Immunoglobulin G3 Antibody

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Michael P Cooke - One of the best experts on this subject based on the ideXlab platform.

  • Production of Ins(1,3,4,5)P_4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation
    Nature Immunology, 2007
    Co-Authors: Andrew T Miller, Mark Sandberg, Karsten Sauer, Michael Young, Yina H. Huang, Susan Sutton, Michael P Cooke
    Abstract:

    Antigen receptor–mediated production of inositol-1,4,5-trisphosphate (Ins(1,4,5)P_3) in lymphocytes triggers the release of Ca^2+ from intracellular stores; this release of Ca^2+ results in the opening of store-operated Ca^2+ channels in the plasma membrane. Here we report that mice lacking Ins(1,4,5)P_3 3-kinase B (Itpkb), which converts Ins(1,4,5)P_3 to inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P_4), had impaired B lymphocyte development and defective Immunoglobulin G3 Antibody responses to a T lymphocyte–independent antigen. Itpkb-deficient B lymphocytes had the phenotypic and functional features of tolerant B lymphocytes and showed enhanced activity of store-operated Ca^2+ channels after B lymphocyte receptor stimulation, which was reversed by the provision of exogenous Ins(1,3,4,5)P_4. Our data identify Itpkb and its product Ins(1,3,4,5)P_4 as inhibitors of store-operated Ca^2+ channels and crucial regulators of B cell selection and activation.

  • Production of Ins(1,3,4,5)P4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation
    Nature Immunology, 2007
    Co-Authors: Andrew T Miller, Karsten Sauer, Mark L. Sandberg, Susan E. Sutton, Yina H. Huang, Mike Young, Michael P Cooke
    Abstract:

    Antigen receptor–mediated production of inositol-1,4,5-trisphosphate (Ins(1,4,5)P3) in lymphocytes triggers the release of Ca2+ from intracellular stores; this release of Ca2+ results in the opening of store-operated Ca2+ channels in the plasma membrane. Here we report that mice lacking Ins(1,4,5)P3 3-kinase B (Itpkb), which converts Ins(1,4,5)P3 to inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), had impaired B lymphocyte development and defective Immunoglobulin G3 Antibody responses to a T lymphocyte–independent antigen. Itpkb-deficient B lymphocytes had the phenotypic and functional features of tolerant B lymphocytes and showed enhanced activity of store-operated Ca2+ channels after B lymphocyte receptor stimulation, which was reversed by the provision of exogenous Ins(1,3,4,5)P4. Our data identify Itpkb and its product Ins(1,3,4,5)P4 as inhibitors of store-operated Ca2+ channels and crucial regulators of B cell selection and activation.

Andrew T Miller - One of the best experts on this subject based on the ideXlab platform.

  • Production of Ins(1,3,4,5)P_4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation
    Nature Immunology, 2007
    Co-Authors: Andrew T Miller, Mark Sandberg, Karsten Sauer, Michael Young, Yina H. Huang, Susan Sutton, Michael P Cooke
    Abstract:

    Antigen receptor–mediated production of inositol-1,4,5-trisphosphate (Ins(1,4,5)P_3) in lymphocytes triggers the release of Ca^2+ from intracellular stores; this release of Ca^2+ results in the opening of store-operated Ca^2+ channels in the plasma membrane. Here we report that mice lacking Ins(1,4,5)P_3 3-kinase B (Itpkb), which converts Ins(1,4,5)P_3 to inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P_4), had impaired B lymphocyte development and defective Immunoglobulin G3 Antibody responses to a T lymphocyte–independent antigen. Itpkb-deficient B lymphocytes had the phenotypic and functional features of tolerant B lymphocytes and showed enhanced activity of store-operated Ca^2+ channels after B lymphocyte receptor stimulation, which was reversed by the provision of exogenous Ins(1,3,4,5)P_4. Our data identify Itpkb and its product Ins(1,3,4,5)P_4 as inhibitors of store-operated Ca^2+ channels and crucial regulators of B cell selection and activation.

