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

  1. [해외논문]   1α,25-Dihydroxyvitamin D3 increases implant osseointegration in diabetic mice partly through FoxO1 inactivation in osteoblasts   SCI SCIE

    Xiong, Yi (State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China ) , Zhang, Yixin (State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China ) , Guo, Yanjun (State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China ) , Yuan, Ying (State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China ) , Guo, Qiang (State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China ) , Gong, Ping (State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China ) , Wu, Yingying (State Key)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 626 - 633 , 2017 , 0006-291x ,

    초록

    Abstract Oral implant osseointegration is delayed by hyperglycemia-generated oxidative stress (OS). Forkhead transcription factor 1 (FoxO1) is known to be viewed as a sensor to OS since reactive oxide species like H 2 O 2 regulates its activity. We previously demonstrated that 1,25(OH) 2 D 3 favored glucose homeostasis and implant osseointegration in diabetic rats. In this study, we investigated the role of FoxO1 OB in the regulation process of 1,25(OH) 2 D 3 on glycometabolism and bone metabolism. We show herein that, with the treatment of 1,25(OH) 2 D 3 , mice lacking FoxO1 in osteoblasts (FoxO1 OB −/- ) exhibited decreased serum glucose that was gradually elevated in untreated diabetic mice. An optimal increase of bone mass and bone-implant contact (BIC) was observed in 1,25(OH) 2 D 3 treated FoxO1 OB −/- mice after 2-month healing. Surprisingly, FoxO1 OB −/- mice without 1,25(OH) 2 D 3 treatment also showed an improvement on bone formation and BIC. Same effect could be found in the expression of bone-related markers Runx2, Osterix and BSP, which elevated in 1,25(OH) 2 D 3 treated FoxO1 OB −/- mice as compared to untreated WT mice. In addition, in vitro study showed that high glucose induced FoxO1 nuclear localization while the effect was ameliorated by 1,25(OH) 2 D 3 treatment. These results suggest that FoxO1 OB might be involved in the regulation of 1,25(OH) 2 D 3 on glucose homeostasis and bone formation, and that FoxO1 OB might act as a key modulator of the capacity of the skeleton regulating metabolic homeostasis. Our study also provides a new idea that a combination of systemic 1,25(OH) 2 D 3 and local FoxO1 inhibitor may be a new approach to enhance implant osseointegration. Highlights FoxO1 ablation in osteoblasts favors glucose homeostasis in diabetic mice. 1,25(OH) 2 D 3 regulates glucose and bone metabolism partly through inactivation of FoxO1. FoxO1 inhibitor may be a novel approach to enhance implant osseointegration.

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  2. [해외논문]   Investigation on temperature-induce conformational change of immobilized β 2 adrenergic receptor   SCI SCIE

    Gao, Xiaokang (School of Pharmaceutical Sciences, Hubei Key Laboratory of Wudang Local Chinese Medicine Research, Hubei Provincial Technology and Research Center for Comprehensive Development of Medicinal Herbs, Hubei University of Medicine, Shiyan 442000, Hubei, China ) , Yang, Lingjian (College of Life Science, Northwest University, Xi'an 710069, China ) , Li, Qian (College of Life Science, Northwest University, Xi'an 710069, China ) , An, Yuxin (College of Life Science, Northwest University, Xi'an 710069, China ) , Liao, Sha (College of Life Science, Northwest University, Xi'an 710069, China ) , Gao, Haiyang (College of Life Science, Northwest University, Xi'an 710069, China ) , Zhao, Xinfeng (College of Life Science, Northwest University, Xi'an 710069, China ) , Bian, Liujiao (College of Life Science, Northwest University, Xi'an 710069, China ) , Zheng, Xiaohui (College of Life Science, Northwest University, Xi'an 710069, China)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 634 - 640 , 2017 , 0006-291x ,

