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Cell reports 28건

  1. [해외논문]   A Mouse Ependymoma Model Provides Molecular Insights into Tumor Formation   SCIE

    Pajtler, Kristian W. (Hopp-Children's Cancer Center at the NCT Heidelberg (KiTZ), 69120 Heidelberg, Germany ) , Pfister, Stefan M. (Hopp-Children's Cancer Center at the NCT Heidelberg (KiTZ), 69120 Heidelberg, Germany)
    Cell reports v.23 no.13 ,pp. 3699 - 3700 , 2018 ,

    초록

    Ozawa et al. present a murine tumor model resembling the most frequent molecular group of human supratentorial ependymoma, ST-EPN-RELA. Their model shows RELA-fusion-based de novo ependymoma tumorigenesis in the forebrain derived from neural stem cells.

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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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  2. [해외논문]   MOXI Is a Mitochondrial Micropeptide That Enhances Fatty Acid β-Oxidation   SCIE

    Makarewich, Catherine A. (Department of Molecular Biology and the Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA ) , Baskin, Kedryn K. (Department of Molecular Biology and the Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA ) , Munir, Amir Z. (Department of Molecular Biology and the Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA ) , Bezprozvannaya, Svetlana (Department of Molecular Biology and the Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA ) , Sharma, Gaurav (Advanced Imaging Research Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA ) , Khemtong, Chalermchai (Advanced Imaging Research Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA ) , Shah, Akansha M. (Department of Molecular Biology and the Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern M) , McAnally, John R. , Malloy, Craig R. , Szweda, Luke I. , Bassel-Duby, Rhonda , Olson, Eric N.
    Cell reports v.23 no.13 ,pp. 3701 - 3709 , 2018 ,

    초록

    Summary M icropeptide regulator of β- oxi dation (MOXI) is a conserved muscle-enriched protein encoded by an RNA transcript misannotated as non-coding. MOXI localizes to the inner mitochondrial membrane where it associates with the mitochondrial trifunctional protein, an enzyme complex that plays a critical role in fatty acid β-oxidation. Isolated heart and skeletal muscle mitochondria from MOXI knockout mice exhibit a diminished ability to metabolize fatty acids, while transgenic MOXI overexpression leads to enhanced β-oxidation. Additionally, hearts from MOXI knockout mice preferentially oxidize carbohydrates over fatty acids in an isolated perfused heart system compared to wild-type (WT) animals. MOXI knockout mice also exhibit a profound reduction in exercise capacity, highlighting the role of MOXI in metabolic control. The functional characterization of MOXI provides insight into the regulation of mitochondrial metabolism and energy homeostasis and underscores the regulatory potential of additional micropeptides that have yet to be identified. Highlights MOXI is a muscle-enriched protein encoded by an RNA that is annotated as non-coding MOXI interacts with the mitochondrial trifunctional protein and enhances β-oxidation MOXI loss- or gain-of-function in mice alters β-oxidation and substrate utilization MOXI knockout mice exhibit a reduced capacity for exercise Graphical Abstract [DISPLAY OMISSION]

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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]   Mitoregulin: A lncRNA-Encoded Microprotein that Supports Mitochondrial Supercomplexes and Respiratory Efficiency  

    Stein, Colleen S. , Jadiya, Pooja , Zhang, Xiaoming , McLendon, Jared M. , Abouassaly, Gabrielle M. , Witmer, Nathan H. , Anderson, Ethan J. , Elrod, John W. , Boudreau, Ryan L.
    Cell reports v.23 no.13 ,pp. 3710 - 3720.e8 , 2018 ,

    초록

    Summary M icropeptide regulator of β- oxi dation (MOXI) is a conserved muscle-enriched protein encoded by an RNA transcript misannotated as non-coding. MOXI localizes to the inner mitochondrial membrane where it associates with the mitochondrial trifunctional protein, an enzyme complex that plays a critical role in fatty acid β-oxidation. Isolated heart and skeletal muscle mitochondria from MOXI knockout mice exhibit a diminished ability to metabolize fatty acids, while transgenic MOXI overexpression leads to enhanced β-oxidation. Additionally, hearts from MOXI knockout mice preferentially oxidize carbohydrates over fatty acids in an isolated perfused heart system compared to wild-type (WT) animals. MOXI knockout mice also exhibit a profound reduction in exercise capacity, highlighting the role of MOXI in metabolic control. The functional characterization of MOXI provides insight into the regulation of mitochondrial metabolism and energy homeostasis and underscores the regulatory potential of additional micropeptides that have yet to be identified. Highlights MOXI is a muscle-enriched protein encoded by an RNA that is annotated as non-coding MOXI interacts with the mitochondrial trifunctional protein and enhances β-oxidation MOXI loss- or gain-of-function in mice alters β-oxidation and substrate utilization MOXI knockout mice exhibit a reduced capacity for exercise Graphical Abstract [DISPLAY OMISSION]