  • Production of Ins(1,3,4,5)P4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation
    Nature Immunology, 2007
    Co-Authors: Andrew T Miller, Karsten Sauer, Mark L. Sandberg, Susan E. Sutton, Yina H. Huang, Mike Young, Michael P Cooke
    Abstract:

    Antigen receptor–mediated production of inositol-1,4,5-trisphosphate (Ins(1,4,5)P3) in lymphocytes triggers the release of Ca2+ from intracellular stores; this release of Ca2+ results in the opening of store-operated Ca2+ channels in the plasma membrane. Here we report that mice lacking Ins(1,4,5)P3 3-kinase B (Itpkb), which converts Ins(1,4,5)P3 to inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), had impaired B lymphocyte development and defective Immunoglobulin G3 Antibody responses to a T lymphocyte–independent antigen. Itpkb-deficient B lymphocytes had the phenotypic and functional features of tolerant B lymphocytes and showed enhanced activity of store-operated Ca2+ channels after B lymphocyte receptor stimulation, which was reversed by the provision of exogenous Ins(1,3,4,5)P4. Our data identify Itpkb and its product Ins(1,3,4,5)P4 as inhibitors of store-operated Ca2+ channels and crucial regulators of B cell selection and activation.

Karsten Sauer - One of the best experts on this subject based on the ideXlab platform.

  • Production of Ins(1,3,4,5)P_4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation
    Nature Immunology, 2007
    Co-Authors: Andrew T Miller, Mark Sandberg, Karsten Sauer, Michael Young, Yina H. Huang, Susan Sutton, Michael P Cooke
    Abstract:

    Antigen receptor–mediated production of inositol-1,4,5-trisphosphate (Ins(1,4,5)P_3) in lymphocytes triggers the release of Ca^2+ from intracellular stores; this release of Ca^2+ results in the opening of store-operated Ca^2+ channels in the plasma membrane. Here we report that mice lacking Ins(1,4,5)P_3 3-kinase B (Itpkb), which converts Ins(1,4,5)P_3 to inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P_4), had impaired B lymphocyte development and defective Immunoglobulin G3 Antibody responses to a T lymphocyte–independent antigen. Itpkb-deficient B lymphocytes had the phenotypic and functional features of tolerant B lymphocytes and showed enhanced activity of store-operated Ca^2+ channels after B lymphocyte receptor stimulation, which was reversed by the provision of exogenous Ins(1,3,4,5)P_4. Our data identify Itpkb and its product Ins(1,3,4,5)P_4 as inhibitors of store-operated Ca^2+ channels and crucial regulators of B cell selection and activation.

  • Production of Ins(1,3,4,5)P4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation
    Nature Immunology, 2007
    Co-Authors: Andrew T Miller, Karsten Sauer, Mark L. Sandberg, Susan E. Sutton, Yina H. Huang, Mike Young, Michael P Cooke
    Abstract:

    Antigen receptor–mediated production of inositol-1,4,5-trisphosphate (Ins(1,4,5)P3) in lymphocytes triggers the release of Ca2+ from intracellular stores; this release of Ca2+ results in the opening of store-operated Ca2+ channels in the plasma membrane. Here we report that mice lacking Ins(1,4,5)P3 3-kinase B (Itpkb), which converts Ins(1,4,5)P3 to inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), had impaired B lymphocyte development and defective Immunoglobulin G3 Antibody responses to a T lymphocyte–independent antigen. Itpkb-deficient B lymphocytes had the phenotypic and functional features of tolerant B lymphocytes and showed enhanced activity of store-operated Ca2+ channels after B lymphocyte receptor stimulation, which was reversed by the provision of exogenous Ins(1,3,4,5)P4. Our data identify Itpkb and its product Ins(1,3,4,5)P4 as inhibitors of store-operated Ca2+ channels and crucial regulators of B cell selection and activation.