    초록

    Abstract The β 2 adrenergic receptor ( β 2 -AR) is a prototypical family A G protein-coupled receptor (GPCR) and an excellent model system for studying the mechanism of GPCR activation. Purified β 2 -AR was immobilized on macroporous silica gel to obtain liquid chromatographic stationary phase. The resulting phase was packed into a stainless steel column (4.6 × 50 mm, 7 μm) and used for on-line chromatographic system. When column oven temperature increased from 20.0 °C to 40.0 °C, uncomplete separate chromatographic peaks of ephedrine and pseudoephedrine as receptor conformational probe were gradually merged into one peak, meanwhile retention time and resolution of the probes were reduced correspondingly, which suggested that temperature could regulate protein conformation. Temperature-induced conformational change of immobilized β 2 -AR, especially changes at higher temperatures, indicated that constructed receptor chromatography could simulate fever disease state of human body and clarify receptor conformation change at pathological condition. At the same time this study could also provide new ideas for screening active components in pathological conditions. Highlights Temperature could regulate protein conformational. The receptor chromatography can simulate the pathological conditions of human fever.

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  3. [해외논문]   Variation in the activity of distinct cytochalasins as autophagy inhibitiors in human lung A549 cells   SCI SCIE

    Takanezawa, Yasukazu (Department of Public Health, School of Pharmacy, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo, 108-8641, Japan ) , Nakamura, Ryosuke (Department of Public Health, School of Pharmacy, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo, 108-8641, Japan ) , Sone, Yuka (Department of Public Health, School of Pharmacy, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo, 108-8641, Japan ) , Uraguchi, Shimpei (Department of Public Health, School of Pharmacy, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo, 108-8641, Japan ) , Kobayashi, Keisuke (Graduate School of Pharmaceutical Sciences, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo, 108-8641, Japan ) , Tomoda, Hiroshi (Graduate School of Pharmaceutical Sciences, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo, 108-8641, Japan ) , Kiyono, Masako (Department of Public Health, School of Pharmacy, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo, 108-8641, Japan)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 641 - 647 , 2017 , 0006-291x ,

    초록

    Abstract Autophagy is a cell survival process that represents a therapeutic target in cancer treatment. Many types of cytochalasins have been identified and some of them have been reported to interfere with the formation of the autophagosome, although only limited data are available to assess their potential effects. Therefore, in this study, we examined the effects of cytochalasins and structurally related compounds on cell survival and the regulation of autophagy in human lung A549 adenocarcinoma cells. Cytochalasin D (CD) and cytochalasin E (CE) prominently inhibited the growth of A549 cells in a dose-dependent manner. Following treatment with CE, F-actin filaments were disrupted, and the proportion of binucleated cells increased, whereas no such effects were observed with the seven other cytochalasins tested. We found that cytochalasin H (CH), CD, and especially CE could induce the up-regulation of autophagy-related protein (LC3-II) and SQSTM1/p62. Using bafilomycin A 1 , we demonstrated that CD, CE, and CH inhibited autophagosome turnover, resulting in a dysfunctional autophagic process. The results of this study reveal that CE is the most potent cytochalasin in terms of its ability to induce cell death and inhibit autophagy. CE may therefore be an effective therapeutic agent against lung cancer. Highlights Cytochalasin E and H are novel inhibitors of autophgic flux. Cytochalasin D, E, and H inhibit autophagy and are new anti-cancer drug candidates. Phenochalasin A inhibits lipid droplet formation without autophagic effects.

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  4. [해외논문]   Exposure to cigarette smoke disturbs adipokines secretion causing intercellular damage and insulin resistance in high fructose diet-induced metabolic disorder mice   SCI SCIE

