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  1. AU="Masaki, Toshihiro"
  2. AU="Ripken, Tammo"
  3. AU="Koekkoek, W A C Kristine"
  4. AU="Hatas, Andrew"
  5. AU="McGregor, T"
  6. AU="De Nisco, Carlo"
  7. AU="Robert A. Harrington"
  8. AU="Xu, Yi-Ming"
  9. AU=Kurokawa Tomohiro
  10. AU="Aggarwal, Samarth"
  11. AU="Lee E. Brown"
  12. AU="Breen, G"
  13. AU="Leung, Tara"

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  1. Artikel ; Online: Polarization and myelination in myelinating glia.

    Masaki, Toshihiro

    ISRN neurology

    2012  Band 2012, Seite(n) 769412

    Abstract: Myelinating glia, oligodendrocytes in central nervous system and Schwann cells in peripheral nervous system, form myelin sheath, a multilayered membrane system around axons enabling salutatory nerve impulse conduction and maintaining axonal integrity. ... ...

    Abstract Myelinating glia, oligodendrocytes in central nervous system and Schwann cells in peripheral nervous system, form myelin sheath, a multilayered membrane system around axons enabling salutatory nerve impulse conduction and maintaining axonal integrity. Myelin sheath is a polarized structure localized in the axonal side and therefore is supposed to be formed based on the preceding polarization of myelinating glia. Thus, myelination process is closely associated with polarization of myelinating glia. However, cell polarization has been less extensively studied in myelinating glia than other cell types such as epithelial cells. The ultimate goal of this paper is to provide insights for the field of myelination research by applying the information obtained in polarity study in other cell types, especially epithelial cells, to cell polarization of myelinating glia. Thus, in this paper, the main aspects of cell polarization study in general are summarized. Then, they will be compared with polarization in oligodendrocytes. Finally, the achievements obtained in polarization study for epithelial cells, oligodendrocytes, and other types of cells will be translated into polarization/myelination process by Schwann cells. Then, based on this model, the perspectives in the study of Schwann cell polarization/myelination will be discussed.
    Sprache Englisch
    Erscheinungsdatum 2012-12-30
    Erscheinungsland Egypt
    Dokumenttyp Journal Article
    ZDB-ID 2612992-9
    ISSN 2090-5513 ; 2090-5513
    ISSN (online) 2090-5513
    ISSN 2090-5513
    DOI 10.5402/2012/769412
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Biological role of dystroglycan in Schwann cell function and its implications in peripheral nervous system diseases.

    Masaki, Toshihiro / Matsumura, Kiichiro

    Journal of biomedicine & biotechnology

    2010  Band 2010, Seite(n) 740403

    Abstract: Dystroglycan is a central component of the dystrophin-glycoprotein complex (DGC) that links extracellular matrix with cytoskeleton, expressed in a variety of fetal and adult tissues. Dystroglycan plays diverse roles in development and homeostasis ... ...

    Abstract Dystroglycan is a central component of the dystrophin-glycoprotein complex (DGC) that links extracellular matrix with cytoskeleton, expressed in a variety of fetal and adult tissues. Dystroglycan plays diverse roles in development and homeostasis including basement membrane formation, epithelial morphogenesis, membrane stability, cell polarization, and cell migration. In this paper, we will focus on biological role of dystroglycan in Schwann cell function, especially myelination. First, we review the molecular architecture of DGC in Schwann cell abaxonal membrane. Then, we will review the loss-of-function studies using targeted mutagenesis, which have revealed biological functions of each component of DGC in Schwann cells. Based on these findings, roles of dystroglycan in Schwann cell function, in myelination in particular, and its implications in diseases will be discussed in detail. Finally, in view of the fact that understanding the role of dystroglycan in Schwann cells is just beginning, future perspectives will be discussed.
    Mesh-Begriff(e) Dystroglycans/metabolism ; Humans ; Myelin Sheath/metabolism ; Peripheral Nervous System Diseases/metabolism ; Peripheral Nervous System Diseases/pathology ; Schwann Cells/metabolism ; Schwann Cells/pathology
    Chemische Substanzen Dystroglycans (146888-27-9)
    Sprache Englisch
    Erscheinungsdatum 2010-06-15
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2052552-7
    ISSN 1110-7251 ; 1110-7243
    ISSN (online) 1110-7251
    ISSN 1110-7243
    DOI 10.1155/2010/740403
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Unexpected Mutations by CRISPR-Cas9 CTG Repeat Excision in Myotonic Dystrophy and Use of CRISPR Interference as an Alternative Approach.

