIE

    Feng, Ruiqi (Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216, USA ) , Liu, Jia (Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216, USA ) , Wang, Zhenhua (School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, 264005, PR China ) , Zhang, Jingwen (School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, 264005, PR China ) , Cates, Courtney (Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216,) , Rousselle, Thomas , Meng, Qingguo , Li, Ji
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 556 - 568 , 2017 , 0006-291x ,

    초록

    Abstract Ginsenosides have been studied extensively in recent years due to their therapeutic effects in cardiovascular diseases. While most studies examined the different ginsenosides individually, few studies compare the therapeutic effects among the different types. This study examined how effective protopanaxadiol, protopanaxatriol ginsenosides Rh2, Rg3, Rh1, and Rg2 of the ginsenoside family are in protecting H9c2 cardiomyocytes from damage caused by hypoxia/reoxygenation. In the current study, a model of myocardial ischemia and reperfusion was induced in H9c2 cardiomyocytes by oxygen deprivation via a hypoxia chamber followed by reoxygenation. Our data show that structures similar to that of protopanaxadiol, which lacked the hydroxide group at C6, were more effective in lowering apoptosis than structures similar to protopanaxatriol with a hydroxide group at C6. As the compounds increased in size and complexity, the cardioprotective effects diminished. In addition, the S enantiomer proved to be more effective in cardioprotection than the R enantiomer. Furthermore, the immunoblotting analysis demonstrated that ginsenosides activate AMPK but suppress JNK signaling pathways during hypoxia/reoxygenation. Thus, ginsenosides treatment attenuated hypoxia/reoxygenation-induced apoptosis via modulating cardioprotective AMPK and inflammation-related JNK signaling pathways. Highlights Ginsenosides have cardioprotective effects on hypoxia and reoxygenation-induced damage. There is a structure-activity relationship regarding ginsenosides' inhibition of apoptosis. AMPK could be an important mediator for ginsenosides' cardioprotection against hypoxic injury.

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  2. [해외논문]   The downregulation of miR-3173 in B-cell acute lymphoblastic leukaemia promotes cell invasion via PTK2   SCI SCIE

    Tian, Lijun (Corresponding author. No. 18 Sudibei Road, Xuzhou 221002, Jiangsu Province, China.) , Cao, Junhua , Ji, Qiang , Zhang, Chuanling , Qian, Tong , Song, Xianchuan , Huang, Baoshan , Tian, Xinyi
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 569 - 574 , 2017 , 0006-291x ,

    초록

    Abstract MicroRNAs are important regulators of the pathogenesis of B-cell acute lymphoblastic leukaemia (B-ALL). In this study, we identified miR-3173 and its predicted target gene PTK2 were correspondingly differentially expressed in B-ALL patients. In B-ALL cell lines, CCK-8 proliferation assay revealed that miR-3173 could inhibit the cell proliferation. Moreover, transwell assay revealed that miR-3173 could also inhibit cell migration and invasion in B-ALL cell lines. Luciferase assays revealed that miR-3173 directly bound to the 3′untranslated region of PTK2, and western blotting showed that miR-3173 suppressed the expression of PTK2 at the protein level. Generally, this study indicates that miR-3173 negatively regulates PTK2 and inhibits proliferation and invasion of B-ALL cell lines. Thus, miR-3173 may represent a potential therapeutic molecule for B-ALL intervention. Highlights miR-3173 is down-regulated in B-ALL patients. miR-3173 inhibits the proliferation and invasion of B-ALL cells. miR-3173 targets the 3′ UTR of PTK2 in B-ALL cells. miR-3173 inhibits PTK2 in B-ALL cells.

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  3. [해외논문]   Structure insights into the molecular mechanism of the interaction between UHRF2 and PCNA   SCI SCIE

