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  1. Article ; Online: Cherish JB, a unique journal that originated from Japan.

    Miyazono, Kohei

    Journal of biochemistry

    2022  Volume 172, Issue 3, Page(s) 137–138

    Abstract: I would like to congratulate the Journal of Biochemistry (JB) on its 100th anniversary. I served as the Editor-in-Chief for four years starting in 2010 and succeeded Dr Naoyuki Taniguchi. ...

    Abstract I would like to congratulate the Journal of Biochemistry (JB) on its 100th anniversary. I served as the Editor-in-Chief for four years starting in 2010 and succeeded Dr Naoyuki Taniguchi.
    Language English
    Publishing date 2022-01-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 218073-x
    ISSN 1756-2651 ; 0021-924X
    ISSN (online) 1756-2651
    ISSN 0021-924X
    DOI 10.1093/jb/mvac004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Receptor-activated transcription factors and beyond: multiple modes of Smad2/3-dependent transmission of TGF-β signaling.

    Miyazawa, Keiji / Itoh, Yuka / Fu, Hao / Miyazono, Kohei

    The Journal of biological chemistry

    2024  Volume 300, Issue 5, Page(s) 107256

    Abstract: Transforming growth factor β (TGF-β) is a pleiotropic cytokine that is widely distributed throughout the body. Its receptor proteins, TGF-β type I and type II receptors, are also ubiquitously expressed. Therefore, the regulation of various signaling ... ...

    Abstract Transforming growth factor β (TGF-β) is a pleiotropic cytokine that is widely distributed throughout the body. Its receptor proteins, TGF-β type I and type II receptors, are also ubiquitously expressed. Therefore, the regulation of various signaling outputs in a context-dependent manner is a critical issue in this field. Smad proteins were originally identified as signal-activated transcription factors similar to signal transducer and activator of transcription proteins. Smads are activated by serine phosphorylation mediated by intrinsic receptor dual specificity kinases of the TGF-β family, indicating that Smads are receptor-restricted effector molecules downstream of ligands of the TGF-β family. Smad proteins have other functions in addition to transcriptional regulation, including post-transcriptional regulation of micro-RNA processing, pre-mRNA splicing, and m
    Language English
    Publishing date 2024-04-02
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2024.107256
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: [113th Scientific Meeting of the Japanese Society of Internal Medicine: Presidential Lecture: Special Lecture: TGF-β Family and Internal Medicine].

    Miyazono, Kohei

    Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine

    2018  Volume 105, Issue 9, Page(s) 1558–1564

    MeSH term(s) Cell Transformation, Neoplastic ; Epithelial-Mesenchymal Transition ; Humans ; Internal Medicine ; Japan ; Neoplasms/metabolism ; Neoplasms/pathology ; Signal Transduction/drug effects ; Societies, Medical ; Transforming Growth Factor beta/metabolism
    Chemical Substances Transforming Growth Factor beta
    Language Japanese
    Publishing date 2018-08-31
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 952816-7
    ISSN 1883-2083 ; 0021-5384
    ISSN (online) 1883-2083
    ISSN 0021-5384
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Bone Morphogenetic Protein Signaling in Cancer; Some Topics in the Recent 10 Years.

    Ehata, Shogo / Miyazono, Kohei

    Frontiers in cell and developmental biology

    2022  Volume 10, Page(s) 883523

    Abstract: Bone morphogenetic proteins (BMPs), members of the transforming growth factor-β (TGF-β) family, are multifunctional cytokines. BMPs have a broad range of functions, and abnormalities in BMP signaling pathways are involved in cancer progression. BMPs ... ...

    Abstract Bone morphogenetic proteins (BMPs), members of the transforming growth factor-β (TGF-β) family, are multifunctional cytokines. BMPs have a broad range of functions, and abnormalities in BMP signaling pathways are involved in cancer progression. BMPs activate the proliferation of certain cancer cells. Malignant phenotypes of cancer cells, such as increased motility, invasiveness, and stemness, are enhanced by BMPs. Simultaneously, BMPs act on various cellular components and regulate angiogenesis in the tumor microenvironment. Thus, BMPs function as pro-tumorigenic factors in various types of cancer. However, similar to TGF-β, which shows both positive and negative effects on tumorigenesis, BMPs also act as tumor suppressors in other types of cancers. In this article, we review important findings published in the recent decade and summarize the pro-oncogenic functions of BMPs and their underlying mechanisms. The current status of BMP-targeted therapies for cancers is also discussed.
    Language English
    Publishing date 2022-05-25
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.883523
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Bone Morphogenetic Protein Signaling in Cancer; Some Topics in the Recent 10 Years

    Shogo Ehata / Kohei Miyazono

    Frontiers in Cell and Developmental Biology, Vol

    2022  Volume 10

    Abstract: Bone morphogenetic proteins (BMPs), members of the transforming growth factor-β (TGF-β) family, are multifunctional cytokines. BMPs have a broad range of functions, and abnormalities in BMP signaling pathways are involved in cancer progression. BMPs ... ...