    Kim, Sanghwa (Division of Basic Radiation Bioscience, Korea Institute of Radiological & Medical Science, Seoul 01812, Republic of Korea ) , Lee, Ah Young (Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University, Seoul 08826, Republic of Korea ) , Kim, Hyeon-Jeong (Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University, Seoul 08826, Republic of Korea ) , Hong, Seong-Ho (Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University, Seoul 08826, Republic of Korea ) , Go, Ryeo-Eun (Laboratory of Biochemistry and Immunology, Veterinary Medical Center and College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 28644, Republic of Korea ) , Choi, Kyung-Chul (Laboratory of Biochemistry and Immunology, Veterinary Medical Center and College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 28644, Republic of Korea ) , Kang, Kyung-Sun (Adult Stem Cell Research Center, College of Veterinary Medicine, Seoul National University, Seoul 08826, Republic of Korea ) , Cho, Myung-Haing (Laboratory of Toxicology, College o)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 648 - 655 , 2017 , 0006-291x ,

    초록

    Abstract A large amount of fructose intake along with smoking is associated with increased incidence of diseases linked to metabolic syndrome. More research is necessary to understand the complex mechanism that ultimately results in metabolic syndrome and the effect, if any, of high fructose dietary intake and smoking on individual health. In this study, we investigated changes in ER-Golgi network and disturbance to secretion of adipokines induced by cigarette smoking (CS) and excess fructose intake and their contribution to the disruption of metabolic homeostasis. We used high fructose-induced metabolic disorder mice model by feeding them with high fructose diet for 8 weeks. For CS exposure experiment, these mice were exposed to CS for 28 days according to OECD guideline 412. Our results clearly showed that the immune system was suppressed and ER stress was induced in mice with exposure to CS and fed with high fructose. Furthermore, their concentrations of adipokines including leptin and adiponectin were aberrant. Such alteration in secretion of adipokines could cause insulin resistance which may lead to the development of type 2 diabetes. Highlights Cigarette smoke and fructose excess intake induce disruption to mechanisms involved in ROS generation and ER stress. Damage of cellular organelles induced by cigarette smoke and high fructose feeding affects inflammatory response and alters secretion of adipokines. Cigarette smoking and fructose excess intake are associated with metabolic syndrome.

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  5. [해외논문]   Supplementing zinc oxide nanoparticles to cryopreservation medium minimizes the freeze-thaw-induced damage to spermatozoa   SCI SCIE

    Isaac, Ann V. (Department of Clinical Embryology, Central Research Lab, Kasturba Medical College, Manipal University, Manipal, 576104, Karnataka, India ) , Kumari, Sandhya (Department of Clinical Embryology, Central Research Lab, Kasturba Medical College, Manipal University, Manipal, 576104, Karnataka, India ) , Nair, Ramya (Department of Clinical Embryology, Central Research Lab, Kasturba Medical College, Manipal University, Manipal, 576104, Karnataka, India ) , Urs, Deepak Raj (Department of Clinical Embryology, Central Research Lab, Kasturba Medical College, Manipal University, Manipal, 576104, Karnataka, India ) , Salian, Sujith Raj (Department of Clinical Embryology, Central Research Lab, Kasturba Medical College, Manipal University, Manipal, 576104, Karnataka, India ) , Kalthur, Guruprasad (Department of Clinical Embryology, Central Research Lab, Kasturba Medical College, Manipal University, Manipal, 576104, Karnataka, India ) , Adiga, Satish Kumar (Department of Clinical Embryology, Central Research Lab, Kasturba Medical College, Manipal University, Manipal, 576104, Karnataka, India ) , Manikkath, Jyothsna (Department of Pharmaceutics) , Mutalik, Srinivas , Sachdev, Divya , Pasricha, Renu
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 656 - 662 , 2017 , 0006-291x ,

    초록

    Abstract The sperm DNA integrity post cryopreservation of human semen samples is one of the serious concerns in human infertility treatment. In the present study, the beneficial effects of zinc oxide nanoparticles in preserving the functional ability of spermatozoa was explored. Ejaculates of normozoospermic men cryopreserved along with Zinc oxide nanoparticles (ZnONPs) exhibited non-significantly higher percentage of total and progressive motility in frozen-thawed samples compared to control. The sperm chromatin damage and malondialdehyde (MDA) level was significantly lower in ZnONPs group ( P P