    Chen, Wanbiao (Hefei National Laboratory for Physical Sciences at Microscale CAS Center for Excellence in Biomacromolecules, Collaborative Innovation Center of Chemistry for Life Sciences, School of Life Sciences, University of Science and Technology of China, 96 Jinzhai Road, Hefei, Anhui 230026, China ) , Wu, Minhao (Hefei National Laboratory for Physical Sciences at Microscale CAS Center for Excellence in Biomacromolecules, Collaborative Innovation Center of Chemistry for Life Sciences, School of Life Sciences, University of Science and Technology of China, 96 Jinzhai Road, Hefei, Anhui 230026, China ) , Hang, Tianrong (Hefei National Laboratory for Physical Sciences at Microscale CAS Center for Excellence in Biomacromolecules, Collaborative Innovation Center of Chemistry for Life Sciences, School of Life Sciences, University of Science and Technology of China, 96 Jinzhai Road, Hefei, Anhui 230026, China ) , Wang, Chengliang (Hefei National Laboratory for Physical Sciences at Microscale CAS Center for Excellence in Biomacromolecules, Collaborative) , Zhang, Xuan , Zang, Jianye
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 575 - 580 , 2017 , 0006-291x ,

    초록

    Abstract UHRF2 (Ubiquitin-like with PHD and ring finger domains 2) is an E3 ubiquitin ligase that plays important roles in DNA methylation, histone modifications and cell cycle regulation by interacting with multiple epigenetic or cell-cycle related proteins. Previous studied have identified PCNA (Proliferating cell nuclear antigen) as an interacting partner of UHRF2 by using the antibody microarray. However, the molecular mechanism and the function of UHRF2-PCNA interaction remains unclear. Here, we report the complex structure of PCNA and the peptide ( 784 NEIL QTLLDLFF PGYSK 800 ) derived from UHRF2 that contains a PIP box. Structural analysis combined with mutagenesis experiments provide the molecular basis for the recognition of UHRF2 by PCNA via PIP-box. Highlights UHRF2 interacts with PCNA through its PIP box. Complex structure of PCNA/UHRF2 PIP reveals the molecular mechanism of how PCNA recognizes UHRF2. UHRF2-PIP box interacts with PCNA mainly via hydrophobic interaction. The hydrogen bond formed between PCNA-H44 and UHRF2 PIP -D792 is critical for the interaction.

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  4. [해외논문]   Characterization of the zinc-induced Shank3 interactome of mouse synaptosome   SCI SCIE

    Lee, Yeunkum (Department of Neuroscience, College of Medicine, Korea University, Seoul, South Korea ) , Ryu, Jae Ryun (Department of Biomedical Sciences, College of Medicine, Korea University, Seoul, South Korea ) , Kang, Hyojin (HPC-enabled Convergence Technology Research Division, Korea Institute of Science and Technology Information, Daejeon, South Korea ) , Kim, Yoonhee (Department of Neuroscience, College of Medicine, Korea University, Seoul, South Korea ) , Kim, Shinhyun (Department of Neuroscience, College of Medicine, Korea University, Seoul, South Korea ) , Zhang, Yinhua (Department of Neuroscience, College of Medicine, Korea University, Seoul, South Korea ) , Jin, Chunmei (Department of Neuroscience, College of Medicine, Korea University, Seoul, South Korea ) , Cho, Hyo Min (Department of Biomedical Sciences, College of Medicine, Korea University, Seoul, South Korea ) , Kim, Won-Ki (Department of Neuroscience, College of Medicine, Korea University, Seoul, South Korea ) , Sun, Woong (Department of Biomedical Sciences, College of Medicine, Korea University, Seoul, South Korea ) , Han, Kihoon (Department of Neuroscience, College of Medicine, Korea)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 581 - 586 , 2017 , 0006-291x ,

    초록

    Abstract Variants of the SHANK3 gene, which encodes a core scaffold protein of the postsynaptic density of excitatory synapses, have been causally associated with numerous brain disorders. Shank3 proteins directly bind zinc ions through their C-terminal sterile α motif domain, which enhances the multimerization and synaptic localization of Shank3, to regulate excitatory synaptic strength. However, no studies have explored whether zinc affects the protein interactions of Shank3, which might contribute to the synaptic changes observed after zinc application. To examine this, we first purified Shank3 protein complexes from mouse brain synaptosomal lysates that were incubated with different concentrations of ZnCl 2 , and analyzed them with mass spectrometry. We used strict criteria to identify 71 proteins that specifically interacted with Shank3 when extra ZnCl 2 was added to the lysate. To characterize the zinc-induced Shank3 interactome, we performed various bioinformatic analyses that revealed significant associations of the interactome with subcellular compartments, including mitochondria, and brain disorders, such as bipolar disorder and schizophrenia. Together, our results showing that zinc affected the Shank3 protein interactions of in vitro mouse synaptosomes provided an additional link between zinc and core synaptic proteins that have been implicated in multiple brain disorders. Highlights The synaptosomal Shank3 complexes incubated with different ZnCl 2 concentrations were analyzed by mass spectrometry. The 71 proteins that specifically interacted with Shank3 under extra ZnCl 2 conditions were identified. The zinc-induced Shank3 interactome is associated with mitochondria and brain disorders.

