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

  1. [해외논문]   Editorial Board  


    Biochemical and biophysical research communications v.494 no.3/4 ,pp. IFC , 2017 , 0006-291x ,

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  2. [해외논문]   Editorial Board   SCI SCIE


    Biochemical and biophysical research communications v.494 no.3/4 ,pp. IFC - IFC , 2017 , 0006-291x ,

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  3. [해외논문]   MiR-126 impairs the intestinal barrier function via inhibiting S1PR2 mediated activation of PI3K/AKT signaling pathway   SCI SCIE

    Chen, Tanzhou (Corresponding author. The Department of Gastroenterology and Hepatology, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Ouhai District, Wenzhou, Zhejiang, 325000, People's Republic of China. ) , Xue, Haibo (Corresponding author. The Department of Gastroenterology and Hepatology, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang, Ouhai District, Wenzhou, Zhejiang, 325000, People's Republic of China.) , Lin, Ruoyang , Huang, Zhiming
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 427 - 432 , 2017 , 0006-291x ,

    초록

    Abstract Background Aberrant expression of miRNAs was a critical element in the pathogenesis of inflammatory bowel disease (IBD). This study aimed to explore the involvement and mechanism of miR-126 in IBD. Methods In this study, the endogenous expressions of miR-126, S1PR2 and S1P in the pathological tissues of patients with IBD were detected using qRT-PCR and western blot assay, respectively. The luciferase reporter gene assay was performed to confirm the targeting regulatory relation between miR-126 and S1PR2. The transendothelial electrical resistance assay was used to measured the value of TEER. Results The expressions of miR-126, S1PR2 and S1P in the pathological tissues of IBD patients were significantly higher than that of the control group. Moreover, miR-126 overexpression contributed to intestinal mucosal barrier dysfunction in vitro . S1PR2 was a direct target of miR-126, and S1PR2 expression was negatively regulated by miR-126 in Caco-2 cells. However, S1PR2 activated by S1P had the protection effect for the integrity and permeability of intestinal mucosal barrier via a PI3K/Akt dependent mechanism. MiR-126 silencing possessed obvious protective effects on the intestinal barrier function, but these effects could be reversed by JTE-013 or LY294002. Conclusion MiR-126 down-regulated S1PR2 and then prevented the activation of PI3K/AKT signaling pathway, which ultimately could damage intestinal mucosal barrier function.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  4. [해외논문]   Peroxiredoxin-1 of macrophage is critical for mycobacterial infection and is controlled by early secretory antigenic target protein through the activation of p38 MAPK   SCI SCIE

    Yabaji, Shivraj M. (Division of Microbiology, CSIR-Central Drug Research Institute, Lucknow 226031, India ) , Mishra, Alok K. (Division of Microbiology, CSIR-Central Drug Research Institute, Lucknow 226031, India ) , Chatterjee, Aditi (Division of Microbiology, CSIR-Central Drug Research Institute, Lucknow 226031, India ) , Dubey, Rikesh K. (Division of Microbiology, CSIR-Central Drug Research Institute, Lucknow 226031, India ) , Srivastava, Kanchan (Department of Pulmonary Medicine, King George Medical University, Lucknow 226003, India ) , Srivastava, Kishore K. (Division of Microbiology, CSIR-Central Drug Research Institute, Lucknow 226031, India)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 433 - 439 , 2017 , 0006-291x ,

