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  1. Article ; Online: CD4 Helper and CD8 Cytotoxic T Cell Differentiation.

    Taniuchi, Ichiro

    Annual review of immunology

    2018  Volume 36, Page(s) 579–601

    Abstract: A fundamental question in developmental immunology is how bipotential thymocyte precursors generate both ... ...

    Abstract A fundamental question in developmental immunology is how bipotential thymocyte precursors generate both CD4
    MeSH term(s) Animals ; CD4 Antigens/genetics ; CD4 Antigens/metabolism ; CD8 Antigens/genetics ; CD8 Antigens/metabolism ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Cell Lineage/genetics ; Cell Lineage/immunology ; Core Binding Factor Alpha 3 Subunit/genetics ; DNA-Binding Proteins/genetics ; Gene Expression Regulation ; Humans ; Immunomodulation/genetics ; Immunomodulation/immunology ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/metabolism ; Regulatory Sequences, Nucleic Acid ; T-Lymphocytes, Cytotoxic/cytology ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Cytotoxic/metabolism ; T-Lymphocytes, Helper-Inducer/cytology ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Helper-Inducer/metabolism ; Transcription Factors/genetics ; Transcription, Genetic
    Chemical Substances CD4 Antigens ; CD8 Antigens ; Core Binding Factor Alpha 3 Subunit ; DNA-Binding Proteins ; Receptors, Antigen, T-Cell ; Transcription Factors ; ZBTB7B protein, human
    Language English
    Publishing date 2018-05-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 604953-9
    ISSN 1545-3278 ; 0732-0582
    ISSN (online) 1545-3278
    ISSN 0732-0582
    DOI 10.1146/annurev-immunol-042617-053411
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Three residues in the BTB domain promote a good partnership between NuRD and Thpok.

    Okuyama, Kazuki / Taniuchi, Ichiro

    Science immunology

    2022  Volume 7, Issue 72, Page(s) eabq1408

    Abstract: Among the BTB-ZF transcription factor family, three amino acids in the BTB domain make Thpok unique in repressing cytotoxic lineage-related genes via recruitment of the NuRD chormatin-remodeling complex (see the related Research Article by ... ...

    Abstract Among the BTB-ZF transcription factor family, three amino acids in the BTB domain make Thpok unique in repressing cytotoxic lineage-related genes via recruitment of the NuRD chormatin-remodeling complex (see the related Research Article by Gao
    MeSH term(s) BTB-POZ Domain ; Gene Expression Regulation ; Protein Binding ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemical Substances Transcription Factors
    Language English
    Publishing date 2022-06-10
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Comment
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.abq1408
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Fine-tuning Notch1 by the stage-specific enhancer.

    Yamashita, Motoi / Taniuchi, Ichiro

    Nature immunology

    2022  Volume 23, Issue 11, Page(s) 1509–1511

    MeSH term(s) Receptor, Notch1/genetics ; Enhancer Elements, Genetic/genetics
    Chemical Substances Receptor, Notch1
    Language English
    Publishing date 2022-10-31
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-022-01341-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Is α1-Antitrypsin Important for Murine Thymocyte Development?

    Nomura, Aneela / Taniuchi, Ichiro

    Trends in immunology

    2021  Volume 42, Issue 3, Page(s) 178–180

    Language English
    Publishing date 2021-01-29
    Publishing country England
    Document type Letter ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2036831-8
    ISSN 1471-4981 ; 1471-4906
    ISSN (online) 1471-4981
    ISSN 1471-4906
    DOI 10.1016/j.it.2021.01.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Views on helper/cytotoxic lineage choice from a bottom-up approach.

    Taniuchi, Ichiro

    Immunological reviews

    2016  Volume 271, Issue 1, Page(s) 98–113

    Abstract: There has been speculation as to how bi-potent CD4(+)  CD8(+) double-positive precursor thymocytes choose their distinct developmental fate, becoming either CD4(+) helper or CD8(+) cytotoxic T cells. Based on the clear correlation of αβT cell receptor ( ... ...