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  6. [해외논문]   PYK2 mediates BzATP-induced extracellular matrix proteins synthesis   SCI SCIE

    Torigoe, Go (Division of Applied Oral Science, Nihon University Graduate School of Dentistry, Tokyo, Japan ) , Nagao, Mayu (Department of Periodontology, Nihon University School of Dentistry, Tokyo, Japan ) , Tanabe, Natsuko (Department of Biochemistry, Nihon University School of Dentistry, Tokyo, Japan ) , Manaka, Soichiro (Department of Periodontology, Nihon University School of Dentistry, Tokyo, Japan ) , Kariya, Taro (Department of Orthodontics, Nihon University School of Dentistry, Tokyo, Japan ) , Kawato, Takayuki (Department of Oral Health Sciences, Nihon University School of Dentistry, Tokyo, Japan ) , Sekino, Jumpei (Division of Applied Oral Science, Nihon University Graduate School of Dentistry, Tokyo, Japan ) , Kato, Shunichiro (Division of Applied Oral Science, Nihon University Graduate School of Dentistry, Tokyo, Japan ) , Maeno, Masao (Nihon University, Tokyo, Japan ) , Suzuki, Naoto (Department of Biochemistry, Nihon University School of Dentistry, Tokyo, Japan ) , Shimizu, Noriyoshi (Department of Orthodontics, Nihon University School of Dentistry, Tokyo, Japan)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 663 - 667 , 2017 , 0006-291x ,

    초록

    Abstract Mechanical stimuli such as fluid shear and cyclic tension force induced extracellular adenosine triphosphate (ATP) release in osteoblasts. In particular, cyclic tension force-induced ATP enhances bone formation through P2X7 activation. Proline-rich tyrosine kinase 2 (PYK2) mediate osteoblasts differentiation is induced by mechanical stimuli. Furthermore, activation of PYK2 also was a response to integrin by mechanical stimuli. Extracellular matrix protein (ECMP)s, which are important factors for bone formation are expressed by osteoblasts. However, the effect of the interaction of 2’(3)- Ο -(4-Benzoylbenzoyl) adenosine-5’-triphosphate (BzATP), which is the agonist of the mechanosensitive receptor P2X7, with PYK2 on ECMP production is poorly understood. Thus, our purpose was to investigate the effects of PYK2 on BzATP-induced ECMP production in osteoblasts. BzATP increased phospho-PYK2 protein expression on days 3 and 7 of culture. Furthermore, the PYK2 inhibitor PF431394 inhibited the stimulatory effect of BzATP on the expression of type I collagen, bone sialoprotein and osteocalcin expression. PF431396 did not inhibit the stimulatory effect of BzATP on osteopontin (OPN) mRNA expression. These results suggest that mechanical stimuli activate P2X7 might induce ECMPs expression through PYK2 except in the case of OPN expression. Altogether, mechanical stimuli-induced ECMPs production might be implicated by extracellular ATP secretion or integrin via PYK2 activation.

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  7. [해외논문]   Stoichiometry and mechanistic implications of the MacAB-TolC tripartite efflux pump   SCI SCIE

    Jo, Inseong (Department of Agricultural Biotechnology, Center for Food Safety and Toxicology, Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea ) , Hong, Seokho (Department of Agricultural Biotechnology, Center for Food Safety and Toxicology, Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea ) , Lee, Minho (Department of Life Science, Chung-Ang University, Seoul 06974, Republic of Korea ) , Song, Saemee (Department of Agricultural Biotechnology, Center for Food Safety and Toxicology, Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea ) , Kim, Jin-Sik (Department of Agricultural Biotechnology, Center for Food Safety and Toxicology, Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea ) , Mitra, Alok K. (School of Biological Sciences, The University of Auckland, Auckland 1010, New Zealand ) , Hyun, Jaekyung (Electron Microscopy Research Center, Korea Basic Scie) , Lee, Kangseok , Ha, Nam-Chul
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 668 - 673 , 2017 , 0006-291x ,