    Abstract Bone morphogenetic proteins (BMPs), members of the transforming growth factor-β (TGF-β) family, are multifunctional cytokines. BMPs have a broad range of functions, and abnormalities in BMP signaling pathways are involved in cancer progression. BMPs activate the proliferation of certain cancer cells. Malignant phenotypes of cancer cells, such as increased motility, invasiveness, and stemness, are enhanced by BMPs. Simultaneously, BMPs act on various cellular components and regulate angiogenesis in the tumor microenvironment. Thus, BMPs function as pro-tumorigenic factors in various types of cancer. However, similar to TGF-β, which shows both positive and negative effects on tumorigenesis, BMPs also act as tumor suppressors in other types of cancers. In this article, we review important findings published in the recent decade and summarize the pro-oncogenic functions of BMPs and their underlying mechanisms. The current status of BMP-targeted therapies for cancers is also discussed.
    Keywords BMPs ; ALKs ; Smads ; cancer ; metastasis ; angiogeneis ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2022-05-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: An

    Nishida, Jun / Miyakuni, Kosuke / Miyazono, Kohei / Ehata, Shogo

    STAR protocols

    2022  Volume 3, Issue 2, Page(s) 101306

    Abstract: We developed ... ...

    Abstract We developed an
    MeSH term(s) Animals ; Diagnostic Imaging ; Female ; Humans ; Kidney/pathology ; Kidney Neoplasms/pathology ; Male ; Mice ; Transplants/pathology ; Tumor Microenvironment
    Language English
    Publishing date 2022-04-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2022.101306
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: An in vivo orthotopic serial passaging model for a metastatic renal cancer study

    Jun Nishida / Kosuke Miyakuni / Kohei Miyazono / Shogo Ehata

    STAR Protocols, Vol 3, Iss 2, Pp 101306- (2022)

    2022  

    Abstract: Summary: We developed an in vivo serial passaging model for renal cancer with orthotopic renal subcapsular inoculation. We detail the procedures for renal subcapsular inoculation of cancer cells in mice, followed by in vivo and ex vivo bioluminescence ... ...

    Abstract Summary: We developed an in vivo serial passaging model for renal cancer with orthotopic renal subcapsular inoculation. We detail the procedures for renal subcapsular inoculation of cancer cells in mice, followed by in vivo and ex vivo bioluminescence imaging, tumor-bearing kidney dissociation, and in vivo passaging. This protocol is capable of reproducing the coevolution between cancer cells and the primary tumor microenvironment. It enables us to unveil the systemic dynamics of metastasis and develop a therapeutic strategy for metastatic renal cancer.For complete details on the use and execution of this protocol, please refer to Nishida et al. (2020).
    Keywords Cell Biology ; Cell culture ; Cancer ; Model Organisms ; Science (General) ; Q1-390
    Language English
    Publishing date 2022-06-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Preparation of monovalent follistatin-like 3-Fc-fusion protein and evaluation of its effects on muscle mass in mice.

    Ozawa, Takayuki / Miyazono, Kohei / Morikawa, Masato

    STAR protocols

    2021  Volume 2, Issue 4, Page(s) 100839

    Abstract: Follistatin-like 3 (FSTL3) is an endogenous antagonist against transforming growth factor-β family ligands. Monovalent FSTL3-Fc fusion protein (mono-FSTL3-Fc) generated with knobs-into-holes technology overcomes limitations of current anti-myostatin ... ...

    Abstract Follistatin-like 3 (FSTL3) is an endogenous antagonist against transforming growth factor-β family ligands. Monovalent FSTL3-Fc fusion protein (mono-FSTL3-Fc) generated with knobs-into-holes technology overcomes limitations of current anti-myostatin therapies. We have developed a facile protocol for affinity purification of the Fc-fused protein from the supernatant of HEK293T cells stably expressing the protein. This protocol is advantageous by only requiring readily accessible equipment. We further outline the steps for validation of mono-FSTL3-Fc increasing systemic muscle mass in mice after intraperitoneal administration. For complete details on the use and execution of this protocol, please refer to Ozawa et al. (2021).
    MeSH term(s) Animals ; Follistatin/metabolism ; Follistatin-Related Proteins/genetics ; HEK293 Cells ; Humans ; Mice ; Muscles/metabolism ; Transforming Growth Factor beta/metabolism
    Chemical Substances Follistatin ; Follistatin-Related Proteins ; Fstl3 protein, human ; Fstl3 protein, mouse ; Transforming Growth Factor beta
    Language English
    Publishing date 2021-09-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2021.100839
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: PolyI:C attenuates transforming growth factor-β signaling to induce cytostasis of surrounding cells by secreted factors in triple-negative breast cancer.

