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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Amino Acid Sequence, Animals, Apoptosis, Arrestins, Cell Line, Tumor, Cytoprotection, Dopaminergic Neurons, Humans, MAP Kinase Kinase Kinase 5, Male, Mice, Mice, Inbred C57BL, Mitochondria, Mitogen-Activated Protein Kinase 10, Molecular Sequence Data, Parkinson Disease, Peptides, Protein Kinase Inhibitors, Protein Structure, Tertiary, Signal Transduction, beta-Arrestins.
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Does small peptide inhibitor of JNK3 protect dopaminergic neurons from MPTP induced injury via inhibiting the ASK1-JNK3 signaling pathway? Context: The ASK1-JNK3 signaling pathway plays a pivotal role in the pathogenesis of Parkinson's disease (PD). The specific binding of β-arrestin2 to JNK3 is essential for activation of the ASK1-JNK3 cascade, representing a potential therapeutic target for preventing dopaminergic neuronal death in PD. The aim of this study was to identify a novel strategy for the prevention of dopaminergic neuronal death in PD. Based on the specific binding of β-arrestin2 to JNK3, a 21-amino-acid fusion peptide, termed JNK3-N-Tat, was synthesized. We evaluated the ability of this peptide to inhibit the binding of β-arrestin2 to its target domain in JNK3 in vitro and in vivo. The JNK3-N-Tat peptide inhibited activation of the ASK1-JNK3 cascade by disrupting the interaction between β-arrestin2 and JNK3. JNK3-N-Tat exerted beneficial effects through pathways downstream of JNK3 and improved mitochondrial function, resulting in attenuated MPP+/MPTP-induced damage. JNK3-N-Tat protected mesencephalic dopaminergic neurons against MPTP-induced toxicity.
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JNK3-N-Tat, a JNK3-inhibitory peptide, protects dopaminergic neurons against MPP+/MPTP-induced injury by inhibiting the ASK1-JNK3 signaling pathway. Final Decision: yes