AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2

AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2 구조식 이미지
카스 번호:
475221-20-6
상품명:
AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2
동의어(영문):
NEP1-40;NOGO-66 (1-40);PubChem ID: 90488731;Nogo Extracellular Peptide;M.W. 4625.11 C206H324N56O65;NOGO EXTRACELLULAR PEPTIDE, 1-40;NOGO-66 (1-40) ANTAGONIST PEPTIDE;NEP1-40; NOGO EXTRACELLULAR PEPTIDE; 1-40;AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2;ARG-ILE-TYR-LYS-GLY-VAL-ILE-GLN-ALA-ILE-GLN-LYS-SER-ASP-GLU-GLY-HIS-PRO-PHE-ARG-ALA-TYR-LEU-GLU-SER-GLU-VAL-ALA-ILE-SER-GLU-GLU-LEU-VAL-GLN-LYS-TYR-SER-ASN-SER-NH2
CBNumber:
CB5110481
분자식:
C206H324N56O65
포뮬러 무게:
4625.11
MOL 파일:
475221-20-6.mol

AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2 속성

저장 조건
-20°C
용해도
H2O: 1 mg/mL
물리적 상태
고체
물리적 상태
단단한 모양
색상
하얀색
수용성
Soluble to 1 mg/ml in water

안전

안전지침서 22-24/25
WGK 독일 3

AC-RIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNS-NH2 C화학적 특성, 용도, 생산

용도

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.

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