    초록

    Abstract The MacAB-TolC tripartite efflux pump is involved in resistance to macrolide antibiotics and secretion of protein toxins in many Gram-negative bacteria. The pump spans the entire cell envelope and operates by expelling substances to extracellular space. X-ray crystal and electron microscopic structures have revealed the funnel-like MacA hexamer in the periplasmic space and the cylindrical TolC trimer. Nonetheless, the inner membrane transporter MacB still remains ambiguous in terms of its oligomeric state in the functional complex. In this study, we purified a stable binary complex using a fusion protein of MacA and MacB of Escherichia coli , and then supplemented MacA to meet the correct stoichiometry between the two proteins. The result demonstrated that MacB is a homodimer in the complex, which is consistent with results from the recent complex structure using cryo-electron microscopy single particle analysis. Structural comparison with the previously reported MacB periplasmic domain structure suggests a molecular mechanism for regulation of the activity of MacB via an interaction between the MacB periplasmic domain and MacA. Our results provide a better understanding of the tripartite pumps at the molecular level. Highlights The exact stoichiometry of the MacAB-TolC pump was confirmed. Structural comparison provides a mechanism for MacA-dependent MacB activation. Improving understanding of the regulatory mechanisms of other efflux pumps.

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  8. [해외논문]   Downregulation of ZMYND11 induced by miR-196a-5p promotes the progression and growth of GBM   SCI SCIE

    Yang, Ji-peng (Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China ) , Yang, Jian-kai (Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China ) , Li, Chen (Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China ) , Cui, Zhi-qiang (Graduate College of Hebei Medical University, Shijiazhuang, People's Republic of China ) , Liu, Hong-jiang (Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China ) , Sun, Xiao-feng (Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China ) , Geng, Shao-mei (Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China ) , Lu, Sheng-kui (Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China ) , Song, Jian (Department of Neurosurgery, The Second Hospital of Hebe) , Guo, Cheng-yong , Jiao, Bao-hua
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 674 - 680 , 2017 , 0006-291x ,

    초록

    Abstract ZMYND11 (zinc finger MYND-type containing 11) has been widely regarded to be involved in a variety of cancers as a potential suppressor. However, the biological role and mechanism of ZMYND11 in glioblastoma multiform (GBM) remain unknown. In this study, we found that ZMYND11 expression was remarkably decreased in GBM tissues from 20 cases and cell line (U87) compared to normal brain tissue from 10 cases ( P Highlights The expression level of ZMYND11 in GBM tumor tissue and U87 cell line. The role of ZMYND11 upregulation in U87 cells in vitro and vivo. The link of expression level between ZMYND11 and miR-196a-5p in GBM tumor and U87 cells.

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  9. [해외논문]   The reason for a high Ca2+-sensitivity associated with Arg91Gly substitution in TPM2 gene is the abnormal behavior and high flexibility of tropomyosin during the ATPase cycle   SCI SCIE

    Borovikov, Yurii S. (Institute of Cytology, Russian Academy of Sciences, 4 Tikhoretsky Avenue, St. Petersburg 194064, Russia ) , Simonyan, Armen O. (Institute of Cytology, Russian Academy of Sciences, 4 Tikhoretsky Avenue, St. Petersburg 194064, Russia ) , Karpicheva, Olga E. (Institute of Cytology, Russian Academy of Sciences, 4 Tikhoretsky Avenue, St. Petersburg 194064, Russia ) , Avrova, Stanislava V. (Institute of Cytology, Russian Academy of Sciences, 4 Tikhoretsky Avenue, St. Petersburg 194064, Russia ) , Rysev, Nikita A. (Institute of Cytology, Russian Academy of Sciences, 4 Tikhoretsky Avenue, St. Petersburg 194064, Russia ) , Sirenko, Vladimir V. (Institute of Cytology, Russian Academy of Sciences, 4 Tikhoretsky Avenue, St. Petersburg 194064, Russia ) , Piers, Adam (Radcliffe Department of Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom ) , Redwood, Charles S. (Radcliffe Department of Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 681 - 686 , 2017 , 0006-291x ,