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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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  4. [해외논문]   Mitoregulin: A lncRNA-Encoded Microprotein that Supports Mitochondrial Supercomplexes and Respiratory Efficiency   SCIE

    Stein, Colleen S. (Department of Internal Medicine, Fraternal Order of Eagles Diabetes Research Center, Abboud Cardiovascular Research Center, Carver College of Medicine, University of Iowa, Iowa City, IA, USA ) , Jadiya, Pooja (Center of Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA ) , Zhang, Xiaoming (Department of Internal Medicine, Fraternal Order of Eagles Diabetes Research Center, Abboud Cardiovascular Research Center, Carver College of Medicine, University of Iowa, Iowa City, IA, USA ) , McLendon, Jared M. (Department of Internal Medicine, Fraternal Order of Eagles Diabetes Research Center, Abboud Cardiovascular Research Center, Carver College of Medicine, University of Iowa, Iowa City, IA, USA ) , Abouassaly, Gabrielle M. (Department of Internal Medicine, Fraternal Order of Eagles Diabetes Research Center, Abboud Cardiovascular Research Center, Carver College of Medicine, University of Iowa, Iowa City, IA, USA ) , Witmer, Nathan H. (Department of Internal Medicine, Fraternal Order of Eagles Diabetes Research Center, Abboud Cardiovascular Research Ce) , Anderson, Ethan J. , Elrod, John W. , Boudreau, Ryan L.
    Cell reports v.23 no.13 ,pp. 3710 - 3720.e8 , 2018 ,

    초록

    Summary Mitochondria are composed of many small proteins that control protein synthesis, complex assembly, metabolism, and ion and reactive oxygen species (ROS) handling. We show that a skeletal muscle- and heart-enriched long non-coding RNA, LINC00116 , encodes a highly conserved 56-amino-acid microprotein that we named mitoregulin (Mtln). Mtln localizes to the inner mitochondrial membrane, where it binds cardiolipin and influences protein complex assembly. In cultured cells, Mtln overexpression increases mitochondrial membrane potential, respiration rates, and Ca 2+ retention capacity while decreasing mitochondrial ROS and matrix-free Ca 2+ . Mtln-knockout mice display perturbations in mitochondrial respiratory (super)complex formation and activity, fatty acid oxidation, tricarboxylic acid (TCA) cycle enzymes, and Ca 2+ retention capacity. Blue-native gel electrophoresis revealed that Mtln co-migrates alongside several complexes, including the complex I assembly module, complex V, and supercomplexes. Under denaturing conditions, Mtln remains in high-molecular-weight complexes, supporting its role as a sticky molecular tether that enhances respiratory efficiency by bolstering protein complex assembly and/or stability. Highlights LINC00116 encodes a single-pass transmembrane protein known as mitoregulin (Mtln) Mtln appears to be a sticky inner mitochondrial membrane protein that binds cardiolipin Mtln levels influence mitochondrial respiration, ROS, and Ca 2+ retention capacity Mtln-KO mice exhibit deficiencies in FAO, mCa 2+ retention, and supercomplexes Graphical Abstract [DISPLAY OMISSION]

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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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  5. [해외논문]   Mutant p53-Expressing Cells Undergo Necroptosis via Cell Competition with the Neighboring Normal Epithelial Cells   SCIE

    Watanabe, Hirotaka (Division of Molecular Oncology, Hokkaido University, Sapporo 060-0815, Japan ) , Ishibashi, Kojiro (Division of Molecular Oncology, Hokkaido University, Sapporo 060-0815, Japan ) , Mano, Hiroki (Division of Molecular Oncology, Hokkaido University, Sapporo 060-0815, Japan ) , Kitamoto, Sho (Division of Molecular Oncology, Hokkaido University, Sapporo 060-0815, Japan ) , Sato, Nanami (Division of Molecular Oncology, Hokkaido University, Sapporo 060-0815, Japan ) , Hoshiba, Kazuya (Division of Molecular Oncology, Hokkaido University, Sapporo 060-0815, Japan ) , Kato, Mugihiko (Division of Molecular Oncology, Hokkaido University, Sapporo 060-0815, Japan ) , Matsuzawa, Fumihiko (Division of Molecular Oncology, Hokkaido University, Sapporo 060-0815, Japan ) , Takeuchi, Yasuto (Division of Molecular Oncology, Hokkaido University, Sapporo 060-0815, Japan ) , Shirai, Takanobu (Division of Molecular Oncology, Hokkaido University, Sapporo 060-0815, Japan ) , Ishikawa, Susumu (Division of Molecular Oncology, Hokkaido University, Sapporo 060-0815, Japan ) , Morioka, Yuka (Division of Disease Model Innovation, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan ) , Imagawa, Toshiaki (Graduate Schoo) , Sakaguchi, Kazuyasu , Yonezawa, Suguru , Kon, Shunsuke , Fujita, Yasuyuki
    Cell reports v.23 no.13 ,pp. 3721 - 3729 , 2018 ,