    Abstract There has been speculation as to how bi-potent CD4(+)  CD8(+) double-positive precursor thymocytes choose their distinct developmental fate, becoming either CD4(+) helper or CD8(+) cytotoxic T cells. Based on the clear correlation of αβT cell receptor (TCR) specificity to major histocompatibility complex (MHC) classes with this lineage choice, various studies have attempted to resolve this question by examining the cellular signaling events initiated by TCR engagements, a strategy referred to as a 'top-down' approach. On the other hand, based on the other correlation of CD4/CD8 co-receptor expression with its selected fate, other studies have addressed this question by gradually unraveling the sequential mechanisms that control the phenotypic outcome of this fate decision, a method known as the 'bottom-up' approach. Bridging these two approaches will contribute to a more comprehensive understanding of how TCR signals are coupled with developmental programs in the nucleus. Advances made during the last two decades seemed to make these two approaches more closely linked. For instance, identification of two transcription factors, ThPOK and Runx3, which play central roles in the development of helper and cytotoxic lineages, respectively, provided significant insights into the transcriptional network that controls a CD4/CD8 lineage choice. This review summarizes achievements made using the 'bottom-up' approach, followed by a perspective on future pathways toward coupling TCR signaling with nuclear programs.
    MeSH term(s) CD4 Antigens/metabolism ; CD8 Antigens/metabolism ; Cell Differentiation/genetics ; Cell Lineage/genetics ; Clonal Selection, Antigen-Mediated ; Core Binding Factor Alpha 3 Subunit/genetics ; Core Binding Factor Alpha 3 Subunit/metabolism ; Cytotoxicity, Immunologic/genetics ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemical Substances CD4 Antigens ; CD8 Antigens ; Core Binding Factor Alpha 3 Subunit ; DNA-Binding Proteins ; Receptors, Antigen, T-Cell, alpha-beta ; Transcription Factors ; ZBTB7B protein, human
    Language English
    Publishing date 2016-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 391796-4
    ISSN 1600-065X ; 0105-2896
    ISSN (online) 1600-065X
    ISSN 0105-2896
    DOI 10.1111/imr.12401
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Oncogenic Runx1–Myc axis in p53-deficient thymic lymphoma

    Date, Yuki / Taniuchi, Ichiro / Ito, Kosei

    Gene. 2022 Apr. 20, v. 819

    2022  

    Abstract: p53 deficiency and Myc dysregulation are frequently associated with cancer. However, the molecular mechanisms linking these two major oncogenic events are poorly understood. Using an osteosarcoma model caused by p53 loss, we have recently shown that ... ...

    Abstract p53 deficiency and Myc dysregulation are frequently associated with cancer. However, the molecular mechanisms linking these two major oncogenic events are poorly understood. Using an osteosarcoma model caused by p53 loss, we have recently shown that Runx3 aberrantly upregulates Myc via mR1, a Runx consensus site in the Myc promoter. Here, we focus on thymic lymphoma, a major tumour type caused by germline p53 deletion in mice, and examine whether the oncogenic Runx–Myc axis plays a notable role in the development of p53-deficient lymphoma. Mice lacking p53 specifically in thymocytes (LP mice) mostly succumbed to thymic lymphoma. Runx1 and Myc were upregulated in LP mouse lymphoma compared with the normal thymus. Depletion of Runx1 or Myc prolonged the lifespan of LP mice and suppressed lymphoma development. In lymphoma cells isolated from LP mice, knockdown of Runx1 led to Myc suppression, weakening their tumour forming ability in immunocompromised mice. The mR1 locus was enriched by both Runx1 and H3K27ac, an active chromatin marker. LP mice with mutated mR1 had a longer lifespan and a lower incidence of lymphoma. Treatment with AI-10-104, a Runx inhibitor, improved the survival of LP mice. These results suggest that Myc upregulation by Runx1 is a key event in p53-deficient thymic lymphoma development and provide a clinical rationale for targeting the Runx family in p53-deficient malignancies.
    Keywords chromatin ; genes ; germ cells ; loci ; longevity ; lymphoma ; mice ; models ; osteosarcoma ; thymocytes
    Language English
    Dates of publication 2022-0420
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 391792-7
    ISSN 1879-0038 ; 0378-1119
    ISSN (online) 1879-0038
    ISSN 0378-1119
    DOI 10.1016/j.gene.2022.146234
    Database NAL-Catalogue (AGRICOLA)

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  7. Article ; Online: The Roles of RUNX Proteins in Lymphocyte Function and Anti-Tumor Immunity.

    Seo, Wooseok / Nomura, Aneela / Taniuchi, Ichiro

    Cells

    2022  Volume 11, Issue 19

    Abstract: The Runt-related transcription factor (RUNX) family of proteins are crucial for many developmental and immuno-physiological processes. Their importance in cellular and tissue development has been repeatedly demonstrated as they are often found mutated ... ...

    Abstract The Runt-related transcription factor (RUNX) family of proteins are crucial for many developmental and immuno-physiological processes. Their importance in cellular and tissue development has been repeatedly demonstrated as they are often found mutated and implicated in tumorigenesis. Most importantly, RUNX have now emerged as critical regulators of lymphocyte function against pathogenic infections and tumorigenic cells, the latter has now revolutionized our current understandings as to how RUNX proteins contribute to control tumor pathogenicity. These multifunctional roles of RUNX in mammalian immune responses and tissue homeostasis have led us to appreciate their value in controlling anti-tumor immune responses. Here, we summarize and discuss the role of RUNX in regulating the development and function of lymphocytes responding to foreign and tumorigenic threats and highlight their key roles in anti-tumor immunity.
    MeSH term(s) Animals ; Core Binding Factor alpha Subunits/genetics ; Core Binding Factor alpha Subunits/metabolism ; Immunity ; Lymphocytes/metabolism ; Mammals/metabolism ; Neoplasms/genetics ; Transcription Factors
    Chemical Substances Core Binding Factor alpha Subunits ; Transcription Factors
    Language English
    Publishing date 2022-10-03
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11193116
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Oncogenic Runx1-Myc axis in p53-deficient thymic lymphoma.

