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Agonist

The Experts below are selected from a list of 321 Experts worldwide ranked by ideXlab platform

Nathanael Gray – 1st expert on this subject based on the ideXlab platform

  • Sphingosine 1-Phosphate (S1P) Receptor Subtypes S1P1and S1P3, Respectively, Regulate Lymphocyte Recirculation and Heart Rate
    Journal of Biological Chemistry, 2004
    Co-Authors: M. Germana Sanna, Jiayu Liao, Euijung Jo, Christopher Alfonso, Min Young Ahn, Melissa S. Peterson, Bill Webb, Sophie Lefebvre, Jerold Chun, Nathanael Gray

    Abstract:

    Sphingosine 1-phosphate (S1P) influences heart rate, coronary artery caliber, endothelial integrity, and lymphocyte recirculation through five related high affinity G-protein-coupled receptors. Inhibition of lymphocyte recirculation by non-selective S1P receptor Agonists produces clinical immunosuppression preventing transplant rejection but is associated with transient bradycardia. Understanding the contribution of individual receptors has been limited by the embryonic lethality of the S1P(1) knock-out and the unavailability of selective Agonists or antAgonists. A potent, S1P(1)-receptor selective Agonist structurally unrelated to S1P was found to activate multiple signals triggered by S1P, including guanosine 5′-3-O-(thio)triphosphate binding, calcium flux, Akt and ERK1/2 phosphorylation, and stimulation of migration of S1P(1)- but not S1P(3)-expressing cells in vitro. The Agonist also alters lymphocyte trafficking in vivo. Use of selective agonism together with deletant mice lacking S1P(3) receptor reveals that agonism of S1P(1) receptor alone is sufficient to control lymphocyte recirculation. Moreover, S1P(1) receptor Agonist plasma levels are causally associated with induction and maintenance of lymphopenia. S1P(3), and not S1P(1), is directly implicated in sinus bradycardia. The sustained bradycardia induced by S1P receptor non-selective immunosuppressive Agonists in wild-type mice is abolished in S1P(3)-/- mice, whereas S1P(1)-selective Agonist does not produce bradycardia. Separation of receptor subtype usage for control of lymphocyte recirculation and heart rate may allow the identification of selective immunosuppressive S1P(1) receptor Agonists with an enhanced therapeutic window. S1P(1)-selective Agonists will be of broad utility in understanding cell functions in vitro, and vascular physiology in vivo, and the success of the chemical approach for S1P(1) suggests that selective tools for the resolution of function across this broad lipid receptor family are now possible.

Jerold Chun – 2nd expert on this subject based on the ideXlab platform

  • sphingosine 1 phosphate s1p receptor subtypes s1p1 and s1p3 respectively regulate lymphocyte recirculation and heart rate
    Journal of Biological Chemistry, 2004
    Co-Authors: Germana M Sanna, Jiayu Liao, Euijung Jo, Christopher Alfonso, Melissa S. Peterson, Bill Webb, Sophie Lefebvre, Jerold Chun, Nathanael S Gray, Hugh Rosen

    Abstract:

    Abstract Sphingosine 1-phosphate (S1P) influences heart rate, coronary artery caliber, endothelial integrity, and lymphocyte recirculation through five related high affinity G-protein-coupled receptors. Inhibition of lymphocyte recirculation by non-selective S1P receptor Agonists produces clinical immunosuppression preventing transplant rejection but is associated with transient bradycardia. Understanding the contribution of individual receptors has been limited by the embryonic lethality of the S1P1 knock-out and the unavailability of selective Agonists or antAgonists. A potent, S1P1-receptor selective Agonist structurally unrelated to S1P was found to activate multiple signals triggered by S1P, including guanosine 5′-3-O-(thio)triphosphate binding, calcium flux, Akt and ERK1/2 phosphorylation, and stimulation of migration of S1P1- but not S1P3-expressing cells in vitro. The Agonist also alters lymphocyte trafficking in vivo. Use of selective agonism together with deletant mice lacking S1P3 receptor reveals that agonism of S1P1 receptor alone is sufficient to control lymphocyte recirculation. Moreover, S1P1 receptor Agonist plasma levels are causally associated with induction and maintenance of lymphopenia. S1P3, and not S1P1, is directly implicated in sinus bradycardia. The sustained bradycardia induced by S1P receptor non-selective immunosuppressive Agonists in wild-type mice is abolished in S1P3-/- mice, whereas S1P1-selective Agonist does not produce bradycardia. Separation of receptor subtype usage for control of lymphocyte recirculation and heart rate may allow the identification of selective immunosuppressive S1P1 receptor Agonists with an enhanced therapeutic window. S1P1-selective Agonists will be of broad utility in understanding cell functions in vitro, and vascular physiology in vivo, and the success of the chemical approach for S1P1 suggests that selective tools for the resolution of function across this broad lipid receptor family are now possible.