    Ikeda, Miki / Taniguchi-Ikeda, Mariko / Kato, Takema / Shinkai, Yasuko / Tanaka, Sonoko / Hagiwara, Hiroki / Sasaki, Naomichi / Masaki, Toshihiro / Matsumura, Kiichiro / Sonoo, Masahiro / Kurahashi, Hiroki / Saito, Fumiaki

    Molecular therapy. Methods & clinical development

    2020  Band 18, Seite(n) 131–144

    Abstract: Myotonic dystrophy type 1 is the most common type of adult-onset muscular dystrophy. This is an autosomal dominant disorder and caused by the expansion of the CTG repeat in the 3' untranslated region of the dystrophia myotonica protein kinase ( ...

    Abstract Myotonic dystrophy type 1 is the most common type of adult-onset muscular dystrophy. This is an autosomal dominant disorder and caused by the expansion of the CTG repeat in the 3' untranslated region of the dystrophia myotonica protein kinase (
    Sprache Englisch
    Erscheinungsdatum 2020-05-22
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2872938-9
    ISSN 2329-0501 ; 2329-0501
    ISSN (online) 2329-0501
    ISSN 2329-0501
    DOI 10.1016/j.omtm.2020.05.024
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  4. Artikel: Reprogramming diminishes retention of Mycobacterium leprae in Schwann cells and elevates bacterial transfer property to fibroblasts.

    Masaki, Toshihiro / McGlinchey, Aidan / Tomlinson, Simon R / Qu, Jinrong / Rambukkana, Anura

    F1000Research

    2013  Band 2, Seite(n) 198

    Abstract: Background: Bacterial pathogens can manipulate or subvert host tissue cells to their advantage at different stages during infection, from initial colonization in primary host niches to dissemination. Recently, we have shown that Mycobacterium leprae (ML) ...

    Abstract Background: Bacterial pathogens can manipulate or subvert host tissue cells to their advantage at different stages during infection, from initial colonization in primary host niches to dissemination. Recently, we have shown that Mycobacterium leprae (ML), the causative agent of human leprosy, reprogrammed its preferred host niche de-differentiated adult Schwann cells to progenitor/stem cell-like cells (pSLC) which appear to facilitate bacterial spread. Here, we studied how this cell fate change influences bacterial retention and transfer properties of Schwann cells before and after reprogramming.
    Results: Using primary fibroblasts as bacterial recipient cells, we showed that non-reprogrammed Schwann cells, which preserve all Schwann cell lineage and differentiation markers, possess high bacterial retention capacity when co-cultured with skin fibroblasts; Schwann cells failed to transfer bacteria to fibroblasts at higher numbers even after co-culture for 5 days. In contrast, pSLCs, which are derived from the same Schwann cells but have lost Schwann cell lineage markers due to reprogramming, efficiently transferred bacteria to fibroblasts within 24 hours.
    Conclusions: ML-induced reprogramming converts lineage-committed Schwann cells with high bacterial retention capacity to a cell type with pSLC stage with effective bacterial transfer properties. We propose that such changes in cellular properties may be associated with the initial intracellular colonization, which requires long-term bacterial retention within Schwann cells, in order to spread the infection to other tissues, which entails efficient bacterial transfer capacity to cells like fibroblasts which are abundant in many tissues, thereby potentially maximizing bacterial dissemination. These data also suggest how pathogens could take advantage of multiple facets of host cell reprogramming according to their needs during infection.
    Sprache Englisch
    Erscheinungsdatum 2013-09-25
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2699932-8
    ISSN 2046-1402
    ISSN 2046-1402
    DOI 10.12688/f1000research.2-198.v3
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Reprogramming adult Schwann cells to stem cell-like cells by leprosy bacilli promotes dissemination of infection.