    Date, Yuki / Taniuchi, Ichiro / Ito, Kosei

    Gene

    2022  Volume 819, Page(s) 146234

    Abstract: p53 deficiency and Myc dysregulation are frequently associated with cancer. However, the molecular mechanisms linking these two major oncogenic events are poorly understood. Using an osteosarcoma model caused by p53 loss, we have recently shown that ... ...

    Abstract p53 deficiency and Myc dysregulation are frequently associated with cancer. However, the molecular mechanisms linking these two major oncogenic events are poorly understood. Using an osteosarcoma model caused by p53 loss, we have recently shown that Runx3 aberrantly upregulates Myc via mR1, a Runx consensus site in the Myc promoter. Here, we focus on thymic lymphoma, a major tumour type caused by germline p53 deletion in mice, and examine whether the oncogenic Runx-Myc axis plays a notable role in the development of p53-deficient lymphoma. Mice lacking p53 specifically in thymocytes (LP mice) mostly succumbed to thymic lymphoma. Runx1 and Myc were upregulated in LP mouse lymphoma compared with the normal thymus. Depletion of Runx1 or Myc prolonged the lifespan of LP mice and suppressed lymphoma development. In lymphoma cells isolated from LP mice, knockdown of Runx1 led to Myc suppression, weakening their tumour forming ability in immunocompromised mice. The mR1 locus was enriched by both Runx1 and H3K27ac, an active chromatin marker. LP mice with mutated mR1 had a longer lifespan and a lower incidence of lymphoma. Treatment with AI-10-104, a Runx inhibitor, improved the survival of LP mice. These results suggest that Myc upregulation by Runx1 is a key event in p53-deficient thymic lymphoma development and provide a clinical rationale for targeting the Runx family in p53-deficient malignancies.
    MeSH term(s) Animals ; Cell Line, Tumor ; Core Binding Factor Alpha 2 Subunit/genetics ; Core Binding Factor Alpha 2 Subunit/metabolism ; Gene Expression Regulation, Neoplastic ; Lymphoma/genetics ; Lymphoma/metabolism ; Mice ; Oncogenes ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Thymus Neoplasms/genetics ; Thymus Neoplasms/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Core Binding Factor Alpha 2 Subunit ; Proto-Oncogene Proteins c-myc ; Runx1 protein, mouse ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2022-01-31
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 391792-7
    ISSN 1879-0038 ; 0378-1119
    ISSN (online) 1879-0038
    ISSN 0378-1119
    DOI 10.1016/j.gene.2022.146234
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The Role of CD8 Downregulation during Thymocyte Differentiation.

    Nomura, Aneela / Taniuchi, Ichiro

    Trends in immunology

    2020  Volume 41, Issue 11, Page(s) 972–981

    Abstract: During mammalian T cell development, ... ...

    Abstract During mammalian T cell development, CD4
    MeSH term(s) Animals ; CD8 Antigens/genetics ; CD8-Positive T-Lymphocytes/metabolism ; Cell Differentiation/genetics ; Down-Regulation ; Humans ; Mice ; Thymocytes/cytology
    Chemical Substances CD8 Antigens
    Language English
    Publishing date 2020-10-07
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2036831-8
    ISSN 1471-4981 ; 1471-4906
    ISSN (online) 1471-4981
    ISSN 1471-4906
    DOI 10.1016/j.it.2020.09.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Transcription Factors in the Development and Function of Group 2 Innate Lymphoid Cells.

    Ebihara, Takashi / Taniuchi, Ichiro

    International journal of molecular sciences

    2019  Volume 20, Issue 6

    Abstract: Group 2 innate lymphoid cells (ILC2s) are tissue-resident cells and are a major source of innate ... ...

    Abstract Group 2 innate lymphoid cells (ILC2s) are tissue-resident cells and are a major source of innate T
    MeSH term(s) Animals ; Core Binding Factor alpha Subunits/metabolism ; Gene Expression Regulation ; Humans ; Immunity, Innate ; Lymphocytes/metabolism ; Models, Biological ; Transcription Factors/metabolism
    Chemical Substances Core Binding Factor alpha Subunits ; Transcription Factors
    Language English
    Publishing date 2019-03-19
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms20061377
    Database MEDical Literature Analysis and Retrieval System OnLINE

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