    초록

    Summary p53 is a tumor suppressor protein, and its missense mutations are frequently found in human cancers. During the multi-step progression of cancer, p53 mutations generally accumulate at the mid or late stage, but not in the early stage, and the underlying mechanism is still unclear. In this study, using mammalian cell culture and mouse ex vivo systems, we demonstrate that when p53R273H- or p53R175H-expressing cells are surrounded by normal epithelial cells, mutant p53 cells undergo necroptosis and are basally extruded from the epithelial monolayer. When mutant p53 cells alone are present, cell death does not occur, indicating that necroptosis results from cell competition with the surrounding normal cells. Furthermore, when p53R273H mutation occurs within RasV12-transformed epithelia, cell death is strongly suppressed and most of the p53R273H-expressing cells remain intact. These results suggest that the order of oncogenic mutations in cancer development could be dictated by cell competition. Highlights Mutant p53 cells undergo necroptosis when surrounded by normal epithelial cells This cell competition process occurs in cell culture and mouse ex vivo systems When p53 mutation occurs in Ras-transformed epithelia, necroptosis is suppressed Graphical Abstract [DISPLAY OMISSION]

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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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  6. [해외논문]   L1 Retrotransposon Heterogeneity in Ovarian Tumor Cell Evolution   SCIE

    Nguyen, Thu H.M. (Mater Research Institute, University of Queensland, TRI Building, Woolloongabba, QLD 4102, Australia ) , Carreira, Patricia E. (Mater Research Institute, University of Queensland, TRI Building, Woolloongabba, QLD 4102, Australia ) , Sanchez-Luque, Francisco J. (Mater Research Institute, University of Queensland, TRI Building, Woolloongabba, QLD 4102, Australia ) , Schauer, Stephanie N. (Mater Research Institute, University of Queensland, TRI Building, Woolloongabba, QLD 4102, Australia ) , Fagg, Allister C. (Mater Research Institute, University of Queensland, TRI Building, Woolloongabba, QLD 4102, Australia ) , Richardson, Sandra R. (Mater Research Institute, University of Queensland, TRI Building, Woolloongabba, QLD 4102, Australia ) , Davies, Claire M. (Mater Health Services, South Brisbane, QLD 4101, Australia ) , Jesuadian, J. Samuel (Mater Research Institute, University of Queensland, TRI Building, Woolloongabba, QLD 4102, Australia ) , Kempen, Marie-Jeanne H.C. (Mater Research Institute, University of Queensland, TRI Building, Woolloongabba, QLD 4102, Australia ) , Troskie, Robin-Lee (Mater Research Institute, University of Queensland, TRI Building, Woolloongabba, QLD 4102, Australia ) , James, Cini (Mater Resear) , Beaven, Elizabeth A. , Wallis, Tristan P. , Coward, Jermaine I.G. , Chetty, Naven P. , Crandon, Alexander J. , Venter, Deon J. , Armes, Jane E. , Perrin, Lewis C. , Hooper, John D. , Ewing, Adam D. , Upton, Kyle R. , Faulkner, Geoffrey J.
    Cell reports v.23 no.13 ,pp. 3730 - 3740 , 2018 ,

    초록

    Summary LINE-1 (L1) retrotransposons are a source of insertional mutagenesis in tumor cells. However, the clinical significance of L1 mobilization during tumorigenesis remains unclear. Here, we applied retrotransposon capture sequencing (RC-seq) to multiple single-cell clones isolated from five ovarian cancer cell lines and HeLa cells and detected endogenous L1 retrotransposition in vitro . We then applied RC-seq to ovarian tumor and matched blood samples from 19 patients and identified 88 tumor-specific L1 insertions. In one tumor, an intronic de novo L1 insertion supplied a novel cis -enhancer to the putative chemoresistance gene STC1 . Notably, the tumor subclone carrying the STC1 L1 mutation increased in prevalence after chemotherapy, further increasing STC1 expression. We also identified hypomethylated donor L1s responsible for new L1 insertions in tumors and cultivated cancer cells. These congruent in vitro and in vivo results highlight L1 insertional mutagenesis as a common component of ovarian tumorigenesis and cancer genome heterogeneity. Highlights Endogenous L1 retrotransposition causes ovarian tumor cell evolution and heterogeneity Hypomethylated donor L1 sequences mobilized consistently in patient tumors and in vitro An intronic L1 mutation in the STC1 oncogene was amplified during chemotherapy The STC1 L1 mutation provided a novel cis -enhancer to activate STC1 expression Graphical Abstract [DISPLAY OMISSION]