    초록

    Abstract Early secretory antigenic target protein (ESAT-6) is an important virulent factor which plays a crucial role in Mycobacterium tuberculosis (MTB) pathogenesis. Here, we demonstrate the role of ESAT-6 in phagocytosis and intracellular survival of mycobacteria through a mechanism mediated by regulation of a host protein; Peroxiredoxin-1 (Prdx-1). Prdx-1 is an anti-apoptotic and stress response protein which protects cells from damage by ROS and H 2 O 2 . The J774 A.1 cells infected with MTB or over-expressing ESAT-6 through eukaryotic promoter vector showed elevated expression of Prdx-1. Further investigation revealed that the up-regulation of Prdx-1 is mediated through the activation of one of the MAP kinases, p38. The NRF-2, a transcriptional activator of Prdx-1 is translocated to the nucleus upon phosphorylation by p38 and subsequently, regulates expression of Prdx-1. Inhibition of the p38 MAPK by a specific inhibitor, SB203580, abrogates the ESAT-6 mediated induction of Prdx-1 expression as well as the phosphorylation of NRF-2 in a time-dependent manner. The inhibition of Prdx-1 expression by specific siRNA in J774 A.1 cells resulted in the reduced bacterial uptake and intracellular survival of the mycobacteria. This is the first report proclaiming that the ESAT-6 regulates Prdx-1 which is involved in the increase of mycobacterial uptake and survival. The intermediate mechanisms involve the increased Prdx-1 production in macrophages through the activation of p38 and NRF-2 dependent signaling. Highlights The mechanism of MTB ESAT-6 protein mediated regulation in host has not been known. The ESAT-6 up-regulates Prdx-1 through p38 MAPK and NRF-2 signaling which increase intracellular survival. First report showing ESAT-6 up-regulates Prdx-1 to increase intracellular survival. The Prdx-1 induction is important mechanism of mycobacteria to survive and multiply within host.

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  5. [해외논문]   DCIR3 and DCIR4 are co-expressed on inflammatory and patrolling monocytes   SCI SCIE

    Hsu, Yu (Corresponding author. Bioscience Bld. Suite 602, The University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa, Chiba, 277-8562, Japan.) , Okada, Ryo , Nishimura, Takashi , Kawasaki, Norihito , Yamamoto, Kazuo , Matsumoto, Naoki
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 440 - 445 , 2017 , 0006-291x ,

    초록

    Abstract Dendritic cell inhibitory receptor 3 (DCIR3) is a member of dendritic immuno-receptor family, of which protein expression has been unknown. We established a specific monoclonal antibody against mouse DCIR3 and investigated the expression of DCIR3 on immune cells of various immune organs. We found that DCIR3 was expressed on monocytes, but not on eosinophils and neutrophils. We also found the existence of a dichotomy in the levels of the expression of DCIR3 on monocytes in bone marrow, blood and spleen. Further investigation of the expression of several cell surface markers on DCIR3 High cells and DCIR3 Low cells revealed that DCIR3 High cells were Ly-6C − CD43 High CD11c + CD80 + NK1.1 + patrolling monocytes and that DCIR3 Low cells were Ly-6C + CD43 Low CD11c − CD80 - NK1.1- inflammatory monocytes. These results and our previous finding that DCIR4 is expressed at high level in patrolling monocytes and at a low level in inflammatory monocytes (Kameda et al., 2016) suggest that DCIR3 and DCIR4 are simultaneously expressed on monocytes. Indeed, DCIR4 + CD11b + monocytes from various immune organs expressed DCIR3. We also found that DCIR1 was expressed on DCIR4 Low inflammatory monocytes but not on DCIR4 HIgh patrolling monocytes. The anti- DCIR3 antibody established in this study, together with the previously established anti-DCIR1 and anti-DCIR4 antibodies, would be a valuable tool to investigate biology and pathophysiology of monocytes. Highlights A monoclonal antibody against mouse DCIR3 was established. DCIR3 is expressed on inflammatory and patrolling monocytes. DCIR3 and DCIR4 are simultaneously expressed on monocytes. Expression of DCIR1 distinguishes inflammatory monocytes from patrolling monocytes.