    초록

    Abstract Substitution of Arg for Gly residue in 91th position in β-tropomyosin caused by a point mutation in TPM2 gene is associated with distal arthrogryposis, characterized by a high Ca 2+ -sensitivity of myofilament and contracture syndrome. To understand the mechanisms of this defect, we studied multistep changes in mobility and spatial arrangement of tropomyosin, actin and myosin heads during the ATPase cycle in reconstituted ghost fibres, using the polarized fluorescence microscopy. The mutation was shown to markedly decrease the bending stiffness of β-tropomyosin in the thin filaments. In the absence of the myosin heads the mutation did not alter the ability of troponin to shift tropomyosin to the blocked position and to switch actin monomers off at low Ca 2+ . During the ATPase cycle the movement of the mutant tropomyosin is restrained, it is located near the open position, which allows strong binding of the myosin heads to actin even at low Ca 2+ . This may be the reason for both high Ca 2+ -sensitivity and contractures associated with the Arg91Gly mutation. The use of reagents that decrease the Ca 2+ sensitivity of the troponin complex may not be appropriate to restore muscle function in patients with this mutation. Highlights Mutation R91G initiates abnormally high flexibility of β-tropomyosin (TM). Troponin moves R91G-TM to the blocked position at low Ca 2+ . This mutation does not alter the ability of troponin to switch off actin monomers. R91G-TM is located near the open position during the ATPase cycle at low Ca 2+ . Mutation R91G increases the fraction of rigor myosin heads at low Ca 2+ . Graphical abstract [DISPLAY OMISSION]

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  10. [해외논문]   MiR-150 deficiency ameliorated hepatosteatosis and insulin resistance in nonalcoholic fatty liver disease via targeting CASP8 and FADD-like apoptosis regulator   SCI SCIE

    Zhuge, Baozhong (Department of Clinical Laboratory, Linyi People's Hospital, Linyi, Shandong, 276000, China ) , Li, Guohong (Department of Clinical Laboratory, Dezhou Municiple Hospital, Dezhou, Shandong, 253000, China)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 687 - 692 , 2017 , 0006-291x ,

    초록

    Abstract The prevalence of Non-alcoholic fatty liver diseases (NAFLD) increased rapidly in the world. However, the pathogenesis of is still unclear. Hepatic steatosis and insulin resistance are considered to be central to the pathophysiology of NAFLD. MicroRNAs are short non-coding RNAs and has been reported to be involved in pathogenesis of NAFLD and related metabolic diseases. Here, we investigated the mechanisms by which miR-150 regulate hepatic steatosis and insulin resistance in high fat diet (HFD) induced NAFLD model. The expression of miR-150 was up-regulated dramatically in both human NAFLD patients and HFD mice model, as well as in hepatocytes treated with oleic acid. miR-150 deficiency ameliorated the hepatic steatosis and insulin resistance significantly in NAFLD mice. miR-150 deficiency decreased the expression of genes related to fatty acid uptake, synthesis and gluconeogenesis, while increased the expression of genes related to fatty acid β-oxidation. Further, we identified that CFLAR is a direct downstream target of miR-150. Overexpression of miR-150 reduced both the mRNA and protein levels of CFLAR in vitro . And overexpression of miR-150 significantly inhibited the luciferase activity of CFLAR 3′-UTR, while the effect of miR-150 was blocked when the binding site of miR-150 within the CFLAR 3′-UTR was mutated. We also found that miR-150 deficiency decreased the expression of p -Jnk1 and p-Ask1, while the effect of miR-150 on steatosis and insulin signaling was blocked by CFLAR overexpression. In conclusion, our data indicated that miR-150 potentially contributes to the hepatic steatosis and insulin resistance in NAFLD. miR-150/CFLAR pathway may be a new therapeutic strategy against NAFLD.

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