    Masaki, Toshihiro / Qu, Jinrong / Cholewa-Waclaw, Justyna / Burr, Karen / Raaum, Ryan / Rambukkana, Anura

    Cell

    2013  Band 152, Heft 1-2, Seite(n) 51–67

    Abstract: Differentiated cells possess a remarkable genomic plasticity that can be manipulated to reverse or change developmental commitments. Here, we show that the leprosy bacterium hijacks this property to reprogram adult Schwann cells, its preferred host niche, ...

    Abstract Differentiated cells possess a remarkable genomic plasticity that can be manipulated to reverse or change developmental commitments. Here, we show that the leprosy bacterium hijacks this property to reprogram adult Schwann cells, its preferred host niche, to a stage of progenitor/stem-like cells (pSLC) of mesenchymal trait by downregulating Schwann cell lineage/differentiation-associated genes and upregulating genes mostly of mesoderm development. Reprogramming accompanies epigenetic changes and renders infected cells highly plastic, migratory, and immunomodulatory. We provide evidence that acquisition of these properties by pSLC promotes bacterial spread by two distinct mechanisms: direct differentiation to mesenchymal tissues, including skeletal and smooth muscles, and formation of granuloma-like structures and subsequent release of bacteria-laden macrophages. These findings support a model of host cell reprogramming in which a bacterial pathogen uses the plasticity of its cellular niche for promoting dissemination of infection and provide an unexpected link between cellular reprogramming and host-pathogen interaction.
    Mesh-Begriff(e) Animals ; Cell Movement ; Cell Survival ; Epigenesis, Genetic ; Epithelial-Mesenchymal Transition ; Granuloma/microbiology ; Host-Pathogen Interactions ; Humans ; Leprosy/genetics ; Leprosy/microbiology ; Leprosy/pathology ; Macrophages/microbiology ; Macrophages/pathology ; Mice ; Mice, Nude ; Mycobacterium leprae ; Peripheral Nerves/pathology ; Schwann Cells/microbiology ; Schwann Cells/pathology ; Stem Cells/pathology
    Sprache Englisch
    Erscheinungsdatum 2013-01-18
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2012.12.014
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel: Secretion of N-terminal domain of α-dystroglycan in cerebrospinal fluid

    Saito, Fumiaki / Saito-Arai, Yuko / Nakamura-Okuma, Ayami / Ikeda, Miki / Hagiwara, Hiroki / Masaki, Toshihiro / Shimizu, Teruo / Matsumura, Kiichiro

    Biochemical and biophysical research communications. 2011 July 29, v. 411, no. 2

    2011  

    Abstract: α-Dystroglycan (α-DG) plays crucial roles in maintaining the stability of cells. We demonstrated previously that the N-terminal domain of α-DG (α-DG-N) is secreted by cultured cells into the culture medium. In the present study, to clarify its function ... ...

    Abstract α-Dystroglycan (α-DG) plays crucial roles in maintaining the stability of cells. We demonstrated previously that the N-terminal domain of α-DG (α-DG-N) is secreted by cultured cells into the culture medium. In the present study, to clarify its function in vivo, we generated a monoclonal antibody against α-DG-N and investigated the secretion of α-DG-N in human cerebrospinal fluid (CSF). Interestingly, we found that a considerable amount of α-DG-N was present in CSF. α-DG-N in CSF was a sialylated glycoprotein with both N- and O-linked glycan. These observations suggest that secreted α-DG-N may be transported via CSF and have yet unidentified effects on the nervous system.
    Schlagwörter cerebrospinal fluid ; culture media ; cultured cells ; glycoproteins ; humans ; monoclonal antibodies ; secretion
    Sprache Englisch
    Erscheinungsverlauf 2011-0729
    Umfang p. 365-369.
    Erscheinungsort Elsevier Inc.
    Dokumenttyp Artikel
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2011.06.150
    Datenquelle NAL Katalog (AGRICOLA)