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  5. [해외논문]   Antidiabetic effect of gomisin N via activation of AMP-activated protein kinase   SCI SCIE

    Jung, Dae Young (Division of Longevity and Biofunctional Medicine, School of Korean Medicine, Pusan National University, Yangsan 50612, Republic of Korea ) , Kim, Ji-Hyun (Division of Longevity and Biofunctional Medicine, School of Korean Medicine, Pusan National University, Yangsan 50612, Republic of Korea ) , Lee, Hoyoung (KM Fundamental Research Division, Korea Institute of Oriental Medicine, Daejeon 34054, Republic of Korea ) , Jung, Myeong Ho (Division of Longevity and Biofunctional Medicine, School of Korean Medicine, Pusan National University, Yangsan 50612, Republic of Korea)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 587 - 593 , 2017 , 0006-291x ,

    초록

    Abstract Gomisin N (GN) is a lignan derived from Schisandra chinensis . AMP-activated kinase (AMPK) has gained attention as a therapeutic target for the treatment of metabolic syndrome. Previously, we reported that GN activated the AMPK pathway and ameliorated high-fat diet (HFD)-induced hepatic steatosis. In this study, we investigated the anti-diabetic effects of GN in C2C12 myotubes and HFD obese mice. GN enhanced the phosphorylation of AMPK/acetyl-CoA carboxylase (ACC) and Akt. In addition, GN promoted glucose uptake in C2C12 myotubes, which was accompanied by the translocation of glucose transporter 4 (GLUT4) to the plasma membrane. Treatment with compound C, an AMPK inhibitor, suppressed GN-mediated stimulation of glucose uptake. Furthermore, GN increased the expression of mitochondria biogenesis and fatty acid oxidation genes in C2C12 myotubes. In the in vivo study, administration of GN to HFD mice decreased the levels of fasting blood glucose and insulin, and improved glucose tolerance in HFD obese mice. GN administration rescued the decreased phosphorylation of AMPK and Akt and stimulated the expression of mitochondria biogenesis genes in the skeletal muscle of HFD mice. These findings suggested that GN exerted anti-hyperglycemic effects through AMPK activation. Highlights Gomisin N activated AMPK/Akt signaling in C2C12 myotubes. Gomisin N stimulated glucose uptake in C2C12 myotubes. Gomisin N promoted mitochondria biogenesis and fatty acid oxidation in C2C12 myotubes. Gomisin N reduced hyperglycemia and improved glucose tolerance in HFD obese mice. Graphical abstract [DISPLAY OMISSION]

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  6. [해외논문]   TRIP6 promotes cell proliferation in hepatocellular carcinoma via suppression of FOXO3a   SCI SCIE

    Zhao, Wenhui (BinZhou Medical University, Yantai 264003, China ) , Dai, Yubin (GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China ) , Dai, Ting (GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China ) , Xie, Tian (GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China ) , Su, Xiaobo (GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China ) , Li, Jing (GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China ) , Zhou, Xiang (Department of Microsurgery, Trauma and Hand Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China ) , Meng, Kewei (Tianjin First Center Hospital, Tianjin 300192, China ) , Zhao, Xiaohui (GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 594 - 601 , 2017 , 0006-291x ,