Yina H. Huang - One of the best experts on this subject based on the ideXlab platform.

  • Production of Ins(1,3,4,5)P_4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation
    Nature Immunology, 2007
    Co-Authors: Andrew T Miller, Mark Sandberg, Karsten Sauer, Michael Young, Yina H. Huang, Susan Sutton, Michael P Cooke
    Abstract:

    Antigen receptor–mediated production of inositol-1,4,5-trisphosphate (Ins(1,4,5)P_3) in lymphocytes triggers the release of Ca^2+ from intracellular stores; this release of Ca^2+ results in the opening of store-operated Ca^2+ channels in the plasma membrane. Here we report that mice lacking Ins(1,4,5)P_3 3-kinase B (Itpkb), which converts Ins(1,4,5)P_3 to inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P_4), had impaired B lymphocyte development and defective Immunoglobulin G3 Antibody responses to a T lymphocyte–independent antigen. Itpkb-deficient B lymphocytes had the phenotypic and functional features of tolerant B lymphocytes and showed enhanced activity of store-operated Ca^2+ channels after B lymphocyte receptor stimulation, which was reversed by the provision of exogenous Ins(1,3,4,5)P_4. Our data identify Itpkb and its product Ins(1,3,4,5)P_4 as inhibitors of store-operated Ca^2+ channels and crucial regulators of B cell selection and activation.

  • Production of Ins(1,3,4,5)P4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation
    Nature Immunology, 2007
    Co-Authors: Andrew T Miller, Karsten Sauer, Mark L. Sandberg, Susan E. Sutton, Yina H. Huang, Mike Young, Michael P Cooke
    Abstract:

    Antigen receptor–mediated production of inositol-1,4,5-trisphosphate (Ins(1,4,5)P3) in lymphocytes triggers the release of Ca2+ from intracellular stores; this release of Ca2+ results in the opening of store-operated Ca2+ channels in the plasma membrane. Here we report that mice lacking Ins(1,4,5)P3 3-kinase B (Itpkb), which converts Ins(1,4,5)P3 to inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), had impaired B lymphocyte development and defective Immunoglobulin G3 Antibody responses to a T lymphocyte–independent antigen. Itpkb-deficient B lymphocytes had the phenotypic and functional features of tolerant B lymphocytes and showed enhanced activity of store-operated Ca2+ channels after B lymphocyte receptor stimulation, which was reversed by the provision of exogenous Ins(1,3,4,5)P4. Our data identify Itpkb and its product Ins(1,3,4,5)P4 as inhibitors of store-operated Ca2+ channels and crucial regulators of B cell selection and activation.

Mark L. Sandberg - One of the best experts on this subject based on the ideXlab platform.

  • Production of Ins(1,3,4,5)P4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation
    Nature Immunology, 2007
    Co-Authors: Andrew T Miller, Karsten Sauer, Mark L. Sandberg, Susan E. Sutton, Yina H. Huang, Mike Young, Michael P Cooke
    Abstract:

    Antigen receptor–mediated production of inositol-1,4,5-trisphosphate (Ins(1,4,5)P3) in lymphocytes triggers the release of Ca2+ from intracellular stores; this release of Ca2+ results in the opening of store-operated Ca2+ channels in the plasma membrane. Here we report that mice lacking Ins(1,4,5)P3 3-kinase B (Itpkb), which converts Ins(1,4,5)P3 to inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), had impaired B lymphocyte development and defective Immunoglobulin G3 Antibody responses to a T lymphocyte–independent antigen. Itpkb-deficient B lymphocytes had the phenotypic and functional features of tolerant B lymphocytes and showed enhanced activity of store-operated Ca2+ channels after B lymphocyte receptor stimulation, which was reversed by the provision of exogenous Ins(1,3,4,5)P4. Our data identify Itpkb and its product Ins(1,3,4,5)P4 as inhibitors of store-operated Ca2+ channels and crucial regulators of B cell selection and activation.