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  7. Artikel: Histone deacetylase inhibitor trichostatin A enhances myogenesis by coordinating muscle regulatory factors and myogenic repressors

    Hagiwara, Hiroki / Saito, Fumiaki / Masaki, Toshihiro / Ikeda, Miki / Nakamura-Ohkuma, Ayami / Shimizu, Teruo / Matsumura, Kiichiro

    Biochemical and biophysical research communications. 2011 Nov. 4, v. 414, no. 4

    2011  

    Abstract: Histone deacetylase inhibitors (HDACIs) are known to promote skeletal muscle formation. However, their mechanisms that include effects on the expression of major muscle components such as the dystrophin-associated proteins complex (DAPC) or myogenic ... ...

    Abstract Histone deacetylase inhibitors (HDACIs) are known to promote skeletal muscle formation. However, their mechanisms that include effects on the expression of major muscle components such as the dystrophin-associated proteins complex (DAPC) or myogenic regulatory factors (MRFs) remain unknown. In this study, we investigated the effects of HDACIs on skeletal muscle formation using the C2C12 cell culture system. C2C12 myoblasts were exposed to trichostatin A (TSA), one of the most potent HDACIs, and differentiation was subsequently induced. We found that TSA enhances the expression of myosin heavy chain without affecting DAPC expression. In addition, TSA increases the expression of the early MRFs, Myf5 and MEF2, whereas it suppresses the expression of the late MRF, myogenin. Interestingly, TSA also enhances the expression of Id1, Id2, and Id3 (Ids). Ids are myogenic repressors that inhibit myogenic differentiation. These findings suggest that TSA promotes gene expression in proliferation and suppresses it in the differentiation stage of muscle formation. Taken together, our data demonstrate that TSA enhances myogenesis by coordinating the expression of MRFs and myogenic repressors.
    Schlagwörter cell culture ; gene expression ; histone deacetylase ; muscle development ; muscles ; myoblasts ; myosin heavy chains ; skeletal muscle
    Sprache Englisch
    Erscheinungsverlauf 2011-1104
    Umfang p. 826-831.
    Erscheinungsort Elsevier Inc.
    Dokumenttyp Artikel
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2011.10.036
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  8. Artikel ; Online: Innate immune response precedes Mycobacterium leprae-induced reprogramming of adult Schwann cells.

    Masaki, Toshihiro / McGlinchey, Aidan / Cholewa-Waclaw, Justyna / Qu, Jinrong / Tomlinson, Simon R / Rambukkana, Anura

    Cellular reprogramming

    2013  Band 16, Heft 1, Seite(n) 9–17

    Abstract: Recently, we showed a natural reprogramming process during infection with Mycobacterium leprae (ML), the causative organism of human leprosy. ML hijacks the notable plasticity of adult Schwann cells in the peripheral nervous system (PNS), bacteria's ... ...