    초록

    Abstract Thyroid hormone receptor-interacting protein 6 (TRIP6), a member of LIM family, acts as an adaptor protein and is overexpressed in several tumor types. However, the clinical significance and biological role of TRIP6 in HCC remains unknown. In our study, we found that TRIP6 was markedly overexpressed in HCC cells and clinical specimens compared with normal hepatocytes and adjacent non-tumor tissues. Immunohistochemical and statistical analysis showed that the expression of TRIP6 significantly correlated with HCC patients' clinical stage and poor survival. Moreover, we demonstrated that overexpressing TRIP6 significantly enhanced, whereas silencing endogenous TRIP6 inhibited, the proliferation and the anchorage-independent growth ability of HCC cells. In addition, overexpression of TRIP6 accelerated, while inhibition of TRIP6 retarded, G1-S phase transition in HCC cells. We further found that overexpression of TRIP6 increased the activation of AKT and suppressed the transactivity of FOXO3a. Meanwhile, overexpression of TRIP6 leaded to the decreased expression of cyclin-dependent kinase inhibitors p21 Cip1 and p27 Kip1 and increased expression of the cell cycle regulator cyclin D1. While silencing TRIP6 triggered the opposite effect. Taken together, these findings showed that TRIP6 plays an important role in promoting HCC cells proliferation and may serve as a novel prognostic biomarker and therapeutic target in HCC. Highlights TRIP6 was upregulated in HCC cells and tissue. TRIP6 expression was correlated with HCC patients’ clinical stage and poor survival. TRIP6 enhanced the proliferation of HCC cells via suppression of FOXO3a. TRIP6 may serve as a novel prognostic biomarker and therapeutic target in HCC.

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  7. [해외논문]   Sequence conservation of protein binding segments in intrinsically disordered regions   SCI SCIE

    Ota, Haruki (Corresponding author.) , Fukuchi, Satoshi
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 602 - 607 , 2017 , 0006-291x ,

    초록

    Abstract Intrinsically disordered proteins are proteins with intrinsically disordered regions (IDRs) that do not adopt a globular structure in their free state. IDRs have unique regions having protein-binding segments of which play pivotal roles in many biological processes. The binding sites in IDRs are heterogeneous in terms of their sequence conservation: some are conserved and others are not. We have been running a database of intrinsically disordered proteins, IDEAL, and collecting such binding segments, which are called protean segments (ProSs), within it. In this study, we compared the sequence conservation of ProSs, structural domains (SDs), and IDRs other than ProSs (non-ProSs) and found that i) functionally constrained residues in ProSs tend to be conserved, ii) the distribution of conservation scores of ProSs is similar to those of SDs but not non-ProSs, and iii) ProSs found in human proteins are mostly conserved only in vertebrates. These results indicate that the conservation patterns in ProSs principally follow the general rules found in SDs. However, we need to consider evolutionary distance when comparing IDR sequences because ProSs can readily emerge and disappear over the course of protein evolution. Moreover, many ProSs may remain to be identified, which may account for the heterogeneity of the sequence conservation of IDRs. Highlights Sequence conservation in protein-binding segments in IDRs is analyzed. Functionally constraint residues in protein-binding segments in IDRs are conserved. Evolutionary distance should be considered in the comparison of IDRs. Cryptic binding regions may influence sequence conservation of IDRs.

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  8. [해외논문]   A novel puromycin decorporation method to quantify skeletal muscle protein breakdown: A proof-of-concept study   SCI SCIE

    Crossland, Hannah (Corresponding author. MRC-ARUK Centre for Musculoskeletal Ageing Research, National Institute for Health Research Biomedical Research Centre, School of Medicine, University of Nottingham, Derby, DE22 3DT, UK.) , Smith, Kenneth , Atherton, Philip J. , Wilkinson, Daniel J.
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 608 - 614 , 2017 , 0006-291x ,

    초록

    Abstract The precise roles that the major proteolytic pathways play in the regulation of skeletal muscle mass remain incompletely understood, in part due to technical limitations associated with current techniques used to quantify muscle protein breakdown (MPB). We aimed to develop a method to assess MPB in cells, based on loss of puromycin labelling of translated polypeptide chains. Following an initial 24 h incubation period with puromycin (1 μM), loss of puromycin labelling from murine C2C12 myotubes was assessed over 48 h, both in the presence or absence of protein synthesis inhibitor cycloheximide (CHX). To validate the method, loss of puromycin labelling was determined from cells treated with selected compounds known to influence MPB (e.g. serum starvation, Dexamethasone (Dex), tumour necrosis factor alpha (TNF-α) and MG-132)). Reported established (static) markers of MPB were measured following each treatment. Loss of puromycin labelling from cells pre-incubated with puromycin was evident over a 48 h period, both with and without CHX. Treatment with Dex (−14 ± 2% vs. Ctl; P P P P in vitro using an established muscle cell line. It is anticipated this non isotopic-tracer alternative to measuring MPB will facilitate insight into the mechanisms that regulate muscle mass/MPB both in vitro , and perhaps, in vivo . Highlights Limitations exist in the techniques used to quantify muscle protein breakdown (MPB). We developed a method for assessing MPB through loss of puromycin labelling in cells. We validated the method using selected compounds known to dynamically modulate MPB.

