Protein Homer 1a

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J Yang - One of the best experts on this subject based on the ideXlab platform.

  • postsynaptic scaffold Protein Homer 1a protects against traumatic brain injury via regulating group i metabotropic glutamate receptors
    Cell Death and Disease, 2014
    Co-Authors: Tao Chen, Yongbo Zhao, Lijun Zhang, Yuefan Yang, Shuang Li, J Yang
    Abstract:

    Traumatic brain injury (TBI) produces excessive glutamate, leading to excitotoxicity via the activation of glutamate receptors. Postsynaptic density scaffold Proteins have crucial roles in mediating signal transduction from glutamate receptors to their downstream mediators. Therefore, studies on the mechanisms underlying regulation of excitotoxicity by scaffold Proteins can uncover new treatments for TBI. Here, we demonstrated that the postsynaptic scaffold Protein Homer 1a was neuroprotective against TBI in vitro and in vivo, and this neuroprotection was associated with its effects on group I metabotropic glutamate receptors (mGluRs). Upon further study, we found that Homer 1a mainly affected neuronal injury induced by mGluR1 activation after TBI and also influenced mGluR5 function when its activity was restored. The ability of Homer 1a to disrupt mGluR-ERK signaling contributed to its ability to regulate the functions of mGluR1 and mGluR5 after traumatic injury. Intracellular Ca2+ and PKC were two important factors involved in the mediation of mGluR-ERK signaling by Homer 1a. These results define Homer 1a as a novel endogenous neuroprotective agent against TBI.

Tao Chen - One of the best experts on this subject based on the ideXlab platform.

  • postsynaptic scaffold Protein Homer 1a protects against traumatic brain injury via regulating group i metabotropic glutamate receptors
    Cell Death and Disease, 2014
    Co-Authors: Tao Chen, Yongbo Zhao, Lijun Zhang, Yuefan Yang, Shuang Li, J Yang
    Abstract:

    Traumatic brain injury (TBI) produces excessive glutamate, leading to excitotoxicity via the activation of glutamate receptors. Postsynaptic density scaffold Proteins have crucial roles in mediating signal transduction from glutamate receptors to their downstream mediators. Therefore, studies on the mechanisms underlying regulation of excitotoxicity by scaffold Proteins can uncover new treatments for TBI. Here, we demonstrated that the postsynaptic scaffold Protein Homer 1a was neuroprotective against TBI in vitro and in vivo, and this neuroprotection was associated with its effects on group I metabotropic glutamate receptors (mGluRs). Upon further study, we found that Homer 1a mainly affected neuronal injury induced by mGluR1 activation after TBI and also influenced mGluR5 function when its activity was restored. The ability of Homer 1a to disrupt mGluR-ERK signaling contributed to its ability to regulate the functions of mGluR1 and mGluR5 after traumatic injury. Intracellular Ca2+ and PKC were two important factors involved in the mediation of mGluR-ERK signaling by Homer 1a. These results define Homer 1a as a novel endogenous neuroprotective agent against TBI.

Yongbo Zhao - One of the best experts on this subject based on the ideXlab platform.

  • postsynaptic scaffold Protein Homer 1a protects against traumatic brain injury via regulating group i metabotropic glutamate receptors
    Cell Death and Disease, 2014
    Co-Authors: Tao Chen, Yongbo Zhao, Lijun Zhang, Yuefan Yang, Shuang Li, J Yang
    Abstract:

    Traumatic brain injury (TBI) produces excessive glutamate, leading to excitotoxicity via the activation of glutamate receptors. Postsynaptic density scaffold Proteins have crucial roles in mediating signal transduction from glutamate receptors to their downstream mediators. Therefore, studies on the mechanisms underlying regulation of excitotoxicity by scaffold Proteins can uncover new treatments for TBI. Here, we demonstrated that the postsynaptic scaffold Protein Homer 1a was neuroprotective against TBI in vitro and in vivo, and this neuroprotection was associated with its effects on group I metabotropic glutamate receptors (mGluRs). Upon further study, we found that Homer 1a mainly affected neuronal injury induced by mGluR1 activation after TBI and also influenced mGluR5 function when its activity was restored. The ability of Homer 1a to disrupt mGluR-ERK signaling contributed to its ability to regulate the functions of mGluR1 and mGluR5 after traumatic injury. Intracellular Ca2+ and PKC were two important factors involved in the mediation of mGluR-ERK signaling by Homer 1a. These results define Homer 1a as a novel endogenous neuroprotective agent against TBI.

Lijun Zhang - One of the best experts on this subject based on the ideXlab platform.

  • postsynaptic scaffold Protein Homer 1a protects against traumatic brain injury via regulating group i metabotropic glutamate receptors
    Cell Death and Disease, 2014
    Co-Authors: Tao Chen, Yongbo Zhao, Lijun Zhang, Yuefan Yang, Shuang Li, J Yang
    Abstract:

    Traumatic brain injury (TBI) produces excessive glutamate, leading to excitotoxicity via the activation of glutamate receptors. Postsynaptic density scaffold Proteins have crucial roles in mediating signal transduction from glutamate receptors to their downstream mediators. Therefore, studies on the mechanisms underlying regulation of excitotoxicity by scaffold Proteins can uncover new treatments for TBI. Here, we demonstrated that the postsynaptic scaffold Protein Homer 1a was neuroprotective against TBI in vitro and in vivo, and this neuroprotection was associated with its effects on group I metabotropic glutamate receptors (mGluRs). Upon further study, we found that Homer 1a mainly affected neuronal injury induced by mGluR1 activation after TBI and also influenced mGluR5 function when its activity was restored. The ability of Homer 1a to disrupt mGluR-ERK signaling contributed to its ability to regulate the functions of mGluR1 and mGluR5 after traumatic injury. Intracellular Ca2+ and PKC were two important factors involved in the mediation of mGluR-ERK signaling by Homer 1a. These results define Homer 1a as a novel endogenous neuroprotective agent against TBI.

Yuefan Yang - One of the best experts on this subject based on the ideXlab platform.

  • postsynaptic scaffold Protein Homer 1a protects against traumatic brain injury via regulating group i metabotropic glutamate receptors
    Cell Death and Disease, 2014
    Co-Authors: Tao Chen, Yongbo Zhao, Lijun Zhang, Yuefan Yang, Shuang Li, J Yang
    Abstract:

    Traumatic brain injury (TBI) produces excessive glutamate, leading to excitotoxicity via the activation of glutamate receptors. Postsynaptic density scaffold Proteins have crucial roles in mediating signal transduction from glutamate receptors to their downstream mediators. Therefore, studies on the mechanisms underlying regulation of excitotoxicity by scaffold Proteins can uncover new treatments for TBI. Here, we demonstrated that the postsynaptic scaffold Protein Homer 1a was neuroprotective against TBI in vitro and in vivo, and this neuroprotection was associated with its effects on group I metabotropic glutamate receptors (mGluRs). Upon further study, we found that Homer 1a mainly affected neuronal injury induced by mGluR1 activation after TBI and also influenced mGluR5 function when its activity was restored. The ability of Homer 1a to disrupt mGluR-ERK signaling contributed to its ability to regulate the functions of mGluR1 and mGluR5 after traumatic injury. Intracellular Ca2+ and PKC were two important factors involved in the mediation of mGluR-ERK signaling by Homer 1a. These results define Homer 1a as a novel endogenous neuroprotective agent against TBI.