The Experts below are selected from a list of 15966 Experts worldwide ranked by ideXlab platform

Cott, Kevin Van - One of the best experts on this subject based on the ideXlab platform.

  • ENGINEERED Clostridium BOTULINUM Toxin ADAPTED TO DELIVER MOLECULES INTO SELECTED CELLS
    DigitalCommons@University of Nebraska - Lincoln, 2020
    Co-Authors: Pavlik, Benjamin J., Blum Paul, Cott, Kevin Van
    Abstract:

    An engineered payload-delivery system includes a target cell binding unit, covlently bound to a pore forming unit, and a payload portion adapted with a region capable of non-covalently binding to the pore forming unit. The pore forming unit is derived from a particular sub-serotype of Clostridium Toxin, while the payload region is derived from a different sub-serotype of Clostridium Toxin. The disclosed chimeri protein-based composition is capable of specifically delivering payload to neural cells

Pavlik, Benjamin J. - One of the best experts on this subject based on the ideXlab platform.

  • ENGINEERED Clostridium BOTULINUM Toxin ADAPTED TO DELIVER MOLECULES INTO SELECTED CELLS
    DigitalCommons@University of Nebraska - Lincoln, 2020
    Co-Authors: Pavlik, Benjamin J., Blum Paul, Cott, Kevin Van
    Abstract:

    An engineered payload-delivery system includes a target cell binding unit, covlently bound to a pore forming unit, and a payload portion adapted with a region capable of non-covalently binding to the pore forming unit. The pore forming unit is derived from a particular sub-serotype of Clostridium Toxin, while the payload region is derived from a different sub-serotype of Clostridium Toxin. The disclosed chimeri protein-based composition is capable of specifically delivering payload to neural cells

Blum Paul - One of the best experts on this subject based on the ideXlab platform.

  • ENGINEERED Clostridium BOTULINUM Toxin ADAPTED TO DELIVER MOLECULES INTO SELECTED CELLS
    DigitalCommons@University of Nebraska - Lincoln, 2020
    Co-Authors: Pavlik, Benjamin J., Blum Paul, Cott, Kevin Van
    Abstract:

    An engineered payload-delivery system includes a target cell binding unit, covlently bound to a pore forming unit, and a payload portion adapted with a region capable of non-covalently binding to the pore forming unit. The pore forming unit is derived from a particular sub-serotype of Clostridium Toxin, while the payload region is derived from a different sub-serotype of Clostridium Toxin. The disclosed chimeri protein-based composition is capable of specifically delivering payload to neural cells

Peter B Simpson - One of the best experts on this subject based on the ideXlab platform.

  • the jak3 inhibitor whi p154 prevents pdgf evoked process outgrowth in human neural precursor cells
    Journal of Neurochemistry, 2006
    Co-Authors: Gillian R Richards, Alison J Smith, P Cuddon, Q P, M Leveridge, Julie Kerby, H L Roderick, Martin D Bootman, Peter B Simpson
    Abstract:

    The prospect of manipulating endogenous neural stem cells to replace damaged tissue and correct functional deficits offers a novel mechanism for treating a variety of CNS disorders. The aim of this study was to investigate pathways controlling neurite outgrowth in human neural precursor cells, in particular in response to platelet-derived growth factor (PDGF). PDGF-AA, -AB and -BB were found to initiate calcium signalling and produce robust increases in neurite outgrowth. PDGF-induced outgrowth of Tuj1-positive precursors was abolished by the addition of EGTA, suggesting that calcium entry is a critical part of the signalling pathway. Wortmannin and PD098059 failed to inhibit PDGF-induced outgrowth. Clostridium Toxin B increased the amount of PDGF-induced neurite branching but had no effect on basal levels. In contrast, WHI-P154, an inhibitor of Janus protein tyrosine kinase (JAK3), Hck and Syk, prevented PDGF-induced neurite outgrowth. PDGF activates multiple signalling pathways with considerable potential for cross-talk. This study has highlighted the complexity of the pathways leading to neurite outgrowth in human neural precursors, and provided initial evidence to suggest that calcium entry is critical in producing the morphological changes observed.

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

  • the jak3 inhibitor whi p154 prevents pdgf evoked process outgrowth in human neural precursor cells
    Journal of Neurochemistry, 2006
    Co-Authors: Gillian R Richards, Alison J Smith, P Cuddon, Q P, M Leveridge, Julie Kerby, H L Roderick, Martin D Bootman, Peter B Simpson
    Abstract:

    The prospect of manipulating endogenous neural stem cells to replace damaged tissue and correct functional deficits offers a novel mechanism for treating a variety of CNS disorders. The aim of this study was to investigate pathways controlling neurite outgrowth in human neural precursor cells, in particular in response to platelet-derived growth factor (PDGF). PDGF-AA, -AB and -BB were found to initiate calcium signalling and produce robust increases in neurite outgrowth. PDGF-induced outgrowth of Tuj1-positive precursors was abolished by the addition of EGTA, suggesting that calcium entry is a critical part of the signalling pathway. Wortmannin and PD098059 failed to inhibit PDGF-induced outgrowth. Clostridium Toxin B increased the amount of PDGF-induced neurite branching but had no effect on basal levels. In contrast, WHI-P154, an inhibitor of Janus protein tyrosine kinase (JAK3), Hck and Syk, prevented PDGF-induced neurite outgrowth. PDGF activates multiple signalling pathways with considerable potential for cross-talk. This study has highlighted the complexity of the pathways leading to neurite outgrowth in human neural precursors, and provided initial evidence to suggest that calcium entry is critical in producing the morphological changes observed.