    Tamura, Yusuke / Tsutsumi, Shuichi / Miyazono, Kohei / Koinuma, Daizo

    Cancer science

    2021  Volume 113, Issue 3, Page(s) 940–949

    Abstract: The activation of RIG-I-like receptor (RLR) signaling in cancer cells is widely recognized as a critical cancer therapy method. The expected mechanism of RLR ligand-mediated cancer therapy involves the promotion of cancer cell death and strong induction ... ...

    Abstract The activation of RIG-I-like receptor (RLR) signaling in cancer cells is widely recognized as a critical cancer therapy method. The expected mechanism of RLR ligand-mediated cancer therapy involves the promotion of cancer cell death and strong induction of interferon (IFN)-β that affects the tumor microenvironment. We have recently shown that activation of RLR signaling in triple-negative breast cancer cells (TNBC) attenuates transforming growth factor-β (TGF-β) signaling, which partly contributes to the promotion of cancer cell pyroptosis. However, the consequences of suppression of TGF-β signaling by RLR ligands with respect to IFN-β-mediated tumor suppression are not well characterized. This study showed that transfection of a typical RLR ligand polyI:C in cancer cells produces significant levels of IFN-β, which inhibits the growth of the surrounding cancer cells. In addition, IFN-β-induced cell cycle arrest in surrounding cancer cells was inhibited by the expression of constitutively active Smad3. Constitutively active Smad3 suppresses IFN-β expression through the alleviation of IFN regulatory factor 3 binding to the canonical target genes, as suggested by ChIP sequencing analysis. Based on these findings, a new facet of the protumorigenic function of TGF-β that suppresses IFN-β expression is suggested when RLR-mediated cancer treatment is used in TNBC.
    MeSH term(s) Cell Death/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Gene Expression Regulation, Neoplastic ; Humans ; Interferon Regulatory Factor-3/metabolism ; Interferon-beta/metabolism ; Poly I-C/genetics ; Poly I-C/pharmacology ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Smad3 Protein/genetics ; Smad3 Protein/metabolism ; Transfection ; Transforming Growth Factor beta/antagonists & inhibitors ; Transforming Growth Factor beta/metabolism ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism ; Triple Negative Breast Neoplasms/pathology ; Tumor Microenvironment/drug effects
    Chemical Substances IRF3 protein, human ; Interferon Regulatory Factor-3 ; SMAD3 protein, human ; Smad3 Protein ; Transforming Growth Factor beta ; Interferon-beta (77238-31-4) ; Poly I-C (O84C90HH2L)
    Language English
    Publishing date 2021-12-23
    Publishing country England
    Document type Journal Article
    ZDB-ID 2115647-5
    ISSN 1349-7006 ; 1347-9032
    ISSN (online) 1349-7006
    ISSN 1347-9032
    DOI 10.1111/cas.15241
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Preparation of monovalent follistatin-like 3-Fc-fusion protein and evaluation of its effects on muscle mass in mice

    Takayuki Ozawa / Kohei Miyazono / Masato Morikawa

    STAR Protocols, Vol 2, Iss 4, Pp 100839- (2021)

    2021  

    Abstract: Summary: Follistatin-like 3 (FSTL3) is an endogenous antagonist against transforming growth factor-β family ligands. Monovalent FSTL3-Fc fusion protein (mono-FSTL3-Fc) generated with knobs-into-holes technology overcomes limitations of current anti- ... ...

    Abstract Summary: Follistatin-like 3 (FSTL3) is an endogenous antagonist against transforming growth factor-β family ligands. Monovalent FSTL3-Fc fusion protein (mono-FSTL3-Fc) generated with knobs-into-holes technology overcomes limitations of current anti-myostatin therapies. We have developed a facile protocol for affinity purification of the Fc-fused protein from the supernatant of HEK293T cells stably expressing the protein. This protocol is advantageous by only requiring readily accessible equipment. We further outline the steps for validation of mono-FSTL3-Fc increasing systemic muscle mass in mice after intraperitoneal administration.For complete details on the use and execution of this protocol, please refer to Ozawa et al. (2021).
    Keywords Developmental biology ; Health Sciences ; Microscopy ; Model Organisms ; Protein expression and purification ; Science (General) ; Q1-390
    Language English
    Publishing date 2021-12-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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