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| | AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2 Basic information |
| | AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2 Chemical Properties |
| storage temp. | -20°C | | solubility | H2O: 1 mg/mL | | form | solid | | color | white | | Water Solubility | Soluble to 1 mg/ml in water |
| | AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2 Usage And Synthesis |
| Uses | Nogo-66(1-40) antagonist peptide has been used as a Nogo-66 receptor antagonist peptide:
- to study the preliminary therapeutic effect after inhibition of Nogo-A in the cauda equina compression (CEC) model
- to determine the effects of Nogo-A/NgR1 on autophagic activation
- to study its role in Nogo-B mediated axonal branching using Schwann cells and sensory neurons of mice
| | Biochem/physiol Actions | Myelin-derived axon outgrowth inhibitors, such as Nogo, may account for the lack of axonal regeneration in the central nervous system (CNS) after trauma in adult mammals. Nogo-66 can inhibit axonal outgrowth through an axonal Nogo-66 receptor (NgR). Competitive antagonists of NgR derived from amino-terminal peptide fragments of Nogo-66. The Nogo-66(1 40) antagonist peptide (NEP1 40) blocks Nogo-66 or CNS myelin inhibition of axonal outgrowth in vitro, demonstrating that NgR mediates a significant portion of axonal outgrowth inhibition by myelin. Intrathecal administration of NEP1 40 to rats with mid-thoracic spinal cord hemisection results in significant axon growth of the corticospinal tract, and improves functional recovery. Thus, Nogo-66 and NgR have central roles in limiting axonal regeneration after CNS injury, and NEP1-40 provides a potential therapeutic agent. | | storage | Store at -20°C |
| | AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2 Preparation Products And Raw materials |
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