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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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  7. [해외논문]   The PARP1-Siah1 Axis Controls HIV-1 Transcription and Expression of Siah1 Substrates   SCIE

    Yu, Dan (Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA ) , Liu, Rongdiao (School of Pharmaceutical Sciences, Xiamen University, Xiamen, Fujian 361005, China ) , Yang, Geng (Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA ) , Zhou, Qiang (Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA)
    Cell reports v.23 no.13 ,pp. 3741 - 3749 , 2018 ,

    초록

    Summary Recent studies have revealed a key role of PARP1 that catalyzes the poly-ADP-ribosylation (PARylation) of substrates in regulating gene transcription. We show here that HIV-1 transcriptional activation also requires PARP1 activity. Because efficient HIV-1 transactivation is known to depend on the ELL2-containing super elongation complex (SEC), we investigated the functional relationship between PARP1 and ELL2-SEC in HIV-1 transcriptional control. We show that PARP1 elevates ELL2 protein levels to form more ELL2-SEC in cells. This effect is caused by PARP1’s suppression of expression of Siah1, an E3 ubiquitin ligase for ELL2, at both mRNA and protein levels. At the mRNA level, PARP1 coordinates with the co-repressor NCoR to suppress Siah1 transcription. At the protein level, PARP1 promotes Siah1 proteolysis, likely through inducing PARylation-dependent ubiquitination (PARdU) of Siah1. Thus, a PARP1-Siah1 axis activates HIV-1 transcription and controls the expression of ELL2 and other Siah1 substrates. Highlights PARP1 activity is required for optimal Tat activation of HIV-1 transcription PARP1 increases levels of ELL2 protein and ELL2-SEC, key for Tat-transactivation PARP1 and NCoR inhibit transcription of Siah1, an E3 ubiquitin ligase for ELL2 PARP1 induces proteosomal degradation of Siah1 likely through a PARdU mechanism Graphical Abstract [DISPLAY OMISSION]

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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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  8. [해외논문]   Anti-microbial Functions of Group 3 Innate Lymphoid Cells in Gut-Associated Lymphoid Tissues Are Regulated by G-Protein-Coupled Receptor 183   SCIE

    Chu, Coco (Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY 10021, USA ) , Moriyama, Saya (Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY 10021, USA ) , Li, Zhi (Institute of Immunology and Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK ) , Zhou, Lei (Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY 10021, USA ) , Flamar, Anne-Laure (Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Me) , Klose, Christoph S.N. , Moeller, Jesper B. , Putzel, Gregory G. , Withers, David R. , Sonnenberg, Gregory F. , Artis, David
    Cell reports v.23 no.13 ,pp. 3750 - 3758 , 2018 ,

    초록

    Summary The intestinal tract is constantly exposed to various stimuli. Group 3 innate lymphoid cells (ILC3s) reside in lymphoid organs and in the intestinal tract and are required for immunity to enteric bacterial infection. However, the mechanisms that regulate the ILC3s in vivo remain incompletely defined. Here, we show that GPR183, a chemotactic receptor expressed on murine and human ILC3s, regulates ILC3 migration toward its ligand 7α,25-dihydroxycholesterol (7α,25-OHC) in vitro , and GPR183 deficiency in vivo leads to a disorganized distribution of ILC3s in mesenteric lymph nodes and decreased ILC3 accumulation in the intestine. GPR183 functions intrinsically in ILC3s, and GPR183-deficient mice are more susceptible to enteric bacterial infection. Together, these results reveal a role for the GPR183-7α,25-OHC pathway in regulating the accumulation, distribution, and anti-microbial and tissue-protective functions of ILC3s and define a critical role for this pathway in promoting innate immunity to enteric bacterial infection. Highlights ILC3s from mouse mesenteric lymph nodes and mouse and human intestine express GPR183 GPR183 and its ligand 7α,25-OHC promote ILC3 migration in vitro GPR183 and 7α,25-OHC regulate the accumulation and function of ILC3s in vivo GPR183 is required for ILC3-mediated immunity against enteric bacterial infection Graphical Abstract [DISPLAY OMISSION]