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  9. [해외논문]   Regulatory effects of the AMPKα-SIRT1 molecular pathway on insulin resistance in PCOS mice: An in vitro and in vivo study   SCI SCIE

    Tao, Xin (Center for Reproductive Medicine, The Third Affiliated Hospital, Sun-Yet Sen University, People's Republic of China ) , Chen, Lei (Center for Reproductive Medicine, The Third Affiliated Hospital, Sun-Yet Sen University, People's Republic of China ) , Cai, Lisi (Center for Reproductive Medicine, The Third Affiliated Hospital, Sun-Yet Sen University, People's Republic of China ) , Ge, Shuqi (Department of Infertility and Sexual Medicine, The Third Affiliated Hospital, Sun-Yet Sen University, People's Republic of China ) , Deng, Xuanying (Center for Reproductive Medicine, The Third Affiliated Hospital, Sun-Yet Sen University, People's Republic of China)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 615 - 620 , 2017 , 0006-291x ,

    초록

    Abstract In order to preliminarily explore the correlation between the AMPKα-SIRT1 pathway and insulin resistance and reproductive function in PCOS mice and find the pathogenesis molecular mechanism and potential therapeutic target of PCOS, we carried out in vitro study of human granulosa KGN cells and in vivo study of PCOS mouse model which was constructed with DHEA, and AICAR and Compound C were applied. We have found that SIRT1 and AMPKα expression in KGN cells gradually decreased as DHEA concentration increased; Mice of the PCOS model were in an obvious status of IR (P Highlights The first research connecting the pathogenesis of IR in PCOS with AMPKα-SIRT1 molecular pathway. Hyperandrogenism decreased the expression of AMPKα and SIRT1 in human ovarian granulosa cells. AMPK agonists AICAR can improve the reproductive and endocrine function of PCOS mice. The AMPKα-SIRT1 pathway could be up-regulated after AICAR treatment in the ovaries PCOS mice. AMPKα-SIRT1 pathway may be a molecular mechanism of IR in PCOS and may serve as a therapeutic target.

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  10. [해외논문]   Crystal structures of Aflatoxin-oxidase from Armillariella tabescens reveal a dual activity enzyme   SCI SCIE

    Xu, Tingting (School of Life Sciences, University of Science and Technology of China, Hefei, 230026, China ) , Xie, Chunfang (National Engineering Research Center of Genetic Medicine, Jinan University, Guangzhou, 510632, China ) , Yao, Dongsheng (National Engineering Research Center of Genetic Medicine, Jinan University, Guangzhou, 510632, China ) , Zhou, Cong-Zhao (School of Life Sciences, University of Science and Technology of China, Hefei, 230026, China ) , Liu, Jinsong (State Key Laboratory of Respiratory Disease, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 621 - 625 , 2017 , 0006-291x ,

    초록

    Abstract Aflatoxin-oxidase (AFO), a newly discovered oxidase isolated from Armillariella tabescens , was reported to perform aflatoxin B1 (AFB1) detoxification through breaking the bisfuran ring of AFB1. However, based on sequence alignment, we found that AFO shares high sequence identities with dipeptidyl peptidase III (DPP III) family members. To understand the functions of AFO, we determined its crystal structures in the absence and presence of zinc, copper ion, and employed HPLC to test if AFO could cleave the substrates of DPP III. Our structures reveal that AFO contains the classic DPP III activity center and the HPLC results further confirm that AFO possesses the dipeptidyl peptidase activity. Therefore, AFO should belong to DPP III family. Interestingly, unlike reported classic DPP III structure that has a large domain movement upon substrate binding, the AFO structures all adopt the closed conformation, independent of substrate binding. This conformation characteristic of AFO may be related to its enzyme activities. Taken together, our results demonstrate that AFO is a dual activity enzyme with both aflatoxin-oxidase and dipeptidyl peptidase activities and its unique conformation feature expands our understanding on the mode of reaction for this enzyme family. Highlights We determined the crystal structure of Aflatoxin-oxidase (AFO). AFO belongs to the DPP III family and possesses dipeptidyl peptidase activity. AFO has a unique conformation characteristic. AFO is a dual activity enzyme.

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