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  6. [해외논문]   SUMOylation represses the transcriptional activity of the Unfolded Protein Response transducer ATF6   SCI SCIE

    Hou, Xia (Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA ) , Yang, Zhao (Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA ) , Zhang, Kezhong (Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA ) , Fang, Deyu (Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA ) , Sun, Fei (Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 446 - 451 , 2017 , 0006-291x ,

    초록

    Abstract The Unfolded Protein Response (UPR) is a cascade of intracellular stress signaling from the endoplasmic reticulum (ER) that protect the cells from the stress caused by accumulation of unfolded or misfolded proteins in the ER. Activating transcription factor 6 (ATF6) is one of primary UPR transducers that remodels the stressed cells through transcriptional regulation. Although the activation mechanism and biological roles of ATF6 have been well studied, the understanding of the negative or feedback regulation of ATF6 remains elusive. In this report, we showed that ATF6 protein can be modified by small ubiquitin-like modification (SUMOylation) and that the transcriptional activity of ATF6 is negatively regulated by SUMOylation. We identified that SUMOylation of ATF6 is significantly increased in the cells expressing misfolded cystic fibrosis transmembrane conductance regulator (CFTR) encoded by the mutant human CFTR gene (dF508CFTR). Further analyses revealed two highly conserved SUMOylation motifs within the trans -activation domain of ATF6 protein of human, mouse, or rat specie. The human ATF6 protein can be SUMOylated mediated through the small ubiquitin-like modifier protein 1 (SUMO-1) and E3 SUMO-protein ligase 1 (PIAS1) at the conserved sumoylation residue Lys 149 that is located at the N-terminal of the activated form of ATF6 protein. Bimolecular fluorescence complementation (BiFC) analysis confirmed that the activated ATF6 protein can be SUMOylated and that the ATF6 sumoylation occurs in the nuclei. Moreover, trans -activation reporter analysis demonstrated that SUMOylation of the ATF6 protein at the conserved residue Lys 149 represses the transcriptional activity of ATF6. In summary, our study revealed a negative regulation of the UPR transducer ATF6 through post-translational SUMOylation. The information from this study will not only increase our understanding of the fine-tuning regulation of the UPR signaling but will also be informative to the modulation of the UPR for therapeutic benefits. Highlights The UPR transducer ATF6 is modified through SUMOylation under ER stress as a feedback regulation. SUMOylation of ATF6 is mediated through SUMO-1 and PIAS1. SUMOylation represses the transcriptional activity of ATF6. Expression of misfolded human cystic fibrosis transmembrane conductance regulator leads to ATF6 SUMOylation.

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  7. [해외논문]   Unique binding mode of Evogliptin with human dipeptidyl peptidase IV   SCI SCIE

    Lee, Hyung Ki (Biomedical Research Institute, Korea Institute of Science and Technology, Seoul, Republic of Korea ) , Kim, Mi-Kyung (Dong-A Socio R&D Center, Yongin, Republic of Korea ) , Kim, Ha Dong (Dong-A Socio R&D Center, Yongin, Republic of Korea ) , Kim, Heung Jae (Dong-A Socio R&D Center, Yongin, Republic of Korea ) , Kim, Ji Won (Department of Chemistry, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea ) , Lee, Jie-Oh (Department of Chemistry, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea ) , Kim, Chan-Wha (School of Life Sciences and Biotechnology Korea University, Seoul, Republic of Korea ) , Kim, Eunice EunKyeong (Biomedical Research Institute, Korea Institute of Science and Technology, Seoul, Republic of Korea)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 452 - 459 , 2017 , 0006-291x ,

    초록

    Abstract Evogliptin (( R )-4-(( R )-3-amino-4-(2,4,5-trifluorophenyl)butanoyl)-3-( tert- butoxymethyl) piperazine-2-one)) is a highly potent selective inhibitor of dipeptidyl peptidase IV (DPP4) that was approved for the treatment of type 2 diabetes in South Korea. In this study, we report the crystal structures of Evogliptin, DA-12166, and DA-12228 ( S,R diastereomer of Evogliptin) complexed to human DPP4. Analysis of both the structures and inhibitory activities suggests that the binding of the trifluorophenyl moiety in the S 1 pocket and the piperazine-2-one moiety have hydrophobic interactions with Phe357 in the S 2 extensive subsite, and that the multiple hydrogen bonds made by the ( R )-β-amine group in the S 2 pocket and the contacts made by the ( R )- tert -butyl group with Arg125 contribute to the high potency observed for Evogliptin.

