Sympathetic Nerve Cell

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 6 Experts worldwide ranked by ideXlab platform

Hanafusa Toshiaki - One of the best experts on this subject based on the ideXlab platform.

  • Biological roles of anti-GM1 antibodies in patients with Guillain–Barré syndrome for Nerve growth factor signaling
    Elsevier B.V., 2007
    Co-Authors: Tanaka Toshifumi, Furutama Daisuke, Sakai Reiko, Fujita Atsushi, Kimura Fumiharu, Tagami Muneyoshi, Ohsawa Nakaaki, Hanafusa Toshiaki
    Abstract:

    AbstractTo reveal the biological and pathological roles of anti-GM1 antibody in Guillain–Barré syndrome (GBS), we examined its effects on Nerve growth factor (NGF) induced TrkA autophosphorylation (NGF-TrkA signaling) in PC12 Cells, a Sympathetic Nerve Cell line. The NGF-TrkA signaling is enhanced by exogenous GM1 ganglioside and this phenomenon is regarded as one of the functional aspects of GM1. The IgGs purified from patients' sera inhibited the NGF-TrkA signaling in GM1 pre-incubated PC12 Cells. The degrees of inhibition by IgGs from patients paralleled their immunological reactivity to GM1. In addition, the IgGs also inhibited the neurite outgrowth of NGF-treated PC12 Cells. Immunoglobulins in the rabbit sera, which were immunized by GM1, also caused a similar suppressive phenomenon. These results suggested that the anti-GM1 antibody could play roles in pathophysiology in anti-GM1 antibody positive GBS through interfering with the neurotrophic action of NGF and GM1 mediated signal modulation including NGF-TrkA signaling. It is suggested that the modulation of GM1 function is one important action of antibodies and could be one of the important mechanisms in GBS

Tanaka Toshifumi - One of the best experts on this subject based on the ideXlab platform.

  • Biological roles of anti-GM1 antibodies in patients with Guillain–Barré syndrome for Nerve growth factor signaling
    Elsevier B.V., 2007
    Co-Authors: Tanaka Toshifumi, Furutama Daisuke, Sakai Reiko, Fujita Atsushi, Kimura Fumiharu, Tagami Muneyoshi, Ohsawa Nakaaki, Hanafusa Toshiaki
    Abstract:

    AbstractTo reveal the biological and pathological roles of anti-GM1 antibody in Guillain–Barré syndrome (GBS), we examined its effects on Nerve growth factor (NGF) induced TrkA autophosphorylation (NGF-TrkA signaling) in PC12 Cells, a Sympathetic Nerve Cell line. The NGF-TrkA signaling is enhanced by exogenous GM1 ganglioside and this phenomenon is regarded as one of the functional aspects of GM1. The IgGs purified from patients' sera inhibited the NGF-TrkA signaling in GM1 pre-incubated PC12 Cells. The degrees of inhibition by IgGs from patients paralleled their immunological reactivity to GM1. In addition, the IgGs also inhibited the neurite outgrowth of NGF-treated PC12 Cells. Immunoglobulins in the rabbit sera, which were immunized by GM1, also caused a similar suppressive phenomenon. These results suggested that the anti-GM1 antibody could play roles in pathophysiology in anti-GM1 antibody positive GBS through interfering with the neurotrophic action of NGF and GM1 mediated signal modulation including NGF-TrkA signaling. It is suggested that the modulation of GM1 function is one important action of antibodies and could be one of the important mechanisms in GBS

Furutama Daisuke - One of the best experts on this subject based on the ideXlab platform.

  • Biological roles of anti-GM1 antibodies in patients with Guillain–Barré syndrome for Nerve growth factor signaling
    Elsevier B.V., 2007
    Co-Authors: Tanaka Toshifumi, Furutama Daisuke, Sakai Reiko, Fujita Atsushi, Kimura Fumiharu, Tagami Muneyoshi, Ohsawa Nakaaki, Hanafusa Toshiaki
    Abstract:

    AbstractTo reveal the biological and pathological roles of anti-GM1 antibody in Guillain–Barré syndrome (GBS), we examined its effects on Nerve growth factor (NGF) induced TrkA autophosphorylation (NGF-TrkA signaling) in PC12 Cells, a Sympathetic Nerve Cell line. The NGF-TrkA signaling is enhanced by exogenous GM1 ganglioside and this phenomenon is regarded as one of the functional aspects of GM1. The IgGs purified from patients' sera inhibited the NGF-TrkA signaling in GM1 pre-incubated PC12 Cells. The degrees of inhibition by IgGs from patients paralleled their immunological reactivity to GM1. In addition, the IgGs also inhibited the neurite outgrowth of NGF-treated PC12 Cells. Immunoglobulins in the rabbit sera, which were immunized by GM1, also caused a similar suppressive phenomenon. These results suggested that the anti-GM1 antibody could play roles in pathophysiology in anti-GM1 antibody positive GBS through interfering with the neurotrophic action of NGF and GM1 mediated signal modulation including NGF-TrkA signaling. It is suggested that the modulation of GM1 function is one important action of antibodies and could be one of the important mechanisms in GBS

Sakai Reiko - One of the best experts on this subject based on the ideXlab platform.

  • Biological roles of anti-GM1 antibodies in patients with Guillain–Barré syndrome for Nerve growth factor signaling
    Elsevier B.V., 2007
    Co-Authors: Tanaka Toshifumi, Furutama Daisuke, Sakai Reiko, Fujita Atsushi, Kimura Fumiharu, Tagami Muneyoshi, Ohsawa Nakaaki, Hanafusa Toshiaki
    Abstract:

    AbstractTo reveal the biological and pathological roles of anti-GM1 antibody in Guillain–Barré syndrome (GBS), we examined its effects on Nerve growth factor (NGF) induced TrkA autophosphorylation (NGF-TrkA signaling) in PC12 Cells, a Sympathetic Nerve Cell line. The NGF-TrkA signaling is enhanced by exogenous GM1 ganglioside and this phenomenon is regarded as one of the functional aspects of GM1. The IgGs purified from patients' sera inhibited the NGF-TrkA signaling in GM1 pre-incubated PC12 Cells. The degrees of inhibition by IgGs from patients paralleled their immunological reactivity to GM1. In addition, the IgGs also inhibited the neurite outgrowth of NGF-treated PC12 Cells. Immunoglobulins in the rabbit sera, which were immunized by GM1, also caused a similar suppressive phenomenon. These results suggested that the anti-GM1 antibody could play roles in pathophysiology in anti-GM1 antibody positive GBS through interfering with the neurotrophic action of NGF and GM1 mediated signal modulation including NGF-TrkA signaling. It is suggested that the modulation of GM1 function is one important action of antibodies and could be one of the important mechanisms in GBS

Fujita Atsushi - One of the best experts on this subject based on the ideXlab platform.

  • Biological roles of anti-GM1 antibodies in patients with Guillain–Barré syndrome for Nerve growth factor signaling
    Elsevier B.V., 2007
    Co-Authors: Tanaka Toshifumi, Furutama Daisuke, Sakai Reiko, Fujita Atsushi, Kimura Fumiharu, Tagami Muneyoshi, Ohsawa Nakaaki, Hanafusa Toshiaki
    Abstract:

    AbstractTo reveal the biological and pathological roles of anti-GM1 antibody in Guillain–Barré syndrome (GBS), we examined its effects on Nerve growth factor (NGF) induced TrkA autophosphorylation (NGF-TrkA signaling) in PC12 Cells, a Sympathetic Nerve Cell line. The NGF-TrkA signaling is enhanced by exogenous GM1 ganglioside and this phenomenon is regarded as one of the functional aspects of GM1. The IgGs purified from patients' sera inhibited the NGF-TrkA signaling in GM1 pre-incubated PC12 Cells. The degrees of inhibition by IgGs from patients paralleled their immunological reactivity to GM1. In addition, the IgGs also inhibited the neurite outgrowth of NGF-treated PC12 Cells. Immunoglobulins in the rabbit sera, which were immunized by GM1, also caused a similar suppressive phenomenon. These results suggested that the anti-GM1 antibody could play roles in pathophysiology in anti-GM1 antibody positive GBS through interfering with the neurotrophic action of NGF and GM1 mediated signal modulation including NGF-TrkA signaling. It is suggested that the modulation of GM1 function is one important action of antibodies and could be one of the important mechanisms in GBS