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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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    Fig. 1 이미지
  9. [해외논문]   NMDA Receptor Autoantibodies in Autoimmune Encephalitis Cause a Subunit-Specific Nanoscale Redistribution of NMDA Receptors   SCIE

    Ladé (ICFO-Institut de Ciències Fotòniques, The Barcelona Institute of Science and Technology, 08860 Castelldefels (Barcelona), Spain ) , pê (ICFO-Institut de Ciències Fotòniques, The Barcelona Institute of Science and Technology, 08860 Castelldefels (Barcelona), Spain ) , che, Laurent (ICFO-Institut de Ciències Fotòniques, The Barcelona Institute of Science and Technology, 08860 Castelldefels (Barcelona), Spain ) , Planagumà (ICFO-Institut de Ciències Fotòniques, The Barcelona Institute of Science and Technology, 08860 Castelldefels (Barcelona), Spain ) , , Jesú (Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital Clínic c/ Villarroel 170, 08036 Barcelona, Spain ) , s (ICFO-Institut de Ciències Fotòniques, The Barcelona Institute of Science and Technology, 08860 Castelldefels (Barcelona), Spain ) , Thakur, Shreyasi (ICFO-Institut de Ciències Fotòniques, The Barcelona Institute of Science and Technology, 08860 Castelldefels (Barcelona),) , Suá , rez, Irina , Hara, Makoto , Borbely, Joseph Steven , Sandoval, Angel , Laparra-Cuervo, Lara , Dalmau, Josep , Lakadamyali, Melike
    Cell reports v.23 no.13 ,pp. 3759 - 3768 , 2018 ,

    초록

    Summary Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe neuropsychiatric disorder mediated by autoantibodies against the GluN1 subunit of the NMDAR. Patients’ antibodies cause cross-linking and internalization of NMDAR, but the synaptic events leading to depletion of NMDAR are poorly understood. Using super-resolution microscopy, we studied the effects of the autoantibodies on the nanoscale distribution of NMDAR in cultured neurons. Our findings show that, under control conditions, NMDARs form nanosized objects and patients’ antibodies increase the clustering of synaptic and extrasynaptic receptors inside the nano-objects. This clustering is subunit specific and predominantly affects GluN2B-NMDARs. Following internalization, the remaining surface NMDARs return to control clustering levels but are preferentially retained at the synapse. Monte Carlo simulations using a model in which antibodies induce NMDAR cross-linking and disruption of interactions with other proteins recapitulated these results. Finally, activation of EphB2 receptor partially antagonized the antibody-mediated disorganization of the nanoscale surface distribution of NMDARs. Highlights NMDARs form nano-objects on the neuronal surface Autoantibodies increase NMDAR nano-object size and content before internalization Cross-linking and disruption of NMDAR-protein interactions cause increased clustering EphB2 receptor activation antagonizes the antibody effects on NMDAR nano-organization Graphical Abstract [DISPLAY OMISSION]

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  10. [해외논문]   An RNA-Binding Multimer Specifies Nematode Sperm Fate   SCIE

    Aoki, Scott T. (Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA ) , Porter, Douglas F. (Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA ) , Prasad, Aman (Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA ) , Wickens, Marvin (Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA ) , Bingman, Craig A. (Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA ) , Kimble, Judith (Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA)
    Cell reports v.23 no.13 ,pp. 3769 - 3775 , 2018 ,

    초록

    Summary FOG-3 is a master regulator of sperm fate in Caenorhabditis elegans and homologous to Tob/BTG proteins, which in mammals are monomeric adaptors that recruit enzymes to RNA binding proteins. Here, we determine the FOG-3 crystal structure and in vitro demonstrate that FOG-3 forms dimers that can multimerize. The FOG-3 multimeric structure has a basic surface potential, suggestive of binding nucleic acid. Consistent with that prediction, FOG-3 binds directly to nearly 1,000 RNAs in nematode spermatogenic germ cells. Most binding is to the 3′ UTR, and most targets (94%) are oogenic mRNAs, even though assayed in spermatogenic cells. When tethered to a reporter mRNA, FOG-3 represses its expression. Together these findings elucidate the molecular mechanism of sperm fate specification and reveal the evolution of a protein from monomeric to multimeric form with acquisition of a distinct mode of mRNA repression. Highlights FOG-3 crystal structure reveals sites of missense mutations FOG-3 assembles into dimers that can multimerize FOG-3 binds directly to mRNAs in the oogenic program FOG-3 recruited to a reporter mRNA represses its expression Graphical Abstract [DISPLAY OMISSION]

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

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