  • Sphingosine 1-Phosphate (S1P) Receptor Subtypes S1P1and S1P3, Respectively, Regulate Lymphocyte Recirculation and Heart Rate
    Journal of Biological Chemistry, 2004
    Co-Authors: M. Germana Sanna, Jiayu Liao, Euijung Jo, Christopher Alfonso, Min Young Ahn, Melissa S. Peterson, Bill Webb, Sophie Lefebvre, Jerold Chun, Nathanael Gray

    Abstract:

    Sphingosine 1-phosphate (S1P) influences heart rate, coronary artery caliber, endothelial integrity, and lymphocyte recirculation through five related high affinity G-protein-coupled receptors. Inhibition of lymphocyte recirculation by non-selective S1P receptor Agonists produces clinical immunosuppression preventing transplant rejection but is associated with transient bradycardia. Understanding the contribution of individual receptors has been limited by the embryonic lethality of the S1P(1) knock-out and the unavailability of selective Agonists or antAgonists. A potent, S1P(1)-receptor selective Agonist structurally unrelated to S1P was found to activate multiple signals triggered by S1P, including guanosine 5′-3-O-(thio)triphosphate binding, calcium flux, Akt and ERK1/2 phosphorylation, and stimulation of migration of S1P(1)- but not S1P(3)-expressing cells in vitro. The Agonist also alters lymphocyte trafficking in vivo. Use of selective agonism together with deletant mice lacking S1P(3) receptor reveals that agonism of S1P(1) receptor alone is sufficient to control lymphocyte recirculation. Moreover, S1P(1) receptor Agonist plasma levels are causally associated with induction and maintenance of lymphopenia. S1P(3), and not S1P(1), is directly implicated in sinus bradycardia. The sustained bradycardia induced by S1P receptor non-selective immunosuppressive Agonists in wild-type mice is abolished in S1P(3)-/- mice, whereas S1P(1)-selective Agonist does not produce bradycardia. Separation of receptor subtype usage for control of lymphocyte recirculation and heart rate may allow the identification of selective immunosuppressive S1P(1) receptor Agonists with an enhanced therapeutic window. S1P(1)-selective Agonists will be of broad utility in understanding cell functions in vitro, and vascular physiology in vivo, and the success of the chemical approach for S1P(1) suggests that selective tools for the resolution of function across this broad lipid receptor family are now possible.

Jiayu Liao – 3rd expert on this subject based on the ideXlab platform

  • sphingosine 1 phosphate s1p receptor subtypes s1p1 and s1p3 respectively regulate lymphocyte recirculation and heart rate
    Journal of Biological Chemistry, 2004
    Co-Authors: Germana M Sanna, Jiayu Liao, Euijung Jo, Christopher Alfonso, Melissa S. Peterson, Bill Webb, Sophie Lefebvre, Jerold Chun, Nathanael S Gray, Hugh Rosen

    Abstract:

    Abstract Sphingosine 1-phosphate (S1P) influences heart rate, coronary artery caliber, endothelial integrity, and lymphocyte recirculation through five related high affinity G-protein-coupled receptors. Inhibition of lymphocyte recirculation by non-selective S1P receptor Agonists produces clinical immunosuppression preventing transplant rejection but is associated with transient bradycardia. Understanding the contribution of individual receptors has been limited by the embryonic lethality of the S1P1 knock-out and the unavailability of selective Agonists or antAgonists. A potent, S1P1-receptor selective Agonist structurally unrelated to S1P was found to activate multiple signals triggered by S1P, including guanosine 5′-3-O-(thio)triphosphate binding, calcium flux, Akt and ERK1/2 phosphorylation, and stimulation of migration of S1P1- but not S1P3-expressing cells in vitro. The Agonist also alters lymphocyte trafficking in vivo. Use of selective agonism together with deletant mice lacking S1P3 receptor reveals that agonism of S1P1 receptor alone is sufficient to control lymphocyte recirculation. Moreover, S1P1 receptor Agonist plasma levels are causally associated with induction and maintenance of lymphopenia. S1P3, and not S1P1, is directly implicated in sinus bradycardia. The sustained bradycardia induced by S1P receptor non-selective immunosuppressive Agonists in wild-type mice is abolished in S1P3-/- mice, whereas S1P1-selective Agonist does not produce bradycardia. Separation of receptor subtype usage for control of lymphocyte recirculation and heart rate may allow the identification of selective immunosuppressive S1P1 receptor Agonists with an enhanced therapeutic window. S1P1-selective Agonists will be of broad utility in understanding cell functions in vitro, and vascular physiology in vivo, and the success of the chemical approach for S1P1 suggests that selective tools for the resolution of function across this broad lipid receptor family are now possible.

  • Sphingosine 1-Phosphate (S1P) Receptor Subtypes S1P1and S1P3, Respectively, Regulate Lymphocyte Recirculation and Heart Rate
    Journal of Biological Chemistry, 2004
    Co-Authors: M. Germana Sanna, Jiayu Liao, Euijung Jo, Christopher Alfonso, Min Young Ahn, Melissa S. Peterson, Bill Webb, Sophie Lefebvre, Jerold Chun, Nathanael Gray

    Abstract:

    Sphingosine 1-phosphate (S1P) influences heart rate, coronary artery caliber, endothelial integrity, and lymphocyte recirculation through five related high affinity G-protein-coupled receptors. Inhibition of lymphocyte recirculation by non-selective S1P receptor Agonists produces clinical immunosuppression preventing transplant rejection but is associated with transient bradycardia. Understanding the contribution of individual receptors has been limited by the embryonic lethality of the S1P(1) knock-out and the unavailability of selective Agonists or antAgonists. A potent, S1P(1)-receptor selective Agonist structurally unrelated to S1P was found to activate multiple signals triggered by S1P, including guanosine 5′-3-O-(thio)triphosphate binding, calcium flux, Akt and ERK1/2 phosphorylation, and stimulation of migration of S1P(1)- but not S1P(3)-expressing cells in vitro. The Agonist also alters lymphocyte trafficking in vivo. Use of selective agonism together with deletant mice lacking S1P(3) receptor reveals that agonism of S1P(1) receptor alone is sufficient to control lymphocyte recirculation. Moreover, S1P(1) receptor Agonist plasma levels are causally associated with induction and maintenance of lymphopenia. S1P(3), and not S1P(1), is directly implicated in sinus bradycardia. The sustained bradycardia induced by S1P receptor non-selective immunosuppressive Agonists in wild-type mice is abolished in S1P(3)-/- mice, whereas S1P(1)-selective Agonist does not produce bradycardia. Separation of receptor subtype usage for control of lymphocyte recirculation and heart rate may allow the identification of selective immunosuppressive S1P(1) receptor Agonists with an enhanced therapeutic window. S1P(1)-selective Agonists will be of broad utility in understanding cell functions in vitro, and vascular physiology in vivo, and the success of the chemical approach for S1P(1) suggests that selective tools for the resolution of function across this broad lipid receptor family are now possible.