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  8. [해외논문]   Dihydroceramide is a key metabolite that regulates autophagy and promotes fibrosis in hepatic steatosis model   SCI SCIE

    Lee, Ah Young (Laboratory of Toxicology, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Republic of Korea ) , Lee, Jae Won (Department of Applied Chemistry, College of Applied Science, Kyung Hee University, Yongin 17104, Republic of Korea ) , Kim, Ji-Eun (Laboratory of Toxicology, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Republic of Korea ) , Mock, Hyuck Jun (Department of Applied Chemistry, College of Applied Science, Kyung Hee University, Yongin 17104, Republic of Korea ) , Park, Sungjin (Laboratory of Toxicology, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Republic of Korea ) , Kim, Sanghwa (Laboratory of Toxicology, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul National University, Seoul 08826, Republic of Korea ) , Hong, Seong-Ho (Laboratory of Toxicology, Research Institute for Veterinary Science and College of Veterinary Medicine, Seoul) , Kim, Ji-Young , Park, Eun-Jung , Kang, Kyung-Sun , Kim, Kwang Pyo , Cho, Myung-Haing
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 460 - 469 , 2017 , 0006-291x ,

    초록

    Abstract Non-alcoholic fatty liver disease (NAFLD) is an increasingly common chronic liver disease worldwide. Sphingolipids are a family of lipids that play essential roles as critical regulators in metabolic disorders. Some sphingolipids are known key factors in metabolic dysfunction. However, the precise effect of dihydroceramide on NAFLD remains unknown. Here, we report how dihydroceramide in autophagosome accumulation activates fibrogenesis in human liver Chang cells treated with free fatty acids (FFA). According to LC/MS lipid profiling, FFA increased the levels of sphingolipids and triacylglycerol (TG). To demonstrate the potential role of dihydroceramide metabolism in autophagy, several sphingolipid synthesis inhibitors were used. Increased dihydroceramide led to impairment of autophagic flux, resulting in increased TG storage in lipid droplets (LD) and upregulated expression of fibrosis markers. Hepatic stellate cells (HSCs, LX-2 cells) were co-cultured with Chang cells to assess the potential fibrogenic response to dihydroceramide, Treatment with rapamycin recovered autophagic flux in Chang cells and fibrogenesis in the co-culture system. Our results identified a critical function of dihydroceramide metabolism in autophagy. It could play an important role in the progression of NAFLD associated with lipid over-accumulation. Therefore, preventing autophagic flux by regulating dihydroceramide could be a potential strategic approach for providing therapy for NAFLD. Highlights FFA uptake increases sphingolipids in liver cells. Dihydroceramide product correlates with autophagosome accumulation. Dihydroceramide impairs autophagic flux and increases lipid droplets. Rapamycin recuperates fibrosis by recovering autophagic flux by increased dihydroceramide.

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  9. [해외논문]   JAK2V617F influences epigenomic changes in myeloproliferative neoplasms   SCI SCIE

    Chen, Chih-Cheng (Department of Hematology and Oncology, Chang Gung Memorial Hospital, Chiayi, Chang Gung University College of Medicine, Taoyuan, Taiwan ) , Chiu, Chia-Chen (Department of Hematology and Oncology, Chang Gung Memorial Hospital, Chiayi, Chang Gung University College of Medicine, Taoyuan, Taiwan ) , Lee, Kuan-Der (Division of Hematology and Oncology, Department of Medicine, Taipei Medical University Hospital, Taipei, Taiwan ) , Hsu, Chia-Chen (Department of Hematology and Oncology, Chang Gung Memorial Hospital, Chiayi, Chang Gung University College of Medicine, Taoyuan, Taiwan ) , Chen, Hong-Chi (Department of Life Science and Gene Therapy Division, Tzu-Chi University and Hospital, Hualien, Taiwan ) , Huang, Tim H.-M. (Cancer Therapy and Research Center, Department of Molecular Medicine and Institute of Biotechnology, School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA ) , Hsiao, Shu-Huei (Human Epigenomics Center, Department of Life Science, Institute of Molecular Biology and Institute of Biomedical Science, National Chung Cheng University,) , Leu, Yu-Wei
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 470 - 476 , 2017 , 0006-291x ,