    Abstract Recently, we showed a natural reprogramming process during infection with Mycobacterium leprae (ML), the causative organism of human leprosy. ML hijacks the notable plasticity of adult Schwann cells in the peripheral nervous system (PNS), bacteria's preferred nonimmune niche, to reprogram infected cells to progenitor/stem cell-like cells (pSLCs). Whereas ML appear to use this reprogramming process as a sophisticated bacterial strategy to spread infection to other tissues, understanding the mechanisms may shed new insights into the basic biology of cellular reprogramming and the development of new approaches for generating pSLC for therapeutic purposes as well as targeting bacterial infectious diseases at an early stage. Toward these goals, we extended our studies to identify other players that might be involved in this complex host cell reprogramming. Here we show that ML activates numerous immune-related genes mainly involved in innate immune responses and inflammation during early infection before downregulating Schwann cell lineage genes and reactivating developmental transcription factors. We validated these findings by demonstrating the ability of infected cells to secrete soluble immune factor proteins at early time points and their continued release during the course of reprogramming. By using time-lapse microscopy and a migration assay with reprogrammed Schwann cells (pSLCs) cultured with macrophages, we show that reprogrammed cells possess the ability to attract macrophages, providing evidence for a functional role of immune gene products during reprogramming. These findings suggest a potential role of innate immune response and the related signaling pathways in cellular reprogramming and the initiation of neuropathogenesis during ML infection.
    Mesh-Begriff(e) Animals ; Cell Dedifferentiation/immunology ; Down-Regulation/immunology ; Humans ; Immunity, Innate ; Inflammation/immunology ; Inflammation/microbiology ; Inflammation/pathology ; Leprosy/immunology ; Leprosy/pathology ; Macrophages/immunology ; Macrophages/pathology ; Mice ; Mice, Inbred ICR ; Mycobacterium leprae/immunology ; Schwann Cells/immunology ; Schwann Cells/microbiology ; Schwann Cells/pathology
    Sprache Englisch
    Erscheinungsdatum 2013-11-26
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2542436-1
    ISSN 2152-4998 ; 1557-7457 ; 2152-4971
    ISSN (online) 2152-4998 ; 1557-7457
    ISSN 2152-4971
    DOI 10.1089/cell.2013.0064
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel: Intrathecal administration of nerve growth factor delays GAP 43 expression and early phase regeneration of adult rat peripheral nerve.

    Hirata, Akira / Masaki, Toshihiro / Motoyoshi, Kazuo / Kamakura, Keiko

    Brain research

    2002  Band 944, Heft 1-2, Seite(n) 146–156

    Abstract: Whether nerve growth factor (NGF) promotes peripheral nerve regeneration in vivo, in particular in adults, is controversial. We therefore examined the effect of exogenous NGF on nerve regeneration and the expression of GAP 43 (growth-associated protein ... ...

    Abstract Whether nerve growth factor (NGF) promotes peripheral nerve regeneration in vivo, in particular in adults, is controversial. We therefore examined the effect of exogenous NGF on nerve regeneration and the expression of GAP 43 (growth-associated protein 43) in adult rats. NGF was infused intrathecally via an osmotic mini-pump, while control rats received artificial cerebrospinal fluid. Two days after the infusion was initiated, the right sciatic nerves were transected or crushed, and the animals allowed to survive for 3 to 11 days. The right DRG, the right proximal stump of the transected sciatic nerve, and the posterior horn of the spinal cord were examined by Western blotting, immunohistochemistry, and electron microscopy. GAP 43 immunoreactivity in the NGF-treated animals was significantly lower than in the aCSF-treated controls. Electron microscopy showed that the number of myelinated and unmyelinated axons decreased significantly in the NGF-treated rats as compared with the controls. These findings are indicative that exogenous NGF delayed GAP 43 induction and the early phase of peripheral nerve regeneration and supports the hypothesis that the loss of NGF supply from peripheral targets via retrograde transport caused by axotomy serves as a signal for DRG neurons to invoke regenerative responses. NGF administered intrathecally may delay the neurons' perception of the reduction of the endogenous NGF, causing a delay in conversion of DRG neurons from the normal physiological condition to regrowth state.
    Mesh-Begriff(e) Animals ; Axons/drug effects ; Axons/metabolism ; Axons/ultrastructure ; Cell Size/drug effects ; Cell Size/physiology ; Dose-Response Relationship, Drug ; Functional Laterality/physiology ; GAP-43 Protein/antagonists & inhibitors ; GAP-43 Protein/metabolism ; Ganglia, Spinal/drug effects ; Ganglia, Spinal/metabolism ; Ganglia, Spinal/physiopathology ; Immunohistochemistry ; Male ; Microscopy, Electron ; Nerve Fibers, Myelinated/drug effects ; Nerve Fibers, Myelinated/metabolism ; Nerve Fibers, Myelinated/ultrastructure ; Nerve Growth Factor/metabolism ; Nerve Growth Factor/pharmacology ; Nerve Regeneration/drug effects ; Nerve Regeneration/physiology ; Neurons, Afferent/drug effects ; Neurons, Afferent/metabolism ; Neurons, Afferent/pathology ; Rats ; Rats, Wistar ; Sciatic Nerve/drug effects ; Sciatic Nerve/metabolism ; Sciatic Nerve/physiopathology ; Sciatic Neuropathy/drug therapy ; Sciatic Neuropathy/metabolism ; Sciatic Neuropathy/physiopathology ; Substance P/metabolism ; Wallerian Degeneration/drug therapy ; Wallerian Degeneration/metabolism ; Wallerian Degeneration/physiopathology
    Chemische Substanzen GAP-43 Protein ; Substance P (33507-63-0) ; Nerve Growth Factor (9061-61-4)
    Sprache Englisch
    Erscheinungsdatum 2002-07-19
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1200-2
    ISSN 1872-6240 ; 0006-8993
    ISSN (online) 1872-6240
    ISSN 0006-8993
    DOI 10.1016/s0006-8993(02)02739-7
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  10. Artikel ; Online: Histone deacetylase inhibitor trichostatin A enhances myogenesis by coordinating muscle regulatory factors and myogenic repressors.

    Hagiwara, Hiroki / Saito, Fumiaki / Masaki, Toshihiro / Ikeda, Miki / Nakamura-Ohkuma, Ayami / Shimizu, Teruo / Matsumura, Kiichiro

    Biochemical and biophysical research communications

    2011  Band 414, Heft 4, Seite(n) 826–831

    Abstract: Histone deacetylase inhibitors (HDACIs) are known to promote skeletal muscle formation. However, their mechanisms that include effects on the expression of major muscle components such as the dystrophin-associated proteins complex (DAPC) or myogenic ... ...

    Abstract Histone deacetylase inhibitors (HDACIs) are known to promote skeletal muscle formation. However, their mechanisms that include effects on the expression of major muscle components such as the dystrophin-associated proteins complex (DAPC) or myogenic regulatory factors (MRFs) remain unknown. In this study, we investigated the effects of HDACIs on skeletal muscle formation using the C2C12 cell culture system. C2C12 myoblasts were exposed to trichostatin A (TSA), one of the most potent HDACIs, and differentiation was subsequently induced. We found that TSA enhances the expression of myosin heavy chain without affecting DAPC expression. In addition, TSA increases the expression of the early MRFs, Myf5 and MEF2, whereas it suppresses the expression of the late MRF, myogenin. Interestingly, TSA also enhances the expression of Id1, Id2, and Id3 (Ids). Ids are myogenic repressors that inhibit myogenic differentiation. These findings suggest that TSA promotes gene expression in proliferation and suppresses it in the differentiation stage of muscle formation. Taken together, our data demonstrate that TSA enhances myogenesis by coordinating the expression of MRFs and myogenic repressors.
    Mesh-Begriff(e) Animals ; Cell Line ; Dystrophin-Associated Protein Complex/metabolism ; Gene Expression/drug effects ; Histone Deacetylase Inhibitors/pharmacology ; Hydroxamic Acids/pharmacology ; Inhibitor of Differentiation Protein 1/metabolism ; Inhibitor of Differentiation Protein 2/metabolism ; Inhibitor of Differentiation Proteins/metabolism ; Mice ; Muscle Development/drug effects ; Muscle Development/genetics ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/growth & development ; Muscle, Skeletal/metabolism ; Myogenic Regulatory Factor 5/metabolism ; Myogenic Regulatory Factors/metabolism ; Myosin Heavy Chains/metabolism
    Chemische Substanzen Dystrophin-Associated Protein Complex ; Histone Deacetylase Inhibitors ; Hydroxamic Acids ; Idb1 protein, mouse ; Idb2 protein, mouse ; Inhibitor of Differentiation Protein 1 ; Inhibitor of Differentiation Protein 2 ; Inhibitor of Differentiation Proteins ; Myogenic Regulatory Factor 5 ; Myogenic Regulatory Factors ; Idb3 protein, mouse (135845-89-5) ; trichostatin A (3X2S926L3Z) ; Myosin Heavy Chains (EC 3.6.4.1)
    Sprache Englisch
    Erscheinungsdatum 2011-11-04
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2011.10.036
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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