    초록

    Abstract Negative valine (V) to phenylalanine (F) switch at the Janus kinase (JAK2) 617 codon (V617F) is the dominant driver mutation in patients with myeloproliferative neoplasms (MPNs). JAK2V617F was proved to be sufficient for cell transformation; however, independent mutations might influence the following epigenomic modifications. To assess the JAK2V617F-induced downstream epigenomic changes without interferences, we profiled the epigenomic changes in ectopically expressed JAK2V617F in Ba/F3 cells. Antibodies against phosphorylated signal transducer and activator of transcription 3 (pSTAT3) and enhancer of zeste homolog 2 (EZH2) were used for chromatin-immunoprecipitation sequencing (ChIP-seq) to detect the downstream epigenomic targets in the JAK2–STAT3 signaling pathway. To confirm the JAK2V617F-induced epigenetic changes in vivo , DNA methylation changes in the target loci in patients with MPNs were detected through methylation-specific polymerase chain reaction and were clustered against the changes within controls. We found that ectopically expressed JAK2V617F in Ba/F3 cells reduced the binding specificity; it was associated with cis -regulatory elements and recognized DNA motifs in both pSTAT3-downstream and EZH2-associated targets. Overlapping target loci between the control and JAK2V617F were FOXH1, HOXC9 , and SRF ) were clustered independently from the control locus ( L1TD1 ) and other mutation genes ( HMGA2 and Lin28A ) in the analyzed MPN samples. Therefore, JAK2V617F influences target binding in both pSTAT3 and EZH2. Without mutations in epigenetic regulators, JAK2V617F can induce downstream epigenomic modifications. Thus, epigenetic changes in JAK2 downstream targets might be trackable in vivo . Highlights Ectopically expressed JAK2V617F in Ba/F3 cells reduced the binding specificity of pSTAT3- and EZH2-associated targets. JAK2V617F can induce downstream epigenomic modifications. The methylation changes in the JAK2-STAT3 target loci were clustered differently from the control and other mutation genes.

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  10. [해외논문]   A chemical screen identifies trifluoperazine as an inhibitor of glioblastoma growth   SCI SCIE

    Pinheiro, Tiago (Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden ) , Otrocka, Magdalena (Chemical Biology Consortium Sweden, Science for Life Laboratory, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden ) , Seashore-Ludlow, Brinton (Chemical Biology Consortium Sweden, Science for Life Laboratory, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden ) , Rraklli, Vilma (Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden ) , Holmberg, Johan (Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden ) , Forsberg-Nilsson, Karin (Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden ) , Simon, Andrá (Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden ) , s (Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden) , Kirkham, Matthew
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 477 - 483 , 2017 , 0006-291x ,

    초록

    Abstract Glioblastoma (GBM) is regarded as the most common malignant brain tumor but treatment options are limited. Thus, there is an unmet clinical need for compounds and corresponding targets that could inhibit GBM growth. We screened a library of 80 dopaminergic ligands with the aim of identifying compounds capable of inhibiting GBM cell line proliferation and survival. Out of 45 active compounds, 8 were further validated. We found that the dopamine receptor D2 antagonist trifluoperazine 2HCl inhibits growth and proliferation of GBM cells in a dose dependent manner. Trifluoperazine's inhibition of GBM cells is cell line dependent and correlates with variations in dopamine receptor expression profile. We conclude that components of the dopamine receptor signaling pathways are potential targets for pharmacological interventions of GBM growth. Highlights Screening of GBM cells uncovers 45 active dopaminergic ligands and 8 were validated. Ligand selectivity suggests dopamine-mediated cell viability regulation in GBM. The DRD2 antagonist trifluoperazine inhibits cell viability and growth of GBM cells. DR expression profile of GBM cells alter the susceptibility to trifluoperazine.

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